Hormones and Heredity
by
J. T. Cunningham
Part 3 out of 4
above proposed, but it must be remembered that the ovum of Monotremes is
known to remain for a short period in the oviduct, or in other words to
pass through it very slowly, and to absorb fluid from its walls, as shown
by the considerable increase in size which the ovarian ovum undergoes
before it is laid. It would be interesting to know how long the
rudimentary corpus luteum persists in _Ornithorhynchus_: the period,
according to my views, should be very short. It is remarkable that in the
results quoted by Marshall a well-developed corpus luteum was found and
exclusively found in the lower Vertebrates which are viviparous. For
example, among fishes in the Elasmobranchs _Myliobatis_ and _Spinax_; in
Teleosteans, in _Zoarces_; in Reptiles, in _Anguis_ and _Seps_. Buehler on
the other hand, confirmed my own negative result with regard to oviparous
Teleosteans, and also found no hypertrophy of the follicle in Cyclostomes
which are also oviparous. In the viviparous forms mentioned there is yolk
in the ovum which is retained in oviduct or ovary, but additional
nutriment is also absorbed from the uterine or ovarian walls. In these
cases there is no placenta and generally no adhesion of ovum or embryo to
walls of oviduct or ovary. These facts alone would be sufficient to
disprove the theory that the corpora lutea are organs producing a
secretion whose function is to cause the attachment of the embryo to the
uterine mucosa. It is also, in my opinion, unreasonable to suppose that
the rudimentary corpora lutea of lower viviparous Vertebrates arose as a
mutation the result of which was to cause internal development of the
ovum. Habits might easily bring about retention of the fertilised ova for
gradually increasing periods, [Footnote: According to Geddes and Thomson
(_Evolution of Sex_, 1889), the common grass-snake has been induced under
artificial conditions to bring forth its young alive.] and the correlation
between the retained developing ova and the hypertrophy of the ruptured
follicles is comprehensible on my theory of the influence of substances
absorbed by the walls of oviduct or ovary from the developing ovum.
The case of _Dasyurus_, however, seems inconsistent with this argument,
for, as previously mentioned, Sandes found that in this Marsupial the
corpora lutea persisted during the greater part of the period of
lactation, which continues for four months after parturition. During the
whole of this time there are no embryos in the uteri, and therefore it
might be urged absorption of hormones from the embryos cannot be the cause
of the persistence of corpora lutea in pregnancy. But it seems to me that
a complete answer to this objection is supplied by the peculiar relations
of the embryos to the pouch in _Dasyurus_ and other Marsupials. The skin
of the pouch while the embryos are in it is very soft, congested, and
glandular; at the same time the embryos when transferred to the pouch at
parturition are very small, immature, and have a soft delicate skin. The
relation of embryos to pouch in _Dasyurus_, therefore, is closely similar
to that of embryos to uterus after the first few days of pregnancy in the
Eutheria. It is true there is no placenta, but the mouths of the embryos
are in very close contact with the teats, and both the skin of the embryos
and that of the pouch are soft and moist. If any special substances are
given off by the embryos in the uterus in ordinary gestation, the same
substances would continue to be given off by the embryos in the marsupial
pouch, and these must be absorbed by the skin of the pouch. In this way it
seems to me we have a logical explanation of the fact that the corpora
lutea in the Marsupial are not absorbed at parturition as in Eutheria. As
Sandes says the 'greater part of the period of lactation,' it would appear
that absorption of the corpora lutea takes place when the young _Dasyurus_
have grown to some size, become covered with hair, and are able to leave
the teats or even the pouch at will. Under these conditions it is obvious
that diffusion of chemical substances from the young through the walls of
the pouch would come to an end. It would be interesting in this connexion
to know more of the relation of egg and embryo to the pouch and to the
corpora lutea in _Echidna_. In _Ornithorhynchus_ the eggs are hatched in a
nest and there is no pouch.
On this view that the corpora lutea are the result, not the cause, of
intra-uterine gestation, it would no longer be possible to maintain the
theory that the corpus luteum in the human species is the cause by its
internal secretion of the phenomenon of menstruation. This was the theory
of Born and Fraenkel. [Footnote: See Biedl, _Internal Secretory Organs_
(Eng. trans.), 1912, p. 404.] Biedl's conclusion is that the periodic
development and disintegration of the uterine mucous membrane in the
menstrual cycle is due to the hormone of the interstitial cells of the
ovary. Leopold and Ravana found that ovulation as a rule coincides with
menstruation, but may take place at any time. Here, again, the problem
must be considered from the point of view of evolution. It can scarcely be
doubted that the thickening and growth of the mucous membrane in the
menstrual cycle is of the same nature as that which takes place in
pregnancy. When the ovum or ova are not fertilised the development comes
to an end after a certain time, differing in different species of Mammals,
and the membrane sloughs, returns to its original, state, and then begins
the same process of development again.
Menstruation, then, must be interpreted as an abortive parturition, both
in woman and lower Mammals, though in the latter it is not usually
accompanied by hemorrhage, and is called pro-oestrus. The question then to
be considered is, what determines parturition and menstruation? The
presence of the fertilised ovum must have been the original cause of the
hypertrophy of the uterine mucous membrane, and in its congenital or
hereditary development the chemical substances diffusing from the ova in
the uterus or even in the Fallopian tube may well be the stimulus starting
the hypertrophy. But what determines the end of the pregnancy? Is it
merely the increasing distension of the uterus by the developing foetus?
This could scarcely be the case in the Marsupials in which the foetus when
born is quite minute. Nor can we attribute parturition to renewed
ovulation, for this occurs in _Dasyurus_ only once a year. All we can
suggest at present is that a certain periodic development takes place by
heredity in presence of the hormones exuded by the fertilised ovum and the
embryo developed from it. When the ovum or ova, not being fertilised, die
the period of development is (usually) shortened and pro-oestrus or
menstruation occurs. In the dog, however, the period of the oestrus cycle
is about the as that of gestation--namely, six months.
The so-called descent of the testicles occurs exclusively in Mammals, in
which with a few important exceptions it is universal. This is a very
remarkable case of the change of position of an organ in the course of
development. The original position of the testis on either side is quite
similar to that of the same organ in birds or reptiles. The genital ridge
runs along the inner edge of the mesonephros, with which the testicular
tubules become connected. The testis, with the mesonephros, forming the
epididymis, closely attached to it, projects into the coelom, and without
losing its connexion with the peritoneum changes its position gradually
during development, passing backwards and downwards until it comes to lie
over the wall of the abdomen just in front of the pubic symphysis of the
pelvic girdle. There the abdominal wall on either side of the middle line
becomes thin and distended to form a pouch, the scrotal sac, into which
the testis passes, still remaining attached to the peritoneum which lines
the pouch, while the distal end of the vas deferens retains its original
connexion with the urethra. The movement of the testis can thus be
accurately described as a transposition or dislocation.
Various causes have been suggested for the formation of the scrotum, but
no one has ever been able to suggest a use for it. It has always been
quite impossible to bring it within the scope of the theory of natural
selection. The evolution of it can only be explained either on the theory
of mutation or some Lamarckian hypothesis. The process of dislocation of
the testis does not conform to the conception of mutation, nor agree with
other cases of that phenomenon. A mutation is a change of structure
affecting more or less the whole soma, but showing itself especially in
some particular organ or structure. But I know of no mutation occurring
under observation which consisted, not in a change of structure or
function, but merely in a change of position of an organ from one part of
the body to another, and moreover a change which takes place by a
continuous process in the course of development. If the testes were
developed from the beginning in a different part of the abdomen, there
might be some reason in calling the change a mutation. Moreover, if it is
a mutation, why has it never occurred in any other class of Vertebrates
except Mammals?
In 1903 Dr. W. Woodland published [Footnote: _Proc. Zool. Soc._, 1903,
Part 1.] a Lamarckian theory of this mammalian feature, the probability of
which it seems to me has been increased rather than decreased by the
progress of research concerning heredity and evolution since that date.
Dr. Woodland correlated the dislocation of the testes with the special
mechanical features of the mode of locomotion in Mammalia. His words are:
'The theory here advocated is to the effect that the descent of the testes
in the Mammalia has been produced by the action of mechanical strains
causing rupture of the mesorchial attachments, such strains being due to
the inertia of the organs reacting to the impulsiveness involved in the
activity of the animals composing the group.' The 'impulsiveness' is the
galloping or leaping movement which is characteristic of most Mammals when
moving at their utmost speed, as seen, for example, in horses, deer,
antelopes, dogs, wolves, and other Ungulata and Carnivora. It is obvious
that when the body is descending to the ground after being hurled upwards
and forwards, the abdominal organs have acquired a rapid movement
downwards and forwards; when the body reaches the ground its movement is
stopped suddenly, while the abdominal organs continue to move. The testes
therefore are violently jerked downwards away from their attachments and
at the same time forward. The check to the forward movement, however, is
momentary, while the body is immediately thrown again upwards and
forwards, which by the law of inertia means that the testes are thrown
still more downwards and backwards. There is no reason to suppose, as Dr.
Woodland suggests, that any rupture of the mesorchium was the usual result
of these strains, but a constant pull or tension was caused in the
direction in which the testes actually move during development. On this
theory we have to consider (1) how such strains could cause a shifting of
the peritoneal attachment, (2) why the testes should be supposed to be
particularly affected more than other abdominal organs. The answer to the
first question is that the strains would cause a growth of the connecting
membrane (mesorchium) at the posterior end, accompanied by an absorption
of it at the anterior end. The answer to the second question is that the
testes are at once the most compact and heaviest organs in the abdomen,
and at the same time the most loosely attached. The latter statement does
not apply to the mesonephros or epididymis which has moved with the
testis, but the latter cannot function without the former, and it may be
supposed that the close attachment of the epididymis to the testis had
come about in the early Mammalia before the change of position was
evolved.
It is evident that the violent shocks of the galloping or leaping movement
do not occur in Birds, Reptiles, or Amphibia. Ostriches run very fast and
do not fly, but their progression is a stride with each foot alternately,
not a gallop. The Anura among the Amphibia are saltatory, but their leaps
are usually single, or repeated only a few times, not sustained gallops.
The exceptions among the Mammalia still more tend to prove the close
correspondence between the 'impulsive' mode of progression and the
dislocation of the male gonads. In the Monotremata there is no scrotum,
the testes are in a position similar to that which obtains in Reptiles,
and they are the only Mammals in which these organs are anterior to the
kidneys. In locomotion they are sluggish, there is no running or galloping
among them. _Ornithorhynchus_ is aquatic in its habits, and _Echidna_ is
nocturnal and moves very slowly. In Marsupials the scrotum is in front of
the penis, but really in the same position as in other Mammals--that is,
in front of the ventral part of the pelvic girdle. It is the penis which
is different, as the skin around the organ has not united in a ventral
suture below it, while the organ itself has not grown forward adnate to
the abdominal skin as in most other Mammals. The scrotum is always
anterior to the origin of the penis, although in the Eutheria apparently
behind that organ. The larger Marsupials like the kangaroos are eminently
saltatory, and the others are active in locomotion. The aquatic Mammals
Sirenia and Cetacea have no scrotum, the testes being abdominal. It is
unnecessary to inquire whether this is the original position, or whether
they are descended from ancestors which had a scrotum: in either case the
position of the testes corresponds to the absence of what Dr. Woodland
calls impulsiveness in progression. The Fissipedia offer an instructive
example, for while the Otariidae have the hind feet turned forward and can
move on land somewhat like ordinary Mammals, the Phocidae cannot move
their hind legs independently or turn them forward, and can only drag
themselves about on land for short distances. In the former the testes are
situated in a well-defined scrotum, in the latter these organs are
abdominal. The Phocidae are probably descended from Mammals of the
terrestrial type with a scrotum, which has disappeared in the course of
evolution. Perhaps the most curious exception is that of the elephants, in
which the testes are abdominal. Here, in consequence of their structure
and massive shape, locomotion in usually a walk, and though they run
occasionally the gait is a trot, not a sustained gallop, and leaping is
out of the question. Sloths which hang from branches upside down have
abdominal testes, but even here they are in a posterior position, between,
the rectum and the bladder, so there has apparently been a degree of
dislocation, probably inherited from ancestors with more terrestrial
habits.
The fact that the ovaries do not occupy normally a position similar to
that of the testes is in accordance with the theory, for they are very
much smaller than the testes; and yet they have undergone some change of
position, for they are posterior to the kidneys.
The facts agree with the hormone theory, for it is to be noted that
although the development of the scrotum is confined to the males, the
'descent' or dislocation takes place in the foetus, and not at the period
of puberty. This is in accordance with the fact that the mechanical
conditions to which the change is attributed are not related to sexual
habits, but to the general habits of life which begin soon after birth.
The development, therefore, may be considered to be related to the
presence of a hormone derived from the normal testis, but not to a special
quantity or quality of hormone associated with maturity or the functional
activity of the organ. In Rodents, however, there is a difference in the
organs, not only at maturity, but in every rutting season, at any rate in
Muridae such as rats and others. In the rutting season the testes become
much larger and descend into the scrotal sacs, at other times of the year
being apparently more or less abdominal. In rabbits and hares, which have
a much more impulsive progression, the organs seem to be always in the
scrotal sacs.
It might be thought that in this case, although the hormone theory of
heredity might be applied, there was no reason to suppose that a hormone
derived from the testis in the individual development was necessary in
order that the hereditary change should take place. If the individual was
male and therefore had a testis, this organ would by heredity go through
the process of dislocation. But there is the curious fact that when the
descent is not normal and complete, in what is called cryptorchidism, the
organs are always sterile. The retention of the testes within the abdomen
may be regarded as a case of arrested development, like many other
abnormalities, but this does not explain why the retained testes should
always be sterile, without spermatogenesis. If the inherited or congenital
process of dislocation requires the presence of hormones produced by a
normal testis, then we can understand why a defective testis does not
descend completely, because it does not produce the hormone which is
necessary to stimulate the hereditary mechanism to complete dislocation.
It is often stated that in cryptorchidic individuals the sexual instincts
and somatic sexual characters are well developed, which would appear
contradictory to the above explanation, but according to Ancel and Bouin
such individuals in the case of the pig show considerable differences in
the secondary signs of sex and in the external genital organs, presenting
variations which lie between the normal and the castrated animal.
We have here, then, in the position of the testes in Mammalia a condition
which is not in the slightest degree 'adaptive' in the ordinary sense--
that is, fulfilling any special function or utility. The condition must be
regarded as distinctly disadvantageous, since the organs are more exposed
to injury, and the abdominal wall is weakened, as we know from the risk of
scrotal hernia in man. But from the Lamarckian point of view the facts
support the conclusion that the condition is the effect of certain
mechanical strains, and is of somatic origin, while the correlations here
reviewed are entirely unexplained by any theory of mutation or blastogenic
origin.
OPPOSING EVIDENCE
We have now to review certain cases which seem to support conclusions
contrary to those which we have maintained in the preceding pages, and to
consider the evidence which has been published in support of other
theories. It must be admitted that the occurrence of male secondary
characteristics on one side of the body, and female on the other, is in
consistent with the view that the development of such characters is due to
the stimulus of a hormone, since the idea of a hormone means something
which diffuses by way of the blood-vessels, lymph-vessels, and interstices
of the tissues, throughout the body, and the hormone theory of secondary
sexual characters assumes that these characters are potentially present by
heredity in both sexes. The occurrence of male somatic characters on one
side or in some part of the body and female on the other, usually
associated with the corresponding gonads, has been termed
gynandromorphism, and has long been known in insects. Cases of this
condition have been observed, though much more rarely, in Vertebrates. I
am not aware of any authentic instances in Mammals, and the supposition
that in stags reduction or abnormality of one antler may be the result of
removal or injury to the testis of one side, or the opposite, have been
completely disproved by experiments in which unilateral castration has
been carried out without any effect on the antlers at all. In birds,
however, a few cases have been recorded by competent observers with a
definiteness of detail which leaves no possibility of doubt. One of the
more recent of these is that of a pheasant of the white-ringed Formosan
variety, _P. torquatus_, of the Chinese pheasant. [Footnote: C. J. Bond,
'Unilateral Development of Secondary Male Characters in a Pheasant,'
_Journ. of Genetics_, vol. iii., 1914.] On the left side this bird shows
the plumage, colour, and the spur of the male; on the right leg there is
no spur except the small rudiment normally occurring in the hen. The
difference in plumage between the two sides, however, is not complete. The
white collar is strictly limited to the left side, but the iridescent blue
green of head and neck is present on both sides, though more marked on the
left. Only a few male feathers appear in the wing coverts of the left
side. The breast feathers are rufous, especially on the left side. The
tail coverts show marked male characters, more especially on the left
side. In the tail, however, the barred character of the male is not
present on one side, absent on the other, but in most of the feathers is
confined to one, the _outer_ side of each feather. With regard to the
gonads, in this bird a single organ was found on the left side, _i.e._ in
the position of the ovary in normal females, and there was no trace of a
gonad on the right side. The organ present was small, 3/4 inch long by 1/2
inch broad, and microscopic sections showed in one part actively growing
areas of tubular gland structure in some of which bodies like spermatozoa
could be detected, while in another were fibrous tissue with degenerating
cysts. The latter appear to have been degenerating egg follicles. The
author concludes that the organ was originally a functional ovary, and
that the ovarian portion had atrophied while a male portion had become
functionally active.
Another case in birds was described by Poll [Footnote: _B.B. Ges. Naturf.
Freunde_, Berlin, 1909.] and is mentioned by Doncaster. [Footnote:
_Determination of Sex_, Cambridge, 1914.] It is that of a Bullfinch
which had the male and female plumage sharply separated on the two sides
of the body. The right side of the ventral surface was red like a normal
male, the left side grey like a normal female. In this case there was a
testis on the right side, on the left an ovary as in normal females.
A third case in birds, somewhat different from the two first mentioned, is
that of a domestic fowl described by Shattock and Seligmann. [Footnote:
_Trans. Pathol. Soc._ (London), vol. 57, Part i., 1906.] It was a bird of
the Leghorn breed, two years old, and had the fully developed comb and
wattles of the cock. Each leg bore a thick blunt spur, nearly an inch in
length, but in the Leghorn breed spurs are by no means uncommon in hens of
mature age, before they have ceased to lay eggs. In plumage the characters
were mainly female. The colour being white could not show sexual
differences, the neck hackles were but moderately developed, saddle
hackles practically absent, the tail resembled that of the hen. There was
a fully developed oviduct on the left side, on the right another less than
half the full length. There was also a vas deferens on each side. There
was a gonad on each side, that of the right about one-fourth the size of
that on the left. In microscopic structure the right gonad resembled a
testis consisting entirely of tubuli lined by an epithelium consisting of
a single layer of cells. In one part of this organ the tubules were larger
than elsewhere, and one of them exhibited spermatogenesis in progress. The
left and larger gonad had a quite similar structure, but at its lower end
were found two ova enclosed within a follicular epithelium.
With regard to the last case it is to be remarked that though the gonad on
the right side was entirely male, there was no unilateral development of
male characters. With regard to the other two cases it must be pointed out
(1) that the difference between the two somatic sex-characters on the two
sides is chiefly a difference of colour, except the difference in the
spurs in Bond's pheasant; (2) that the evidence already cited shows that
in fowls castration does not prevent the development of the colour and
form of the male plumage, nor of the spurs: that in drakes, although
castration does not seem to have been carried out on young specimens
before the male plumage was developed, when performed on the mature bird
it prevents the eclipse, and does not cause the male to resemble the hen.
Castration, then, tends to prove that in Birds the development of the male
characters is not so closely dependent on the stimulation of testicular
hormone as in Mammals. The characters must therefore be developed by
heredity in the soma, which implies that the soma must itself be
differentiated in the two sexes. The development must therefore be more
in the nature of gametic coupling. It does not follow that the primary
sex-character or the somatic characters are exclusive in either sex.
We may suppose that the zygote contains both sexes, one or other of which
is dominant, and that dominance of one primary sex involves dominance of
the corresponding sexual characters. This does not, however, agree with
the result of removal of the ovaries in ducks, for this causes the
characters of the male to appear, so that the dominance of the female is
not a permanent condition of the soma but is dependent on the ovarian
hormone.
In the hermaphrodite individuals mentioned above the difference of
dominance is on two sides of the body instead of two different
individuals. It may also be remarked here that while it is very difficult
to believe that spurs were not due in evolution to the mechanical
stimulation of striking with the legs in combat, and while specially
enlarged feathers are erected in display, we cannot at present attribute
the varied and brilliant _colour_ of male birds to the direct influence of
external stimuli.
In Lepidoptera among insects the evidence concerning castration tends to
prove that hormones from the gonads play no part at all in the development
of somatic sexual characters. Kellog, an American zoologist, in 1905
[Footnote: _Journ. Exper. Zool._ (Baltimore), vol. i., 1905.] described
experiments in which he destroyed by means of a hot needle the gonads in
silkworm caterpillars (_Bombyx mori_), and found no difference in the
sexual characters of the moths reared from such caterpillars. Oudemans had
previously obtained the same result in the Gipsy Moth, _Limantria dispar_.
Meisenheimer [Footnote: _Experimentelle Studien zur Soma- und
Geschlechtedifferenzierung_. Jena, 1909.] made more extensive
experiments on castration of caterpillars in the last-mentioned species,
in which the male is dark in colour and has much-feathered antennae, while
the female is very pale and has antennae only slightly feathered. In the
moths developed from the castrated larvae there was no alteration in the
male characters, and in the females the only difference was that some of
them were slightly darker than the normal. Meisenheimer and Kopee after
him claim to have grafted ovaries into males and testes into females, with
the result that the transplanted organs remained alive and grew, and in
some cases at least became connected with the genital ducts. Even in these
cases the moth when developed showed the original characters of the sex to
which belonged the caterpillar from which it came, although it was
carrying a gonad of the opposite sex. It will be seen that these results
are the direct opposite of those obtained by Steinach on Mammals. We have
no evidence that the darker colour of the normal male in this case is
adaptive, or due to external stimuli, but the feathering of the antennae
is generally believed to constitute a greater development of the olfactory
sense organs, and is therefore adaptive, enabling the male to find the
female. This is therefore the kind of organ which would be expected to be
affected by hormones from the generative organs. It is stated that the
sexual instincts were also unaltered, a male containing ovaries instead of
testes readily copulating with a normal female.
These results, almost incredible as they appear, are in harmony with the
relatively frequent occurrence of gynandromorphism in insects.[Footnote:
See Doncaster, _Determination of Sex_ (Camb. Univ. Press, 1914), chap.
ix.] One of the most remarkable cases of this is that of an ant
(_Myrmica scabrinodis_) the left half of which is male, the right half not
merely female, but worker--that is, sterile female, without wing. Cases in
Lepidoptera, _e.g. Amphidasys betularia_, have frequently been recorded.
Presumably not only the antennae and markings, but also the genital
appendages and the gonads themselves, are male and female on the two
sides. On the view that both sexes and the somatic sex-characters of both
sexes are present in each zygote, and that the actual sex is due to
dominance, we must conclude that the male primary and secondary characters
are dominant on one side, and the female on the other, and it is evident
that hormones diffusing throughout the body cannot determine the
development of somatic sexual characters here. Various attempts have been
made to explain gynandromorphism in insects in accordance with the
chromosome theory of sex-determination. These are discussed by Doncaster
in the volume already cited, but from the point of view of the present
work the important question is that concerning the somatic sex-characters.
According to Doncaster it has been found that in some Lepidoptera the
different sex-chromosomes occur in the female, not in the male as in other
insects. Half the eggs, therefore, contain an X chromosome, and half a Y,
while all the sperms contain an X chromosome. Doncaster has seen in
_Abraxas grossulariata_ ova with two nuclei both undergoing maturation.
If one of these in reduction expelled a Y chromosome, the other an X,
then one would retain an X and the other a Y. Each was fertilised by a
sperm, one becoming therefore XX or male and the other XY or female. It
may be supposed that as there was only the cytoplasm of one ovum, each
nucleus would determine the characters of half the individual developed.
The question remains, therefore, where are the factors of the somatic
sex-characters? One suggestion which might be made is that the female
characters are present in the _Y_, in this case female producing
chromosome, or, if the female characters are merely negative, that the
male characters are in the _X_ chromosome, but only show themselves in the
homozygous condition, thus:--
FEMALE x MALE
XY XX
| \/ |
| /\ |
XX YX
MALE FEMALE
The male characters in the male, _XX_, would appear because present in two
chromosomes, but would be recessive in the female because present only in
one chromosome. The validity of this scheme, however, is disproved by the
fact that males can transmit the female characters of their race, as in
the case mentioned by Doncaster where a male _Nyssia zonaria_ when crossed
transmits the wingless character of its own female.
Another, perhaps better, suggestion is that the somatic characters of both
sexes are present in each. Then as each somatic cell is descended without
segregation from the fertilised ovum, we may suppose that the presence of
the sex-chromosomes in the somatic cells themselves in some way determines
whether male or female characters shall develop, without the aid of any
hormones from the gonads. This theory would be quite compatible with
the belief that adaptive somatic sex-characters may be due to external
stimulation, for supposing that the hypertrophy or modification is
conveyed to the determinants in the gametocytes, and was confined to
one sex, _e.g._ the male, then these determinants would be modified in
association with the sex-chromosomes of that sex, and thus though
after reduction and fertilisation they would be present in the female
zygote also, they would not develop in that sex. Thus supposing _M_ to
represent a modification acquired in the male and _m_ the absence of
the modification, such as the feathered antenna of a moth, and the
sex-chromosomes to be _X_ and _Y_, then we should have in the
gametocytes--
Male Female
_MM mm_
_XX XY_
Gametes _MX, MX: mXmY_
Zygotes _MmXX male, MmXY female_,
and the character _M_ would only appear in the male because it only
develops in association with _XX_ in the somatic cells descended from the
male zygote. This would be the result in the first generation in which a
somatic modification affected the factors in the chromosomes. In the next
generation _m_ in the male would be affected, and the male for the sake of
simplicity might be supposed to become _MMXX_. When the female gametes
segregated, some would always be _mY_, and some zygotes therefore _MXmY_.
Others might be _MMXY_. On this theory, therefore, there would always be
some females heterozygous for the male character.
Geoffrey Smith, one of the many promising young scientific investigators
whose careers were cut short in the War, maintained views concerning
somatic sex-characters different from that which explains their
development as due to a hormone from the testis or ovary. Nussbaum in 1905
[Footnote: 'Ergebuisse der Anat. und Entwicklungsgesch.,' Bd. xv.;
_Pflügers Archiv_, Bd. cxxvi, 1909.] had recorded experiments on _Rana
fusca_ (which is identical with the British species commonly called _R.
temporaria_) which appeared to prove that in the male frog after
castration the annual development of the thumb-pad and the muscles of the
fore-leg does not take place, and if these organs have begun to enlarge
before castration they atrophy again. When pieces of testis were
introduced into the dorsal lymph-sac of a castrated frog the thumb-pads
and muscles developed as in a normal frog. Geoffrey Smith and Edgar
Schuster [Footnote: _Quart Journ. Mic. Sci_., lvii, 1911-12.] investigated
the subject again with results contrary to those of Nussbaum.
Smith and Schuster begin by describing the normal cycle of changes in the
testes on the one hand and the thumb-pad on the other. After the discharge
of the spermatozoa in March or April the testes are at their smallest
size. From this time onwards till August they steadily increase in size,
attaining their maximum at the beginning of September. From then till the
breeding season no increase in size or alteration of cellular structure
occurs, the testes apparently remaining in a state of complete inactivity
during this period. With regard to internal development, after the
discharge of spermatozoa in the breeding season the spermatogonia divide
and proliferate, forming groups of cells known as spermatocysts. In June
and July spermatogenesis is active, and from August to October the
formation of ripe spermatozoa is completed.
The corresponding changes in the thumb-pads are as follows. Immediately
after the breeding season the horny epidermis of the pad with its deeply
pigmented papillae is cast off, and the thumb remains comparatively smooth
from April or May until August or September. When the large papillae are
shed, smaller papillae remain beneath, and are gradually obliterated by
the epidermis growing up between them. The epidermis is therefore growing
while the spermatogenesis is taking place. In August and September the
epidermic papillae begin to be obvious, and from this time till February a
continuous increase in the papillae and their pigmentation occur. Geoffrey
Smith argues that the development of this somatic character occurs while
the testes are inactive and unchanged. Considering that the testes
throughout the winter months are crammed with spermatozoa, which must
require some nourishment, and which may be giving off a hormone all the
time, the argument has very little weight. Smith and Schuster found that
ovariotomy, with or without subsequent implantation of testes or injection
of testis extract, had no effect in causing the thumb of the female to
assume any male characters.
Castration during the breeding season causes the external pigmented
layer with its papillae to be cast off very soon--that is to say, it
has the same effect as the normal discharge of the spermatozoa. Smith
and Schuster found that castration at other seasons caused the pad to
remain in the condition in which it was at the time, that there was no
reduction or absorption as Nussbaum and Meisenheimer found, and that
allo-transplantation of testes--that is, the introduction of testes from
other frogs either into the dorsal lymph-sacs or into the abdominal
cavity--or the injection of testis extract, had no effect in causing
growth or development of the thumb-pad.
There seems to be one defect in the papers of both Nussbaum and Smith and
Schuster--namely, that neither of them mentions or apparently appreciates
the fact that the thumb-pads, apart from the dermal glands, consist of
horny epidermis developed from the living epidermis beneath. The horny
layer is not shown clearly in the figures of Smith and Schuster. It seems
impossible that the horny layer or its papillae could atrophy in
consequence of castration, or be absorbed. The horny part of the frog's
thumb-pad is comparable with the horny sheath of the horns in the
mammalian Prong-buck (_Antilocapra_) which are shed after the breeding
season and annually redeveloped. Meisenheimer claims that he produced
development of papillae on the thumb-pad, not only by implantation of
pieces of testis, but also by implantation of pieces of ovary. This seems
so very improbable that it suggests a doubt whether the same investigator
was not mistaken with regard to the results of his experiments in
transplanting gonads in Moths.
Smith and Schuster conclude that the normal development of the thumb-pad
depends on the presence of normal testes, but that there is no sufficient
evidence that the effect is due to a hormone derived from the testis. It
is equally probable, according to Smith, that the testicular cells take up
some substance or substances from the blood, thus altering the composition
of the latter and perhaps stimulating the production of these substances
in some other organ of the body. These substances may be provisionally
called sexual formative substances. Smith's theory therefore is that the
action of the testes in metabolism is rather to take something from the
blood than to add something to it, and that it is this subtractive effect
which influences the development of somatic sexual organs.
Geoffrey Smith in fact, in the paper above considered, attempts to apply
to the frog the views he put forward [Footnote: _Fauna und Flora des
Golfes van Neapel_, 29 Monographie Rhizocephala.] in relation to the
effect of the parasite _Sacculina_ on the sexual organs of crabs. The
species in which he made the most complete investigation of the influence
of the parasite was _Inachus scorpio_ (or _dorsettensis_). Figures showing
the changes in the abdomen produced by the presence of _Sacculina_ are
given in Doncaster's _Determination of Sex_, Pl. xv. _Sacculina_ is one of
the Cirripedia, and therefore allied to the Barnacles. It penetrates into
the crab in its larval stage, and passes entirely into the crab's body,
where it develops a system of branching root-like processes. When mature
the body of the _Sacculina_ containing its generative organs forms a
projection at the base of the abdomen of the crab on its ventral surface,
and after this is formed the crab does not moult. Crabs so affected do not
show the usual somatic sexual characters, and at one time it was supposed
that only females were attacked. It is now known that both sexes of the
host may be infected by the parasite, but the presence of the latter
causes suppression of the somatic sex-differences. The entry of the
parasite is effected when the crab is young and small, before the somatic
sex-characters are fully developed. The gonads are not actually
penetrated, at least in some cases, by the fibrous processes of the
parasite, but nevertheless they are atrophied and almost disappear. In
_Inachus_ the abdomen of the normal male is very narrow and has no
appendages except two pairs of copulatory styles. The abdomen of the
female is very broad, and has four pairs of biramous appendages covered
with hairs, the normal function of which is to carry the eggs. The effect
of the parasite in the male is that the abdomen is broader, the copulatory
styles reduced, and biramous hairy appendages are developed similar to
those of the female, but smaller. In the female the abdomen remains broad,
but the appendages are much smaller than in the normal female, about equal
in size to those of the 'sacculinised' male. Smith interpreted the
alteration in the male as a development of female secondary characters,
but it is obvious from the condition in Macrura or tailed Decapods, like
the lobster or crayfish, that the abdomen or tail of the male originally
carried appendages similar to those of the female, and that the male
character is a loss of these appendages. The absence of the male character
therefore necessarily involves a development of these appendages, and
there is not much more reason for saying that the male under the influence
of the parasite develops female characters, than for saying that the male
character is absent. There is no evidence in the facts concerning
parasitic castration for Geoffrey Smith's conclusion that the female
characters are latent in the male, but the male characters not latent in
the female: both return to a condition in which they resemble each other,
and the primitive form from which they were differentiated.
By his studies of parasitic castration Geoffrey Smith was led to formulate
a theory for the explanation of somatic sex-characters different from that
of hormones. He found that in the normal female crab the blood contained
fatty substances which were absorbed by the ovaries for the production of
the yolk of the ova. When _Sacculina_ is present these substances are
absorbed by the parasite; the ovary is deprived of them, and therefore
atrophies. In the male the parasite requires similar substances, and its
demand on the blood of the host stimulates the secretion of such
substances, so that the whole metabolism is altered and assimilated to
that of the female. It is this physiological change which causes the
development of female secondary characters. He describes this change as
the production of a hermaphrodite sexual formative substance, on the
ground that in at least one case eggs were found in the testis of a male
_Inachus_ which had been the host of a _Sacculina_, but had recovered. It
must however be noted that the _Sacculina_ itself is hermaphrodite, with
ovaries much larger than the testes. It is possible that while the
parasite prevents the development of testis or ovary in the host, it gives
up to the body of the host a hormone from its own ovaries which tends to
develop the female secondary characters: for the parasite is itself a
Crustacean, and therefore the hormone from its ovaries would not be of too
different a nature to act upon the tissues of the host.
The observation of Geoffrey Smith that eggs may occur in the testis of a
crab after recovery from the parasite appears of more importance than his
peculiar theoretical suggestions, for it tends to show that sex is not
always unalterably fixed at fertilisation. In this case the influence of a
parasite predominantly female would seem to be the real cause of the
development of eggs in the testis of the host. Geoffrey Smith does not
discuss the origin of the somatic sexual characters in evolution, or
attempt to show how his theories of sexual formative substance, and of the
influence of the gonads by subtraction rather than addition, would bear
upon the problem.
CHAPTER VI
Origin Of Non-Sexual Characters: The Phenomena Of Mutation
According to the theory here advocated, modifications produced by external
stimuli in the soma will also be inherited in some slight degree in each
generation when they have no relation to sex or reproduction. In this case
the habits and the stimuli which they involve will be common to both
sexes, and the hormones given off by the hypertrophied tissues will act
upon the corresponding determinants in the gametocytes. The modifications
thus produced will therefore be related to habits, and the theory will
include all adaptations of structure to function, but other characters may
also be included which are the result of stimuli and yet have no function
or utility.
The majority of evolutionists in recent years have taught that influences
exerted through the soma have no effect on the determinants in the
chromosomes of the gametes, that all hereditary variations are gametogenic
and none somatogenic. Mendelians believe that evolution has been due to
the appearance of characters or factors of the same kind as those which
distinguish varieties in cultivated organisms, and which are the subject
of their experiments, but they have found a difficulty, as already
mentioned in Chapter II, in forming any idea of the origin of a new
dominant character. A recessive character is the absence of some positive
character, and if in the cell-divisions of gametogenesis the factor for
the positive character passes wholly into one cell, the other will be
without it, will not 'carry' that factor. If such a gamete is fertilised
by a normal gamete the organism developed from the zygote will be
heterozygous, and segregation will take place in its gametes between the
chromosome carrying the factor and the other without it, so that there
will now be many gametes destitute of the factor in question. When two
such gametes unite in fertilisation the resulting organism will be a
homozygous recessive, and the corresponding character will be absent. In
this way we can conceive the origin of albino individuals from a coloured
race, supposing the colour was due to a single factor.
In Bateson's opinion the origin of a new dominant is a much more difficult
problem. In 1913 he discussed the question in his Silliman Lectures.
[Footnote: _Problems of Genetics_, Oxford Univ. Press, 1913.] He considers
the difficulty is equally hopeless whether we imagine the dominants to be
due to some change internal to the organism or to the assumption of
something from without. Accounts of the origin of new dominants under
observation in plants usually prove to be open to the suspicion that the
plant was introduced by some accident, or that it arose from a previous
cross, or that it was due to the meeting of complementary factors. In
medical literature, however, there are numerous records of the spontaneous
origin of various abnormalities which behave as dominants, such as
brachydactyly, and Bateson considers the authenticity of some of these to
be beyond doubt. He concludes that it is impossible in the present state
of knowledge to offer any explanation of the origin of dominant
characters. In a note, however, he suggests the possibility that there are
no such things as new dominants. Factors have been discovered which simply
inhibit or prevent the development of other characters. For example, the
white of the plumage in the White Leghorn fowl is due to an inhibiting
factor which prevents the development of the colour factor which is also
present. Withdraw the dominant inhibiting factor, and the colour shows
itself. This is shown by crossing the dominant white with a recessive
white, when some birds of the F(2) generation are coloured.[Footnote:
Bateson, _Principles of Heredity_, p. 104.] Similarly, brachydactyly in
man may be due to the loss of an inhibiting factor which prevents it
appearing in normal persons. It is evident, however, that it is difficult
to apply this suggestion to all cases. For example, the White Leghorn fowl
must have descended from a coloured form, probably from the wild species
_Gallus bankiva_. If Bateson's suggestion were valid we should have to
suppose that the loss of the factor for colour caused the dominant white
to appear, and then when this is withdrawn colour appears again, so that
the colour factors and the inhibiting factors must lie over one another in
a kind of stratified alternation. And then how should we account for the
recessive white?
In his Presidential Address to the meeting of the British Association in
Australia, 1914, Bateson explains his suggestion somewhat more fully with
a command of language which is scarcely less remarkable than the subject
matter. The more true-breeding forms are studied the more difficult it is
to understand how they can vary, how a variation can arise. When two forms
of _Antirrhinum_ are crossed there is in the second generation such a
profusion of different combinations of the factors in the two
grandparents, that Lotsy has suggested that all variations may be due to
crossing. Bateson does not agree with this. He believes that genetic
factors are not permanent and indestructible, but may undergo quantitative
disintegration or fractionation, producing subtraction or reduction
stages, as in the Picotee Sweet Pea, or the Dutch Rabbit. Also variation
may take place by loss of factors as in the origin of the white Sweet Pea
from the coloured. But regarding a factor as something which, although it
may be divided, neither grows nor dwindles, neither develops nor decays,
the Mendelian cannot conceive its beginning any more than we can conceive
the creation of something out of nothing. Bateson asks us to consider
therefore whether all the divers types of life may not have been produced
by the gradual unpacking of an original complexity in the primordial,
probably unicellular forms, from which existing species and varieties have
descended. Such a suggestion in the present writer's opinion is in one
sense a truism and in another an absurdity. That the potentiality of all
the characters of all the forms that have existed, pterodactyls,
dinosaurs, butterflies, birds, etc. etc., including the characters of all
the varieties of the human race and of human individuals, must have been
present in the primordial ancestral protoplasm, is a truism, for if the
possibility of such evolution did not exist, evolution would not have
taken place. But that every distinct hereditary character of man was
actually present as a Mendelian factor in the ancestral _Amoeba_, and that
man is merely a group of the whole complex of characters allowed to
produce real effects by the removal of a host of inhibiting factors, is
incredible. The truth is that biological processes are not within our
powers of conception as those of physics and chemistry are, and Bateson's
hypothesis is nothing but the old theory of preformation in ontogeny. Just
as the old embryologists conceived the adult individual to be contained
with all its organs to the most minute details within the protoplasm of
the fertilised ovum or one of the gametes, so the modern Mendelian,
because he is unable to conceive or to obtain the evidence of the gradual
development of a hereditary factor, conceives all the hereditary factors
of the whole animal kingdom packed in infinite complexity within the
protoplasm of the primordial living cells. That man is complex and
_Amoeba_ simple is merely a delusion; the truth according to Mendelism is
that man is merely a fragment of the complexity of the original _Amoeba_.
Mendelism studies especially the heredity of characters, and only
incidentally deals with recorded instances of the appearance of new forms,
such as the origin of a salmon-coloured variety of _Primula_ from a
crimson variety. The occurrence of new characters, or mutations as they
are called, has been specially studied by other investigators, and I
propose briefly to consider the two most important examples of such
research, namely, that by Professor T. H. Morgan, which deals with the
American fruit-fly _Drosophla_, and the other which concerns the mutations
of the genus of plants OEnothera, exemplified by our well-known Evening
Primrose.
Professor T. H. Morgan informs us [Footnote: _A Critique of the Theory of
Evolution_ (Oxford Univ. Press, 1916), p. 60] that within five or six
years in laboratory cultures of the fruit-fly, _Drosophila ampelophila_,
arose over a hundred and twenty-five new types whose origin was completely
known. The first of these which he mentions is that of eye colour,
differing in the two sexes, in the female dark eosin, in the male
yellowish eosin. Another mutation was a change of the third segment of the
thorax into a segment similar to the second. Normally the third segment
bears minute appendages which are the vestiges of the second pair of
wings; in the mutant the wings of the third segment are true wings though
imperfectly developed. A factor has also occurred which causes duplication
of the legs. Another mutation is loss of the eyes, but in different
individuals pieces of the eye may be present, and the variation is so wide
that it ranges from eyes which until carefully examined appear normal, to
the total absence of eyes. Wingless flies also arose by a single mutation.
These were found on mating with normal specimens to be all recessive
characters, thus agreeing with Bateson's views. The next one described is
dominant. A single male appeared with a narrow vertical red bar instead of
the broad red normal eye. When this male was bred with normal females all
the eyes of the offspring were narrower than the normal eye, though not so
narrow as in the abnormal male parent. It may be pointed out that this is
scarcely a sufficient proof of dominance. If the mutation were due to the
loss of one factor affecting the eye, the heterozygote carrying the normal
factor from the mother only might very well develop a somewhat imperfect
eye.
Morgan arranges the numerous mutations observed in _Drosophila_ in four
groups, corresponding in his opinion to the four pairs of chromosomes
occurring in the cells of the insect. After the meiotic or reduction
divisions each gamete of course contains in its nucleus four single
chromosomes. One of the four pairs consists of the sex-chromosomes. All
the factors of one group are contained in one chromosome, and it is found
in experiments that the members of each group tend to be inherited
together--that is to say, if two or more enter a cross together, in other
words, if a specimen possessing two or more mutations is crossed with
another in which they are absent, they tend to segregate as though they
were a single factor. This fact agrees with the hypothesis that the
factors in such a case are contained in a single chromosome which
segregates from the fellow of its pair in the reduction divisions.
Exceptions may occur, however, and these are explained by what is called
'crossing over.' When one chromosome of a pair, instead of being parallel
to the other in the gametocyte, crosses it at a point of contact, then
when the chromosomes separate, part of one chromosome remains connected
with the part of the other on the same side and the two parts separate as
a new chromosome, so that two factors originally in the same chromosome
may thus come to lie in different chromosomes. In consequence of this, two
or more factors which are usually 'coupled' or inherited together may come
to appear in different individuals.
Morgan emphasises the statement that a factor does not affect only one
particular organ or part of the body. It may have a chief effect in one
kind of organ, _e.g._ the wings or eyes, but usually affects several parts
of the body. Thus the factor that causes rudimentary wings also produces
sterility in females, general loss of vigour, and short hind legs.
The facts to which I shall refer concerning _Oenothera_ are for the most
part quoted on the authority of Dr. Ruggles Gates, and taken from his book
_The Mutation Factor in Evolution_ (London, 1915). The occurrence of
mutations in _Oenothera_ was first noticed by De Vries, the Dutch
botanist, in the neighbourhood of Amsterdam in 1886. He found a large
number of specimens of _Oenothera Lamarckiana_ growing in an abandoned
potato-field at Hilversum, and these plants showed an unusual amount of
variation. He transplanted nine young plants to the Botanic Garden of
Amsterdam, and cultivated them and their descendants for seven generations
in one experiment. Similar experiments have been made by himself and
others. The large majority of the plants produced from the _Oe.
Lamarckiana_ by self-fertilisation were of the same form with the same
characters, but a certain percentage presented 'mutations'--that is,
characters different from the parent form, and in some cases identical
with those of plants occurring occasionally among those growing wild in
the field where the observations began. Nine of these mutants have been
recognised and defined, and distinguished by different names. The
characters are precisely described and in many cases figured by Gates in
the volume cited above. The first mutant to be recognised--in 1887--was
one called _lata._ It must be explained that the young plant of
_Oenothera_ has practically no stem, but a number of leaves radiating in
all directions from the growing point which is near the surface of the
soil. The plant is normally biennial, and in the first season the
internodes are not developed. This first stage is called the 'rosette.'
From the reduced stem are afterwards developed one or more long stems with
elongated internodes, bearing leaves and flowers. In the mutation _lata_
the rosette leaves are shorter and more crinkled than those of
_Lamarckiana,_ and the tips of the leaves are very broad and rounded.
The stems of the mature plant are short and usually more or less decumbent
with irregular branches. The flower-buds are peculiarly stout and
barrel-shaped, with a protrusion on one side. The seed-capsules are
short and thick, containing relatively few seeds, and the pollen is
wholly or almost wholly sterile.
It is to be noted here, a fact emphasised by DeVries in his earliest
publications on the subject, that in nearly all, if not all cases, a
mutation does not consist in a peculiarity of a single organ, but in an
alteration of the whole plant in every part. In this respect mutations as
observed in _Oenothera_ seem to be in striking contrast to the majority of
Mendelian characters. Mutation in fact seems to be a case of what the
earlier Darwinians called correlation, while Mendelian characters may
apparently be separated and rejoined in any combination. For example, in
breeds of fowls any colour or any type of plumage may be obtained with
single comb or with rose comb. In my own experiments on fowls the loose
kind of plumage first known in the Silky fowl, which is white, could be
combined with the coloured plumage of the type known as black-red. At the
same time it must be borne in mind that since the factor, whether a
portion of a chromosome or not, is transmitted in heredity as a part of a
single cell, the gamete, and since every cell of the developed individual
is derived by division from the single zygote cell formed by the union of
the two gametes, the factor or determinant must be contained in every cell
of the soma, except in cases where differential division, or what is
called somatic segregation, takes place. Thus the factor which causes the
comb to be a rose comb in a fowl must be present in the cells that produce
the plumage or the toes or any other part of the body. Morgan, as
mentioned above, finds in _Drosophila_ that factors do affect several
parts of the body. It is, however, curious to consider that the factor
which produces intense pigmentation of the skin and all the connective
tissue in the Silky fowl has no effect on the colour of the plumage in
that breed, which is a recessive white. The plumage is an epidermic
structure, and therefore distinct from the connective tissue, but it is
difficult to understand why a pigment factor though present in every cell
has no effect on epidermic cells.
The Mendelians, when the mutations of _Oenothera_ were first described,
endeavoured to show that they were merely examples of the segregation of
factors from a heterozygous combination. They suggested in fact that
_Oenothera Lamarckiana_ was the result of a cross, or repeated crosses,
between plants differing in many factors, that the numerous mutations were
similar to the variety of different types which are produced by breeding
together the grey mice arising from a cross between an albino and a
Japanese waltzing mouse in Darbishire's experiment. Since that time,
however, the natural distribution and the cultural history of _Oenothera_
has been very thoroughly worked out. _Oenothera Lamarckiana_ is the common
Evening Primrose of English gardens. The species of the sub-genus _Onagra_
to which _Lamarckiana_ belongs were originally confined to America
(Canada, United States, and Mexico), but _Lamarckiana_ itself has never
been found there in a wild state. Attempts, however, to produce it by
crossing of other forms have not succeeded, and a specimen has been
discovered at the Museum d'Histoire Naturelle at Paris, collected by
Michaux in North America about 1796, which agrees exactly with the
_Oenothera Lamarckiana_ naturalised or cultivated in Europe. The plant was
first described by Lamarck from plants grown in the gardens of the Museum
d'Histoire Naturelle, under the name _OE. grandiflora_, which had been
introduced by Solander from Alabama, but Seringe subsequently decided that
Lamarck's species was distinct from _grandiflora_, and named it
_Lamarckiana_. Gates states that Michaux was in the habit of collecting
seeds with his specimens, and that it is therefore highly probable that
Lamarck's specimens were grown directly from seeds collected in America by
Michaux. Gates considers that the suggestion of the hybrid origin of
_Lamarckiana_ in culture is thus finally disposed of. By the year 1805,
_Lamarckiana_ was apparently naturalised and flourishing on the coast of
Lancashire, and in 1860 it was brought into commerce, probably from these
Lancashire plants, by Messrs, Carter. The cultures of De Vries are
descended from these commercial seeds, but the Swedish race of
_Lamarckiana_, as well as those of English gardens, differ in several
features and must have come from another source or been modified by
crossing with _grandiflora_. This last remark is quoted from Gates, but it
seems improbable that the Dutch plants should be derived from those of
Lancashire, and those of English gardens from a different source. The fact
seems to be, according to other parts of Gates's volume, that there are
various races of _Lamarckiana_ in English gardens and in the Isle of
Wight, as well as in Sweden, etc., and that these races differ from one
another less than the mutants of De Vries and his followers.
An important point about these mutations is that their production is a
constant feature of _Lamarckiana_. Whenever large numbers of the seeds of
this plant are grown, a certain proportion of the plants developed present
these _same_ mutations; not always all of them--some may be absent in one
culture, present in another, but four of them are fairly common and of
constant occurrence. The total proportion of mutant plants compared with
the normal was 1*55 per cent. in one family, 5*8 per cent. in another. It
would appear therefore, supposing that mutations arose subsequently in the
same determinate way from previous mutations, that evolution, though in a
number of divergent directions from one ancestral form, would proceed
along definite lines, and that there would be nothing accidental about it.
We should thus arrive at a demonstration of what Eimer called
orthogenesis, or evolution in definite directions.
The mutation _lata_ cannot be said to breed true, as the pollen is almost
entirely sterile. It has therefore been propagated by crossing with
_Lamarckiana_ pollen, with the result that both forms are obtained
with _lata_ varying in proportion from 4 per cent. to 45 per cent.
_Rubrinervis_ is a mutation from _Lamarckiana_, chiefly distinguished by
red midribs in the leaves and red stripes on the sepals. When propagated
from self-fertilised seed it produced about 95 per cent. of offspring with
the same characters, and the remaining 5 per cent. mutants, one of which
was _laevifolia_ which had been found by De Vries among plants growing
wild at Hilversum. Gates obtained a single plant among offspring of
_rubrinervis_ in which the sepals were red throughout, and to this he gave
the name _rubricalyx_. When selfed this plant gave rise to both
_rubricalyx_ and _rubrinervis_, and in the second generation when the
_rubricalyx_ was selfed again the numbers of the two were approximately 3
to 1. _Rubricalyx_ is therefore a dominant heterozygote, and this fact was
further confirmed in the third generation when a selfed plant gave 200
offspring all _rubricalyx_, the mother plant having evidently been
homozygous for the red character. In this case, therefore, we have what
Bateson was seeking, the origin of a new dominant character under
observation, the original mutation having arisen in a single gamete of the
zygote which gave rise to the plant. It is claimed by mutationists that
mutations are not new combinations or separations of Mendelian unit
characters already present, but are themselves new characters, though not
always necessarily, as in the case of _rubricalyx_, new unit characters in
the Mendelian sense.
Perhaps the most interesting of the researches on the phenomena of
mutation are those concerning the relation of the characters to the
chromosomes of the cell, in which Gates has been a pioneer and one of
the most industrious and successful investigators. The behaviour of
the chromosomes in meiosis or reduction division both in the pollen
mother-cells and in the megaspore mother-cells which give rise to the
so-called embryo-sac are fully described by Gates. Here it is only
necessary to refer to the abnormalities in the reduction division which
are related to mutation, and the results of these abnormalities in the
number of chromosomes. The original number of chromosomes in _OEnothera_
is 14. In the mutation _lata_ this has become 15, and also in another
mutation called _semilata_. The chromosomes before the reduction division
are arranged in pairs, each pair consisting, it is believed, of one
paternal and one maternal chromosome. One of each pair goes into one
daughter-cell and the other into the other, but not all maternal into one
and all paternal into the other. Thus each daughter-cell after the first
or heterotypic division in normal cases contains 7 chromosomes. A second
homotypic division takes place in which each chromosome splits into two as
in somatic divisions, and thus we have 4 gametes with 7 chromosomes each.
Now when _lata_ is produced it is believed that in the heterotypic
division one pair passes into one daughter-cell instead of one chromosome
of the pair into each daughter-cell, the other pairs segregating in the
usual way. We thus have one daughter-cell with 8 chromosomes and the other
with 6. This 6+8 distribution has actually been observed in the pollen
mother-cell in _rubrinervis_. When a gamete with 8 chromosomes unites in
fertilisation with a normal gamete with 7 the zygote has 15. The _lata_
mutants having an odd chromosome are almost completely male-sterile, and
their seed production is also much reduced: but this partial sterility
cannot be attributed entirely to the odd chromosome because _semilata_,
which has also 15 chromosomes, does not show the same degree of sterility.
Other cases occur in which the number of chromosomes in the somatic cells
is double the ordinary number--namely, 28--and others in which the number
is 21. The normal number in the gamete, 7, is considered the simple
or haploid number, and therefore the number 28 is called tetraploid.
This doubling of the somatic number of chromosomes is now known in a
number of plants and animals. It occurs in the _OEnothera_ mutant _gigas_.
The origin of it has not been clearly made out, but it must result either
from the splitting of each chromosome or from the omission of the
chromosome reduction. In many cases the more numerous chromosomes are
individually as large as those in normal plants, and consequently the
nucleus is larger, the cell is larger, and the whole plant is larger in
every part. But giantism may occur without tetraploidy, and vice versa. In
the _OEnothera gigas_ the rosette leaves are broadly lanceolate with
obtuse or rounded tips, more crinkled than in _Lamarckiana_, petioles
shorter. The stem-leaves are also larger, broader, thicker, more obtuse,
and more crinkled than in _Lamarckiana_. The stem is much stouter, almost
double as thick, but not taller because the upper internodes are shorter
and less numerous. It is difficult to avoid the conclusion that the
stouter character of the organs in this plant is causally connected with
the increased number of chromosomes. Where the number of cells formed is
approximately similar, as in two allied forms of plant in this case, the
greater size of the cells would naturally give a stouter habit, but it is
clear that large cells do not necessarily mean greater size. The cells of
_Salamander_ and _Proteus_ are the largest found among Vertebrates, but
those Amphibia are not the largest Vertebrates. It is curious to note how
different are these discoveries concerning differences in the _number_ of
chromosomes from the conception of Morgan that a mutation depends on a
factor situated in a part of one chromosome.
More copious details concerning mutations will be found in the
publications cited. The question to be considered here is how far the
claim is justified that the facts of this kind hitherto discovered afford
an explanation of the process of evolution. It seems probable that
mutations are of different kinds, as exemplified in _Oenothera_ by _gigas_
and _rubricalyx_ respectively, the former producing only sterile hybrids,
the latter behaving exactly like a Mendelian unit. There can be little
doubt that, as Bateson states, numerous forms recognised as species or
varieties in nature differ in the same way as the races or breeds of
cultivated organisms which differ by factors independently inherited.
There are facts, however, which prove that all species are not sterile
_inter se_, and that their characters when they are hybridised do not
always segregate in Mendelian fashion. John C. Phillips, [Footnote:
_Journ. Exper. Zool._, vol. xviii., 1915.] for example, crossed three wild
species of duck, _Anas boscas_ (the Mallard) with _Dafila acuta_ (the
Pintail) and with _Anas tristis_. In the former cross he states that
except for one or two characters there seemed to be no more tendency to
variation in the _F2_ generation than in the _F1_. An _F1_ Pintail-Mallard
[female] was mated with a wild Pintail [male]. According to Mendelian
expectation the offspring of this mating should have been half Pintail and
half Pintail-Mallard hybrids, but Phillips states that on casual
inspection the plumage of all the males appeared pure Pintail although the
shape was distinctly Mallard-like. The statement is, however, open to
criticism. The question is, what were the unit characters in the parent
species? If the unit characters were very small and numerous, an
individual in which all the characters of the Pintail existed together
among the offspring of the hybrid mated with pure Pintail would be rare in
proportion to the individuals presenting other combinations. Of the _F2_'s
obtained from crossing _Anas tristis_ [male] with _Anas boscas_ [female]
Phillips obtained 23 females and 16 males. The females were all alike and
similar to _F1_ females. Of the males one was a variate specially marked,
about half-way between the _F1_ type and the Mallard parent. This,
according to Phillips, was a segregate. The rest showed a range of
variation but no distinct segregation.
It is somewhat surprising that Mendelian experts, who seem to believe that
species are distinguished by Mendelian characters, have not made
systematic experiments on the crossing of species in order to prove or
disprove their belief.
For my own part I cannot help thinking that the origin of varieties in
species in a domesticated or cultivated state is in a sense pathological.
Such variation doubtless occurs in nature, but not with such luxuriance.
The breeds of domestic fowls differ so greatly that Bateson and others
refuse to believe that they have all arisen from the single species
_Gallus bankiva_. It seems to me from the evidence that there cannot be
any doubt that they have so arisen. One fact that impresses my mind is
that if we consider colour variations in domesticated animals, we find
that a similar set of colours has arisen in the most diverse kinds of
animals with sometimes certain markings or colours peculiar to one group,
_e.g._ dappling in horses, wing bars in pigeons. Thus in various kinds of
Mammals and Birds we have white and black, red or yellow, chocolate with
various degrees of dilution, and piebald combinations. Why should forms
originally so different, as the cat with its striped markings and the
rabbit with no markings at all, give rise to the same colour varieties? It
seems probable that the reason is that the original form had the small
number of pigments which occur mixed together in very small particles, and
that in the descendants the single pigments have separated out, with
increase or decrease in different cases. It is true that historical
evidence tends to show that the greatest variations, such as albinism in
one direction or excess of pigment in the other in the Sweet Pea, were the
first to arise (see Bateson, Presidential Address to British Association,
Australia, 1914, Part I.), and the splitting appears often to be
intentionally produced by crossing these extreme variations with the
original form, but the possibility remains that the conditions of
domestication, abundant food, security and reduced activity, lead to
irregularity in the process of heredity. In any case the mere separation
among different individuals of factors originally inherited together in
one complex does not account for the origin of the complex or of the
factors. This is somewhat the same idea as that of Bateson when he states
that it is easy to understand the origin of a recessive character but
difficult to conceive the origin of a dominant.
The point, however, which I desire most to emphasise is that the
investigations we have been discussing are concerned with variations which
have no relation whatever to adaptation, and afford no explanation of the
evolution of adaptations. These variations perform no function in the life
of the individual, have no relation to external conditions, either in the
sense of being caused by special conditions or fitting the individual to
live in special conditions. A still more important fact is that they do
not explain the origin of metamorphosis. They do not arise by a
metamorphosis: in the case of the rose comb of fowls the chick is not
hatched with a single comb which gradually changes into a rose comb, but
the rose comb develops directly from the beginning. Mutationists and
Mendelians do not seem in the least to appreciate the importance of
metamorphosis or of development generally in considering the relation of
the mutations or factors which they study to evolution in general, because
they have not grasped the fact that there are two kinds of characters to
be explained, adaptational and non-adaptational. T. H. Morgan, for
example, [Footnote: _A Critique of the Theory of Evolution_, p. 67
(Princeton, U.S.A., and London, 1916).] describes a mutation in
_Drosophila_ consisting in the loss of the eyes, and triumphantly remarks:
'Formerly we were taught that eyeless animals arose in caves. This case
shows that they may also arise suddenly in glass milk-bottles by a change
in a single factor.' As it stands the statement is perfectly true, but it
is obvious that the writer does not believe that the darkness of caves
ever had anything to do with the loss of eyes. It is almost as though a
man should discover that blindness in a certain case was due to a
congenital, i.e. gametic, defect, and should then scoff at the idea that
any person could become blind by disease. Some of those who specialise in
the investigation of genetics seem to give inadequate consideration to
other branches of biology. It is a well-established fact that in the mole,
in _Proteus_, and in _Ambtyopsis_ (the blind fish of the Kentucky caves),
the eyes develop in the embryo up to a certain stage in a perfectly normal
way and degenerate afterwards, and that they are much better developed in
the very young animal than in the adult. Does this metamorphosis take
place in the blind _Drosophila_ of the milk-bottle? The larva of the fly
is, I believe, eyeless like the larvae of other Diptera, but Morgan says
nothing of the eye being developed in the imago or pupa and then
degenerating. There is therefore no relation or connexion between the
mutation he describes and the evolution of blindness in cave animals. It
is a truth, too often insufficiently appreciated by biologists, that sound
reasoning is quite as important in science as fact or experiment. Loeb
[Footnote: _The Organism as a Whole_, p. 319 (New York and London, 1916).]
also endeavours to prove that the blindness of cave animals is no evidence
of the influence of darkness in causing degeneration of the eyes. He
refers to experiments by Uhlenhuth, who transplanted eyes of young
Salamanders into different parts of their bodies where they were no longer
connected with the optic nerves. These eyes underwent a degeneration which
was followed by a complete regeneration. He showed that this regeneration
took place in complete darkness, and that the transplanted eyes remained
normal when the Salamanders were kept in the dark for fifteen months.
Hence the development of the eyes does not depend on the influence of
light or on the functional action of the organs. But it must be obvious to
any biologist who has thoroughly considered the problem, that this
experiment has little to do with the question of the cause of blindness in
cave animals. No one ever supposed that cave fishes became blind in
fifteen months, or in fifteen years. The experiment cited merely proves
that in the individual the embryonic or young eye will continue developing
by heredity even after it is transplanted and in the absence of light. But
the eye of the Mammal normally develops in the uterus in the absence of
light.
In his remarks concerning _Typhlogobius_, a blind fish on the coast of
southern California, Loeb seems to be mistaken with regard to the facts.
He states that this fish lives 'in the open, in shallow water under rocks,
in holes occupied by shrimps.' According to Professor Eigenmann the same
species of shrimp is found all over the Bay of San Diego, and is
accompanied by other genera of goby, such as _Clevelandia_ and
_Gillichthys_, which have eyes; but these fishes live outside the holes,
and only retreat into them when frightened, while the blind species is
found only at Point Loma, and never leaves the burrows of the shrimp. It
would appear, therefore, that _Typhlogobius_ lives in almost if not quite
complete darkness, instead of being, as Loeb states, 'blind in spite of
exposure to light,' while the closely allied forms which are exposed to
light are not blind.
Loeb states, on the authority of Eigenmann, that all those forms which
live in caves were adapted to life in the dark before they entered the
cave, because they are all negatively heliotropic and positively
stereotropic, and with these tropisms would be forced to enter a cave
whenever they were put at the entrance. Even those among the Amblyopsidae
which live in the open have the tropisms of the cave dweller. But these
latter are not blind, and the argument only tends to show that the blind
fish _Amblyopsis_ entered the caves before it was blind. Nocturnal animals
generally must be said to be negatively heliotropic, but these usually
have larger and more sensitive eyes than the diurnal.
It is said, however, that _Chologaster agassizii_, which is not blind,
lives in the underground streams of Kentucky and Tennessee, but I think it
is open to doubt whether it is a species entirely confined to darkness.
Another point which Loeb omits to mention is the absence of pigment in
cave animals, especially Vertebrates such as _Amblyopsis_ and _Proteus_.
If absence of light is not the cause of blindness in these cases, how is
it that the blindness is always associated with absence of pigment, since
we know that the latter in Fishes and Amphibia is due to the absence of
light? It has been shown that _Proteus_ when kept in the light develops
some amount of pigment, although it does not become pigmented to the same
degree as ordinary Amphibia. We have here, I think, an example of the
essential difference between mutations and somatic modifications. Absence
of the gametic factor or factors for pigmentation results in albinism, and
no amount of exposure to light produces pigmentation in albinos, _e.g._
albino Axolotls which are well known in captivity. Absence of light, on
the other hand, prevents the development of pigment. The question
therefore is whether the somatic modification is inherited. The fact that
_Proteus_ does not rapidly become as deeply coloured when exposed to light
as ordinary Amphibia shows that the gametic factors for pigmentation have
been modified as well as the somatic tissues.
Loeb attributes the blindness of cave fishes to a disturbance in the
circulation and mutation of the eyes originally occurring as a mutation.
But how could an explanation of this kind be applied to the case of
_Anableps tetrophthalmus_, in which each eye is divided by a partition of
the cornea and lens into an upper half adapted for vision in air and a
lower half for vision in water? This fish lives in the smooth water of
estuaries in Central America, and swims habitually with the horizontal
partition of the lens level with the surface of the water. It is
impossible to understand in this case, firstly, how a mutation could cause
the eyes to be divided and doubly adapted to two different optic
conditions, and, secondly, how at the same time a convenient 'tropism'
should occur which caused the animal to swim with its eyes half in and
half out of water. Are we to suppose that the upper half of the body or
eye had a positive heliotropism and the lower half a negative
heliotropism? The fact is that the fish swims at the surface in order to
watch for and feed on floating particles. The tropism concerned is the
food tropism, but what is gained by calling the search for food common to
all active animals a tropism, and how is the search for food before the
food is perceptible to the senses, before it can act as a stimulus on a
food-sensitive substance in the body, to be compared to a tropism at all?
Loeb undertakes to prove that the organism as a whole acts automatically
according to physicochemical laws. But he misses the question of evolution
altogether. For example, he quotes Gudernatsch as having proved that legs
can be induced to grow in tadpoles at any time, even in very young
specimens, by feeding them with thyroid gland. Loeb writes: 'The earlier
writers explained the growth of the legs in the tadpole as a case of an
adaptation to life on land. We know through Gudernatsch that the growth of
the legs can be produced at any time by feeding the animal with the
thyroid gland.' Obviously he thinks that these two propositions are
contradictory to each other, whereas there is no contradiction, between
them at all. Loeb actually supposes that the thyroid is the cause of the
development of the legs. Logically, if this were the case it would follow
that if we fed an eel or a snake with thyroid it would develop legs like
those of a frog, and if a man were injected with extract of the testes of
a stag he would develop antlers on his forehead. It will be obvious to
most biologists that the thyroid, whether that of the tadpole itself or
that which is supplied as food, only causes the development of legs
because the hereditary power to develop legs is already present. The
question is how this hereditary power was evolved. Legs _are_ an
adaptation to life on land. What we have to consider and to investigate is
whether the legs arose as a gametic mutation or as a direct result of
locomotion on land.
The general result of clinical and experimental evidence is to show that
the hormone of the thyroid is necessary to normal development. The arrest
of development in cretinous children is due to some deficiency of thyroid
secretion, and is counteracted by the administration of thyroid extract.
Excess of the secretion produces a state of restlessness and excitement
associated with an abnormally rapid rate of metabolism and protrusion of
the eye-balls (Graves' disease). The physiological text-books, however,
say nothing of precocity of development in children as a result of
hyperthyroidism. This, however, is undoubtedly what occurs in the case of
tadpoles. The legs would naturally develop at some time or other, after a
prolonged period of larval life. Feeding with thyroid causes them to
develop at once. I have repeated Gudernatsch's experiment with the
following results:--
This year I had a considerable number of tadpoles of the common English
frog, which were hatched between March 26 and March 29. On April 12,
when they had all passed the stage of external gills and developed
internal gills and opercula, I divided them into two lots, one in a
shallow pie-dish, the other in a glass cylinder. To one lot I gave a
portion of rabbit's thyroid, to the other a piece of rabbit's liver. They
fed eagerly on both. Afterwards I obtained at intervals of a week or so
the thyroid of a sheep. I have seen no precise details of Gudernatsch's
method of feeding tadpoles, but my own method was simply to put a piece of
thyroid into the water containing the tadpoles and leave it there for
several days, then to take it out and put in another piece, changing the
water when it seemed to be getting foul.
April 22. Noticed that the non-thyroid tadpoles were larger than those fed
on thyroid. Changed the former into the pie-dish and the latter into the
glass jar, to make sure that the difference in size was not due to larger
space.
May 3. Only eighteen of the non-thyroid tadpoles surviving, owing to the
water having become foul, but these are three times as large as those fed
on thyroid. In the latter no trace of hind-legs was visible, but the
abdominal region was much emaciated and contracted, while the head region
was broader.
May 4. Noticed minute white buds of hind-legs in the thyroid-fed tadpoles.
May 6. A number of the thyroid-fed were dying, and the skin and opercular
membranes were swollen out away from the tissues beneath.
Largest normal tadpole, 2.7 cm. long.
body, 1.0 "
tail, 1.7 "
Largest thyroid-fed tadpole, 1.1 cm. long.
body, 0.5 "
tail, 0.6 "
May 10. A great number of the thyroid-fed dead and the rest dying, lying
at the bottom motionless. They now had the tail much shorter, and the
fore-legs showing as well as the hind, but the latter not very long, and
without joints or toes.
Period from first feeding with thyroid, thirty days. I now decided to feed
the controls with thyroid, expecting that as they were large and vigorous
they would have strength enough to complete the metamorphosis and become
frogs.
May 15. Fed the controls with thyroid for first time.
The smallest of them was in total length 1.7 cm.
body, 0.7 "
tail, 1.0 "
The largest measured was in total length 2.2 "
body, 0.8 "
tail, 1.4 "
May 25. All but two of the tadpoles dead. The tails were only half the
original length, all had well-developed hind-legs, some with toes, but the
fore-legs were beneath the opercula, not projecting from the surface.
Smallest total length, 1.2 cm.
body, 0.5 "
tail, 0.7 "
Largest total length, 1.8 "
body, 0.7 "
tail, 1.1 "
These last measurements were made after the tadpoles had been preserved in
spirit, and were therefore doubtless somewhat less than in the fresh
condition. Making allowance for this it is evident that the tails had
undergone reduction as part of the metamorphosis, but the body was also
shorter. There is some reason therefore for concluding that actual
reduction in size of body occurs as the result of metamorphosis induced by
thyroid feeding. As in the other case the skin and opercular membranes
were distended by liquid beneath them.
The total period of the change in this second experiment was ten days.
I conclude that the amount of thyroid eaten was so excessive as to cause
pathological conditions as well as precocious metamorphosis, so that the
animals died without completing the process.
On June 10 I still had four tadpoles which had never had thyroid, but only
pieces of meat, earthworm, or fish. These were very much larger than any
of the others, were active and vigorous, and the largest one showed small
rudiments of hind-legs, the others none at all.
CHAPTER VII
Metamorphosis And Recapitulation
As one of the most remarkable examples of metamorphosis and recapitulation
in connexion with adaptation we will consider once more the case of the
Flat-fishes which I have already mentioned in an earlier chapter. These
fishes offer perhaps the best example of the difference between
gametogenic mutations and adaptive modifications. In several species
specimens occur occasionally in which the asymmetry is not fully
developed. [Footnote: See 'Coloration of Skins of Fishes, especially of
Pleuronectidae,' _Phil. Trans. Royal Soc_., 1894.] These abnormalities are
most frequent in the Turbot, Brill, Flounder, and Plaice. The chief
abnormal features are pigmentation of the lower side as well as of the
upper, the eye of the lower side, left or right according to the species,
on the edge of the head instead of the upper side, and the dorsal fin with
its attachment ceasing behind this eye, the end of the fin projecting
freely forwards over the eye in the form of a hook. Such specimens have
been called ambicolorate, but it is an important fact that they are also
ambiarmate--that is to say, the scales or tubercles which in the normal
Flat-fish are considerably reduced or absent on the lower side, in these
abnormal specimens are developed on the lower side almost as much as on
the tipper. Minor degrees of the abnormality occur: in Turbot with the
hook-like projection of the dorsal fin the lower side of the head is often
without pigment, while the rest of the lower side is pigmented. Less
degrees of pigmentation of the lower side occur without structural
abnormality of the eye and dorsal fin.
There is no evidence that these abnormalities are due to abnormal
conditions of life. One specimen of Plaice of this type was kept alive in
the aquarium, and it lay on its side, buried itself in the sand, and when
disturbed swam horizontally, like a normal specimen. The abnormalities are
undoubtedly mutations of gametic origin. The development of one of these
abnormal specimens from the egg has not to my knowledge been traced, but
there is no reason to suppose that the fish develops first into the normal
asymmetrical condition and then changes gradually to the abnormal condition
described. On the contrary, everything points to the conclusion that the
abnormality is an arrest or incomplete occurrence of the normal process of
development, _i.e._ of the normal metamorphosis. T. H. Morgan, in a volume
published some years ago, [Footnote: _Evolution and Adaptation_.] put
forward the extraordinary view that the Pleuronectidae arose from
symmetrical fishes by a mutation which was entirely gametogenetic and
entirely independent of habits or external conditions, and then finding
itself with two eyes on one side of its head, and no air-bladder, adopted
the new mode of life, the new habit of lying on the ground on one side in
order to make better use of its asymmetrically placed eyes. According to
this view habits have been adapted to structure, not structure to habits.
We are thus to believe that Amphibia came out of the water and breathed
air because by an accidental mutation they possessed lungs and a pulmonary
circulation capable of atmospheric respiration. Such is the result of
applying conclusions derived from phenomena of one kind to phenomena of a
totally different kind. One of the chief differences between structural
features and correlations which are adaptive from those which are not is
the process of metamorphosis, where we see the structure changing in
the individual life history as the mode of life changes. The egg of the
Flat-fish develops into a symmetrical pelagic larva similar to that of
many other marine fishes. The larva has an eye on each side of its head
and swims with its plane of symmetry in a vertical position: it has also
colour on both sides equally. When the skeleton begins to develop the
transformation takes place: the eye of one side, left in some species,
right in others, moves gradually to the edge of the head and then on to
the other side. The dorsal fin extends forward, preserving its original
direction, and so passes between the eye that has changed its position and
the lower side of the fish, on which that eye was originally situated. In
some cases this extension of the fin takes place earlier and the eye
passes beneath the base of the fin to reach the other side. Any one who
takes the trouble to make himself acquainted with the facts will see that
the three chief features of the Pleuronectid--namely, the position of the
eyes, the extension of the dorsal and ventral fins, and the absence of
pigment from the lower side--are not structurally correlated with one
another at all as changes in different parts of the organism in a mutation
are said to be, but are all closely related to their functions in the new
position of the body. A mutation consisting in general asymmetry would be
comprehensible, but the head of the Pleuronectid is not asymmetrical in a
general sense, but only so far as to allow of the changed position of the
eyes. The posterior end of the skull is as symmetrical as in any other
fish, and in some cases the mouth and jaws are also symmetrical, entirely
unaffected by the change in the position of the eyes. In other cases the
jaws are asymmetrical in a direction opposite to that of the eyes, there
is no change of position but a much greater development of the lower half
of the jaws, reduction, with absence of teeth, of the upper half. In the
latter case the fish feeds on worms and molluscs living on the ground and
seized with the lower half of the jaws, in the former the food consists of
small fish swimming above the Flat-fish and seized with the whole of the
jaws (Turbot, Halibut, etc.).
I contend, then, that the mode in which the normal Flat-fish develops is
quite different from that in which mutations arise. T. H. Morgan
[Footnote: _A Critique of the Theory of Evolution_ (1916), p. 18.] states
that a variation arising in the germ-plasm, no matter what its cause, may
affect any stage in the development of the next individuals that arise
from it. In certain cases this is true, that is to say, when there are
very distinct stages already. For example, a green caterpillar becomes a
white butterfly with black spots. A mutation might affect the black spots,
an individual might be produced which had two spots on each wing instead
of one, and no sign of this mutation would be evident in the caterpillar.
But my contention is that when this mutation occurred, the original
condition of one spot would not be first developed and then gradually
split into two. Morgan proceeds to state clearly what I wish to insist
upon concerning mutations. He writes that in recent times the idea that
variations are discontinuous has become current. Actual experience, he
tells us, shows that new characters do not add themselves to the line of
existing characters, but if they affect the adult characters, they change
them without as it were passing through and beyond them.
Now in the case of the ancestors of the Flat-fish the adult and the larva
must have had the same symmetry with regard to eyes and colour and the
dorsal fin terminated behind the level of the eyes. Thus the variations
which gave rise to the Flat-fish were not discontinuous but continuous. In
each individual development now, not merely hypothetically in the
ancestor, the condition of the adult arises by an absolutely continuous
change of the eyes, fins, and colour. Such a continuous change cannot be
explained by a discontinuous variation, _i.e._ a mutation. The
abnormalities above mentioned on the other hand, although they doubtless
arise from the same kind of symmetrical larva as the normal Flat-fish, and
develop by a gradual and continuous process, do not presumably pass
through the condition of the normal adult Flat-fish and then change
gradually into the condition we find in them. As compared with the normal
Flat-fish they arise by a discontinuous variation, they are mutations,
whereas the normal Flat-fish as compared with its symmetrical ancestor
arises by a continuous change.
In order to make my meaning clear I must point out that I have been using
the word continuous in a different sense from that in which it is used by
other biologists, Bateson for example. The word has been applied
previously to variations which form a continuous series in a large number
of individuals, each of which differs only slightly from those most
similar to it. No two individuals are exactly alike, and thus such
continuous variations are universal. According to the theory of natural
selection the course of evolutionary change in any organ or character
would form a similar continuous series, the mean of each generation
differing only by a small difference from that of the preceding. According
to the modern mutationists such small differences are to be called
fluctuations, and have no effect on evolution at all, are not even
hereditary, are not due to genetic factors in the gametes. Discontinuous
variations, on the other hand, are as a rule differences in an individual
from the normal type and from its parents of considerable degree, and are
conspicuous: these are what are called mutations.
The mutationists and Mendelians have not shown how the essential
characteristics of mutations are to be reconciled with the facts of
metamorphosis, or with recapitulation in development which is so often
associated with metamorphosis. T. H. Morgan is the only mutationist, so
far as my reading has gone, who has attempted to do this, and he seems to
me to have failed to understand the difficulties or even the nature of the
problem. He points out that the embryos of Birds and Mammals have gill
slits representing the same structures as those of the adult Fish, but the
young stage of the Fish also possessed gill slits, therefore it is 'more
probable that the Mammal and Bird possess this stage in their development
simply because it has never been lost.' He concludes therefore that the
gill slits of the embryo Bird represent the gill slits of the embryo Fish,
and not the adult gill slits of the Fish, which have been in some
mysterious way pushed back into the embryo of the Bird.
Morgan evidently does not realise that the Birds and Reptiles must have
been derived from Amphibia, and that the embryo Reptile or Bird with gill
slits and gill arches is merely a tadpole enclosed in an egg shell. The
Frog in its adult state differs much from a Fish, while the larva in its
gill arches and gill slits resembles a Fish. Morgan contends that the new
characters do not add themselves to the end of the line of already
existing characters. But in the case of the Frog this is exactly what they
have done. The existing characters were in this case the gill arches and
slits. Those who believe in recapitulation do not suppose that the animal
had to live a second life added on to the life of its ancestors and that
the new characters appeared in the second life. They believe that in the
ancestor a certain character or general structure of body when developed
persisted without change throughout life like the gill arches and slits in
a Fish. At some stage of life before maturity this character underwent a
change, and in the descendants the development of the original character
and the change were repeated by heredity. There is no 'mysterious pushing
back of adult characters into the embryo,' although it is possible or even
probable that in some cases the change gradually became earlier in the
life history: it is the new character which is pushed back, not the adult
character of the ancestor.
It is perfectly true, as Morgan says, that new characters which arise as
discontinuous variations--in other words, those kinds of variation which
are called mutations--do not add themselves to the line of already
existing characters, but 'change the adult characters without as it were
passing through and beyond them.' The mutations which Morgan describes in
his own experiments on _Drosophila_ illustrate this in every case. In no
case is the original organ or character, _e.g._ wings, of the normal Fly
first developed and then changed by a gradual continuous process into the
new character. It might perhaps be said that this took place in the pupa,
but that seems impossible, for the complete wing is not fully developed in
the pupa. The same truth is equally apparent in the mutations described
in _OEnothera_. It follows, therefore, that none of the evolutionary
changes which have produced what are called recapitulations can have been
due to changes of that kind which is known as mutation.
The abnormalities in Pleuronectidae to which I have referred are of the
kind usually regarded as due to arrested development. But closer
consideration gives rise to doubt concerning the validity of this
explanation. It might be supposed that the attached base of the dorsal fin
is unable to extend forward because the eye on the edge of the head is in
the way, but if the metamorphosis is arrested, why should the fin grow
forward in a free projection? I have described a very abnormal specimen of
Turbot in a paper communicated to the Zoological Society of London,
[Footnote: _Proc. Zool Soc._, 1907.] and in that paper have discussed
other possible explanations of these mutations. In the specimen to which I
refer the pigmentation instead of being present on both sides was
reversed: the lower side was pigmented from the posterior end to the edge
of the operculum (Plate II, fig. 2), while the upper side was unpigmented
excepting a scattering of minute black specks and a little pigment on the
head (Plate II., fig. 1).
[Illustration: PLATE II, Fig. 1 and Fig. 2,
Abnormal Specimen Of Turbot]
I have suggested that the explanation here is that in the zygote the
primordia of a normal body and a reversed head have been united together.
We may suppose that different parts of the body are represented in the
gametes by different determinants or factors, and therefore it is possible
that these factors may be separated. In the specimen we are considering
the body is normal or nearly so, with the pigmentation on the left side,
which is normal for the Turbot, while the head has both eyes with some
pigment on the right side and the left side unpigmented. Reversed
specimens occasionally occur in many species of Pleuronectidae, and if the
determinants for a reversed head and a normal body were united in one
zygote, the curious abnormality observed might be the result. It is just a
possibility that if this fish which was only 4.4 cm. long had lived to
adult size, the upper side would have become pigmented under the influence
of light, while the strong hereditary influence would have prevented the
disappearance of the pigment from the lower side. In that case the adult
condition would have been similar to that of ordinary ambicolorate
specimens, but reversed, with eyes on the right side instead of the left.
Other explanations of the more frequent ambicolorate mutation are
possible: the body may consist of two left sides instead of a left and
right, joined on to a normal head. But the first suggestion seems the more
probable, as two rights or two lefts would not be symmetrical. Supposing
the head and body not properly to belong to each other, one being reversed
and one normal, we can in a way understand why the dorsal fin does not
form the usual connexion with the edge of the head, because the
determinants would not be in the normal intimate relation to each other.
In thus writing of reversed and normal it must be understood that the
former word does not mean merely turned over, for in that case right side
of the body would be joined to the left side of the head, and the dorsal
fin would be next to the ventral side of the head, which is not the case.
What is meant is that a left side of the body which is normally pigmented
is joined to a left side of the head which instead of having both eyes has
neither, the two eyes being on the right side of the head which is joined
to the right side of the body, and this is normal and unpigmented. The
dorsal fin belonging to the normal sinistral body would therefore have a
congenital tendency in the metamorphosis to unite with the head on the
outer side of the original lower or right eye after it has moved to the
left side. Actually, however, in this abnormal specimen it finds itself on
the outer side of the left eye which has passed to the right side, and it
has no tendency to unite with this part of the head. At the same time it
has no tendency to bend over at an angle to reach the outer side of the
right eye, and therefore it grows directly forward without attachment to
the head at all.
It will be seen, therefore, that what is changed in relative position in
these mutations is not the actual parts of the body, but merely the
_characters_ of those parts. In a sinistral Flat-fish, whether it is
normally sinistral like the Turbot or abnormally like a 'reversed'
Flounder, the viscera are in the same position as in a dextral specimen:
the liver is on the left side, the coils of the intestine on the right.
Thus in a reversed or sinistral Flounder, which is normally dextral, the
left side which is uppermost is still the left side, but it has colour and
two eyes, whereas in the normal specimen the right side has these
characters and not the left. Thus we are forced to conceive of the
determinants in the chromosomes of the fertilised ovum which correspond to
the two sides of the body, as entirely distinct from the determinants
which cause the condition or 'characters' of the two sides, unless indeed
we suppose that determinants of right side with eyes and colour occur in
some gametes and of right side without eyes and colour in others, and vice
versa, and that homozygous and heterozygous combinations occur in
fertilisation. On this last hypothesis the mutation here considered might
be a heterozygous specimen, with the dextral condition dominant in the
head and the sinistral in the body. Or it might be somehow due to what
Morgan and his colleagues have called crossing over in the segregation of
heterozygous chromosomes, so that a part corresponding to a sinistral body
is united with a part corresponding to a dextral head.
My conclusion from the evidence is that any process of congenital
development may in particular zygotes exhibit a mutation, a departure from
the normal. We need not use the term heredity at all, or if we do, must
remember that in the present argument it does not refer to any
transmission from the parent. The factors in the gametes of the normal
Flat-fish egg cause the normal metamorphosis to take place after the
larval symmetry has lasted a certain time. In occasional individuals the
factors whatever they are, portions of the chromosomes or arrangement of
the chromosomes or anything else, are different from those of the normal
egg, and in consequence the abnormalities above described are developed.
But the chief fact which I cannot too strongly emphasise is that the
development of the abnormality from the symmetrical larva is direct,
whether it is merely an arrest of development or an abnormal combination
of reversed and normal parts. The abnormal development is not due to a
change occurring _after_ the normal asymmetry has been developed. These
abnormalities are true mutations.
The evolution of the normal Flat-fish, on the other hand, was obviously
due to a change of a different kind. Here we are dealing with the change
from a symmetrical fish to the asymmetrical. Judging from what takes place
in other mutations, it was quite possible for asymmetry to have developed
directly from the egg, in consequence of some difference in the
chromosomes of the nucleus. It has been shown that placing a fish egg for
a short time in MgCl[2] [Footnote: Stockard, _Arch. Eut. Mech._, xxiii.
(1907).] causes a cyclopean monstrosity to be developed in which the two
eyes are united into one: but the two eyes do not develop separately first
and then gradually approach each other and unite, the development of the
optic cups is different from the first. In the normal Flat-fish the
evolution that has occurred is the original development of the symmetrical
fish, and the subsequent _continuous gradual_ change in eyes, fin, and
colour to the adult Flat-fish as we see it. All the evidence accumulated
by the experiments and observations of mutationists and Mendelians goes to
prove that this change is of an entirely different kind from those
variations which are described as mutations, or as loss or addition of
genetic factors.
This being the case, we have to inquire what is the explanation of the
evolution of the normal metamorphosis.
The important fact is that the original symmetrical structure of the larva
and the asymmetrical structure of the adult Flat-fish correspond to the
different positions of the body of the fish in relation to the vertical,
the horizontal ground at the bottom of the water, and incidence of light.
The larva swims with its plane of symmetry vertical like most other
fishes; its locomotion requires symmetrical development of muscles and
fins; the two sides being equally exposed to light, it requires an eye on
each side, and the pigment on each side is also related to the equal
exposure to light. The adult lying with one side on the ground has its
original plane of symmetry horizontal and parallel to the ground, and only
the other side exposed to light, and on this side only eyes and colour,
_i.e._ pigment. The change of structure corresponds with the change of
habit. It consists in the change of position of the lower eye, the
extension of the dorsal fin forwards, and the disappearance of pigment
from the lower side. In the actual metamorphosis these changes take place
as the skeleton develops, before the hard bones are fully formed, while
the fish is still small, but the young Turbot reaches a much larger size
before metamorphosis is complete, namely, about one inch in length, than
the young Plaice or Flounder. It is of little importance to consider
whether at the beginning of the evolution the change of position occurred
late or early in life. It may have become earlier in the course of the
evolution. The important matter is to consider the evidence in support of
the conclusion that the relation to external conditions has been the cause
of the evolutionary change. We have already seen that the nature of the
change and the relation of the change of structure to the change of
conditions necessarily tend to the inference that the latter is the cause
of the former. But we have to consider the particular changes in detail.
To take first the loss of pigmentation from the lower side. I have shown
experimentally that exposure of the lower sides of Flounders to light
reflected upwards from below causes development of pigment on the lower
side. At the same time the experiments proved that the loss of pigment in
the fish in the natural state and the development of it under exposure to
light were not merely direct results of the presence or absence of light
in the individual, for in some cases the young fish were placed in the
apparatus before the pigment had entirely disappeared from the lower side,
and the metamorphosis went on, the lower side becoming quite white, and
the pigment only developed gradually after long exposure to the light. In
the principal experiment four specimens were placed in the apparatus on
September 17, 1890, when about six months old and 7 to 9 cm. in length.
One of these died on July 1, 1891, and had no pigment on the lower side.
The other three all developed pigment on that side. In one it was first
noticed in April 1891, and in the following November the fish was 22 cm.
long and had pigmentation over the greater part of the lower side (Plate
III.). Microscopically examined, the pigmentation was found to consist of
black and orange chromatophores exactly similar to those of the upper
side. Some hundreds of young Flounders were reared at the same time under
ordinary conditions and none of them developed pigment.
It is clear, therefore, that exposure of the lower side to light and
reduction of the amount of light falling on the upper side (for the tops
of the aquaria used were covered with opaque material) does not cause the
two sides to behave in the same way in respect of pigment, as they would
if the normal condition of the fish was merely due to the difference in
the exposure to light of the two sides in the individual life. There is a
very strong congenital or hereditary tendency to the disappearance of
pigment from the lower side, and this is only overcome after long exposure
to the light. On the other hand, if the disappearance of the pigment were
due to a mutation, were gametogenic and entirely independent of external
conditions, there would be no development of pigment after the longest
exposure. To prove that an inherited character is an acquired character is
quite as good evidence as to show that an acquired character is inherited.
The latter kind of evidence is very difficult to get, for the effect of
conditions in a single lifetime is but slight, and is not likely to show a
perceptible inherited effect. The theory that adaptations are due to the
heredity of the effects of stimulation assumes that the same stimulus has
been acting for many generations.
[Illustration: PLATE III - Flounder, Showing Pigmentation Of Lower Side
After Exposure To Light]
It is necessary, however, to consider how far the conclusions drawn from
these experiments are contradicted by the mutations occurring in nature,
some of which have already been mentioned. We will consider first
ambicolorate specimens. If the absence of pigment from the lower side in
normal Flat-fishes is due to the absence of light, how is it that the
pigmentation persists on the lower side of ambicolorate specimens, which
is no more exposed to light than in normal specimens? The answer is that
in the mutants the determinants for pigmentation are united with the
determinants for the lower side of the fish. My view is that the
differentiation of these determinants for the two sides was due in the
course of evolution to the different exposure to light, was of somatic
origin, but once the congenital factors or determinants were in existence
they were liable to mutation, and thus in the ambicolorate specimens there
is a congenital tendency to pigmentation on the lower side, which would
only be overcome by exclusion of light for another series of generations.
Mutations also occur in which part or whole of the upper side is white and
unpigmented. Several such specimens are mentioned in the memoir by myself
and Dr. MacMunn in the _Phil. Trans._ already cited, one being a Sole
which was entirely white on the lower side, and also on the upper, which
was pigmented only over the head region from the free edge of the
operculum forwards. Since the upper sides in these specimens are fully
exposed to light in the natural state and yet remain unpigmented, it would
appear impossible to believe that the action of light was the cause of the
development of pigment on the lower sides of normal specimens in my
experiments. To some it may be so, but in my own opinion the one fact is
as certain as the other. I believe the two facts can be reconciled. I had
one specimen of Plaice in the living condition which had the middle third
of its upper surface white, and the whole of the lower side white as
usual. This specimen was kept for 4-1/2 months with its _lower_ surface
exposed to light and the upper side shaded. At the end of that period
there were numerous small patches of pigment scattered over the lower side
principally in the regions of the interspinous bones, above and below the
lateral line. In the area of the upper side, which was originally
unpigmented, there were also numerous small pigment spots. I believe,
therefore, that in this case there were determinants for absence of
pigment not only on the lower side but on part of the upper side also, and
that so long as light was excluded from the lower side the patch on the
upper side remained unpigmented in sympathy. When the congenital tendency
of the determinants on the lower side was overcome by the action of light,
the white patch on the upper side also began to develop pigment.
Lastly, I may refer again to the specially abnormal Turbot mentioned
above. In this case the lower side was over the greater part pigmented and
the upper side white, and this would appear to contradict the conclusion
just drawn concerning the piebald Plaice. But this Turbot was only 4.4 cm.
long, and is the only case known to me where so much of the lower side was
pigmented with the upper side almost entirely white. The theory of
sympathy or correlation might apply here since the lower side of the head
was unpigmented, but from the small size of the specimen and the amount of
pigment on the lower side, it seems to me most probable that if the
specimen had lived to be adult the upper side would have developed pigment
under the action of light and the specimen would have become ambicolorate.
When we compare the results reached by the mutationists with those
obtained by the Mendelians we find that they tend to two different
conceptions of the relation between the gametes and the organism developed
from them. The effect of a change in the determinants of the gametes
according to the mutationists is evident in every part of the plant. A
factor in Mendelian experiments usually affects only one organ or one part
of the organism. The factor for double hallux in fowls, for instance, may
coexist with single comb or rose comb. The general impression produced on
the mind by study of Mendelian phenomena is that the organism is a mosaic
of which every element corresponds to a separate element in the
chromosomes. Thus we know that what we call a single factor may cause the
whole plumage of a fowl to have the detached barbs, which constitutes the
Silky character, but we also know that an animal may be piebald, strongly
pigmented in one part and white or unpigmented in another. So we find in
these Flat-fish mutations mosaic-like forms which evidently result from
mosaic-like factors in the gametes, or in the chromosomes of the gametes.
Experimental evidence concerning the movement of the lower eye to the
upper side and of the forward extension of the dorsal fin has not been
obtained, though years ago I made some attempts, at the suggestion of Mr.
G. J. Romanes, to obtain such evidence with regard to the eye by keeping
young Flounders, already partially metamorphosed, in a reversed position.
I did not succeed in devising apparatus which would keep the young fish
alive in the reversed position for a sufficiently long time. We can only
consider, therefore, whether those other changes can reasonably be
attributed to the conditions of life. Anatomical investigation shows that
the bony interorbital septum composed principally of the frontal bones,
which in symmetrical fish passes between the eyes, is still between the
eyes in the Flat-fish, but has been bent round through an angle of 90
degrees on the upper side, while in the lower side a new bony connexion
has been formed on the outer side of the eye which has moved from the
lower side. This connexion is due to a growth from the prefrontal
backwards to join a process of the frontal, and is entirely absent in
symmetrical fishes. It is along this bony bridge that the dorsal fin
extends. The origin of the eye muscles and of the optic nerves is
morphologically the same as in symmetrical fishes. On the theory of
modification by external stimuli we must naturally attribute the
dislocation of the eye of the lower side to the muscular effort of the
fish to direct this eye to the dorsal edge, but something may also be due
to the pressure of the flat ground on the eye-ball. There is little
difficulty in attributing the bending of the interorbitl septum to
pressure of the lower eye-ball against it, pressure which is probably due
partly if not chiefly to the action of the eye muscles. The formation of
the bony bridge outside the dislocated eye is more difficult to explain,
as I have never had the opportunity to study the relation of this bridge
to the muscles. It is worth mentioning that in the actual development of
Turbot and Brill the metamorphosis takes place to a considerable degree
while the young fish is pelagic, before the habit of lying on the ground
is assumed, but of course this is no evidence that the change was not
originally caused by the habit of lying on the ground.
With regard to the extension of the dorsal fin there is no difficulty in
discovering a stimulus which would account for it. Symmetrical fishes
propel themselves chiefly by the tail; in shuffling over the ground or
swimming a little above it. Flat-fishes move by means of undulations of
the dorsal and ventral fins. Increased movement produces hypertrophy, and
according to the theory here maintained, not merely enlargement of parts
existing, but phylogenetic increase in the number of such parts, here fin
rays and their muscles. In Flat-fishes the dorsal and ventral fins extend
along the whole length of the dorsal and ventral edges: the dorsal from
the head, in some cases from a point anterior to the eyes, to the base of
the tail, the ventral from the anus, which is pushed very far forward, to
the base of the tail, and in some species of Solidae these fins are
confluent with the caudal fin.
Formerly it was dogmatically maintained that the effect of an external
stimulus on somatic organs or tissues could have no influence on the
determinants in the chromosomes of the gametes to which the hereditary
characters of the organism were due. As we have tried to show, this dogma
is no longer credible in face of the discoveries concerning hormones. The
hormone theory supposes that the somatic modifications due to external
stimuli--in the case of the Flat-fish the disappearance of pigment from
the lower side, the torsion of the orbital region of the skull, and the
extension of the dorsal fin--modify the hormones given off by these parts,
increasing some and decreasing others, and that these changes in the
hormones affect the determinants, whatever they are, in the gametocytes
within the body.
Here arises an interesting question--namely, how does the hormone theory
explain the phenomenon of metamorphosis any better than the mutation
theory? It might be agreed that if the determinants are stimulated or
deprived of stimulation, the effect of the change should logically show
itself from the beginning of development, and that therefore the process
of metamorphosis or indirect development does not support the hormone
theory any more than the theory of gametogenic mutations. This objection
may be answered in the following way. The reason why the determinants give
rise to the original structure first and then change it into the new
structure is probably the same as that which causes secondary sexual
characters to develop only at the stage of puberty. By the hypothesis the
new habits and new stimuli begin to act at some stage after the complete
development of the original structure of the body. The differences in the
original hormones of the modified parts are therefore acting
simultaneously with the hormones, that is, the chemical substances derived
from all other parts of the body in its fully developed condition. It is
very probable that in the early stages of development the metabolism of
the body would be considerably different from that of the adult stage, and
the same combination of hormones would not be present. We may suppose,
therefore, that the determinants of the zygote have acquired a tendency
to produce the increases and decreases of tissue which constitute a
certain modification, _e.g._ the change in the position of the eyes in a
Flat-fish, but the stimulus which caused this tendency has always acted
when the adult combination of hormones was present. In consequence of this
the developed tissues do not undergo the inherited modification until the
adult combination is again present. In this way we can form a definite
conception of the reason why an adaptive modification is inherited at the
same stage in which it was produced, just as the antlers of a stag are
only developed when the hormone of the mature testis is present. At the
same time it is probable that the age at which the inherited development
takes place tends to become earlier in later generations, to occur in fact
as soon as the necessary hormone medium is present.
The diagnostic characters, of some of the species of Pleuronectidae have
been mentioned in an earlier part of this volume, in order to point out
that they have no relation to differences of habit or external conditions.
Here it is to be pointed out that there is no evidence that they arise by
metamorphosis. The scales, for example, afford distinct and constant
diagnostic characters both of species and genera, but their peculiarities
have not been found to arise by modification of a primitive form. The
rough tubercles of the Flounder, and the scattered thornlike tubercles of
the Turbot, develop directly, not by the continuous modification of
imbricated scales. There is, however, one scale-character among the
Pleuronectidae which appears to stand in direct contradiction to the
conclusions drawn by me concerning scales in general. It not only develops
by a gradual change, but it is a secondary sexual character developing in
the males only at maturity. The character was described by E. W. L. Holt
in specimens of the Baltic variety of the Plaice, _Pleuronectes platessa_,
[Footnote: _Journ. Mar. Biol. Assn._, vol iii. (Plymouth, 1893-95.)] and
consists in the spinulation of the posterior edges of the scales,
especially on the upper side, in mature males. The same condition, but to
a much slighter degree, was afterwards shown by myself to occur constantly
in Plaice from the English Channel and North Sea. [Footnote: _Ibid._, vol.
iv. p. 323.] It occurs also in _P. glacialis_, the representative of the
Plaice in more northern seas. I have shown that the spinules develop in
the mature males not as a modification of the scale, but as separate
calcareous deposits the bases of which afterwards become united to the
scale. It would seem that the development of this character is dependent
on the hormone from the mature testis, and in order to conform with the
arguments used by me in other cases, the spinulation should have some
definite function in relation to the habits of the sexes, and this
function should involve some kind of external stimulation restricted to
the mature male. So far, however, no evidence whatever of such function or
such stimulation has been discovered. It is possible that the case differs
from other secondary sexual characters as the antlers of stags in one
respect, namely, that the Dab (_P. limanda_), the Sole, and other species
of _Solea._ and several other Pleuronectidae have what are called etenoid
scales--that is, scales furnished with spines on the posterior edge--and
since the ordinary scales of the Plaice are reduced, the spinulation of
scales in the mature male Plaice is not a new character but the retention
of a primitive character. Then the question would remain why the scales in
the mature female and immature male have degenerated, or rather why the
primitive character develops only in the mature stage of the male.
There is one point in which this sexual dimorphism in the Plaice appears
to differ from typical cases, and which suggests that the greater
spinulation of scales in the males has no function at all in the relations
of the sexes, and is therefore not subject to and external stimulation.
This point is the remarkable way in which the degree of development of
spiny armature differs in different regions and in local races, and seems
to correspond to different climatic conditions. Both Plaice and Flounders
in the Baltic are much more spiny than in the North Sea, although in the
Flounder no sexual difference in this respect has been noted. On the east
coast of North America occurs _P. glacialis_, in which the scales of the
male are strongly spinulate and those of the female smooth. On the coast
of Alaska females of this species seem to be more spinulate than
elsewhere. The Flounder does not occur in the Arctic, but on the west
coast of North America occurs a local form called _P. stellatus_,
scarcely distinct as a species, which has a strong development of spiny
tubercles all over the upper side. The Flounders of the Mediterranean are
much less spinous than those of the North Sea or Channel. The Dab (_P.
limanda_) occurs on the American coast in a local form called _Limanda
ferruginea_, and in the North Pacific there is a rougher form called _L.
aspera_. In these three species therefore, apart from mutations, the
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