Hormones and Heredity / A Discussion of the Evolution of Adaptations and the Evolution of Species

by J. T. Cunningham

CHAPTER IV

Origin Of Somatic Sex-Characters In Evolution

In his Mendel's Principles of Heredity, 1909, Bateson does not discuss the nature of somatic sex-characters in general, but appears to regard them as essential sex-features, as male or female respectively. As mentioned above, he argues from the fact that injury or disease of the ovaries may lead to the development of male characters in the female, that the female is heterozygous for sex, and from the supposed fact that castration of the male leads merely to the non-appearance of male somatic characters, that the female sex-factor is wanting in the male. He does not distinguish somatic sex-characters from primary sex-factors, and discusses certain cases of heredity limited by sex as though they were examples of the same kind of phenomenon as somatic sex-characters in general. One of these cases is the crossing by Professor T. B. Wood of a breed of sheep horned in both sexes with another hornless in both sexes. In the F1 generation the males were horned, the females hornless. Here, with regard to the horned character, both sexes were of the same genetic composition, i.e. heterozygous, or if we represent the possession of horns by H, and their absence by h, both sexes were Hh. Thus Hh[male] was horned and Hh[female] was hornless, or, as Bateson expresses it, the horned character was dominant in males, recessive in females. Bateson offers no explanation of this, but it obviously suggests that some trace of the original dimorphism of the sheep in this character was retained in both horned and hornless breeds. We may suppose that the factor for horns had disappeared entirely from the hornless sheep by a mutation, but in the horned breed another mutation had been a weakening of the influence of the sexual hormones on the development of the character, which, as in all such cases, is really inherited in both sexes. In the F1, when the horned character in the female is only inherited from one side, the hereditary tendency is not enough to overcome the influence of the absence of the testis hormone and presence of the ovarian hormone, and so the horns do not develop. The Mendelian merely sees a relation of the character to sex, but overlooks entirely the question of the dimorphism in the original species from which the domesticated breeds are descended. Similarly, with regard to cattle where it has been found that hornlessness is dominant or nearly so in both sexes, no reference is made to the opposite fact that wild cattle have horns in both sexes and are not dimorphic in this character.

Bateson proceeds to consider colour-blindness as though its heredity were of similar kind. He refers to it as a male character latent in the female, remarks that we should expect that disease or removal of the ovaries might lead to the occasional appearance of colour-blindness in females. He also discusses the case of Abraxas grossulariata and its variety lacticolor, and other cases of sex-linked heredity, apparently with the idea that all such cases are similar to those of sexual dimorphism. A. lacticolor occurs in nature only in the female sex, and when bred with grossulariata [male] produces [male]'s and [female]'s all grossulariata, these of course being heterozygous. When the F1 grossulariata [male] was bred with the wild lacticolor [female] it produced both forms in both sexes, and thus lacticolor [male] was obtained for the first time. When this lacticolor [male] was bred with F1 grossulariata[female] it produced all the [male]'s grossulariata and all the [female]'s lacticolor. Bateson's explanation is that the female, according to the Mendelian theory of sex, is heterozygous in sex, the male homozygous and recessive, and that lacticolor is linked with the female sex-character, grossulariata being repelled by that character. Thus we have, the lacticolor character being recessive,

lact. male, LL male male x F, gross. female, GL female male
Gametes L male + L male x G male + L female
_____________________|______________________
| |
GL male male LL male female
gross. male lact. female

It will be seen that although in the progeny of this mating all the grossulariata were males and all the lacticolor females, yet this case is by no means similar to that of sexual dimorphism in which the characters are normally always confined to the same sex. For the lacticolor character in the parent was in the male, while in the offspring it was in the female. We cannot say here that in the theoretical factors which are supposed to represent what happens, the lacticolor character is coupled with the female sex-factor, for we find it with the male sex-character in the lacticolor [male]. It is so coupled only in the heterozygous grossulariata [female], and at the same time the grossulariata character is repelled.

According to Doncaster [Footnote: Determination of Sex, Camb. Univ. Press, 1914.] sex-limited, or as it is now proposed to call it sex-linked, transmission in this case means that the female grossulariata transmits the character to all her male offspring and to none of the female, while a heterozygous male grossulariata mated with lacticolor female transmits the character equally to both sexes: that is to say, the heredity is completely sex-limited in the female but not at all in the male. This is evidence that the female produces two kinds of eggs, one male producing and the other female producing.

With regard to the ordinary form of colour-blindness, Bateson's first explanation was that it was like the horns in the cross-bred sheep, dominant in males, recessive in females. About 4 per cent. of males in European countries are colour-blind, but less than 1/2 per cent. of females. Affected males may transmit the defect to their sons but not to their daughters: but daughters of affected persons transmit the defect frequently to their sons. Bateson gives [Footnote: Mendel's Principles of Heredity, 1909.] a scheme of the transmission, but corrects this in a note stating that colour-blindness does not descend from father to son, unless the defect was introduced by the normal sighted mother also, i.e. was carried by her as a recessive. The fact that unaffected males do not transmit the defect shows, according to Bateson, that it is due to the addition of a factor to the normal, not to omission of a factor.

According to later researches as quoted by Doncaster, colour-blindness is due to the loss of some factor which is present in the normal individual. The normal male is heterozygous for this normal factor. If we denote the presence of the normal factor by N and its absence or recessive by n, then the male is Nn, while the female is homozygous or NN. But in addition to this it is the male in this case which is heterozygous for sex, and n goes to the male-producing sperms, N to the female-producing. Thus in the mating of normal man with normal woman the transmission is as follows:—

Nn (male) x NN (female)
Gametes n (male) + N (female) x N + N

n (male) + N N (female) + N
| |
Nn (male) NN (female)

That is all offspring normal, but the males again heterozygous.

An affected male has the constitution nn, and if he marries a normal woman the descent is as follows:—

nn (male) x NN (female)
Gametes n (male) + n (female) x N + N

n (male) + N N (female) + N
| |
nN (male) nN (female)

When a normal male is mated with a heterozygous nN female we get

nN (male) x nN (female)
Gametes n (male) + N (female) x n + N
______________________|______________________
| | | |
nn (male) nN (male) nN (female) NN (female)

that is, half the sons are normal and half colour-blind, while half the females are homozygous and normal, and the other half heterozygous and normal.

T. H. Morgan [Footnote: A Critique of the Theory of Evolution.] has observed a number of cases of sex-linked inheritance in the mutations which occurred in his cultures of Drosophila. The eye of the wild original fly is red, one of the mutants has a white eye, i.e. the red colour and its factor are absent. When a white-eyed male is mated to a red-eyed female all the offspring have red eyes. If these are bred inter se, there are, as in ordinary Mendelian cases, three red-eyed to one white-eyed in the F2 generation, but white eyes occur only in the males, in other wards half the males are white-eyed. On the other hand, when a white-eyed female is mated to a red-eyed male all the daughters have red eyes, and all the sons white eyes. This has been termed crisscross inheritance. If these are bred together the result in F2 is equal numbers of red-eyed and white-eyed females, and equal numbers of red-eyed and white-eyed males. The ration of dominant to recessive is 2 to 2 instead of the usual Mendelian ration of 3 to 1.

According to Morgan the interpretation is as follows: In the nucleus of the female gametocytes there are two X chromosomes related to sex, in those of the male there is one X chromosome and one Y chromosome of slightly different shape. The factor for red eye occurs in the sex-chromosomes, that is to say, according to this theory, the sex-chromosome does not merely determine sex but carries other factors as well, and this fact is the explanation of sex-linked inheritance. The factor for red eye then is present in both X chromosomes of the wild female, absent from both X and Y chromosomes of the white-eyed male. The gametes of the female each carry one X red chromosome, of those of the male half carry an X white chromosome, and half the Y white chromosome. The fertilised female ova therefore carry an X red chromosome + an X white chromosome, the male producing ova one X red chromosome and one Y white chromosome. They are all therefore red-eyed, but heterozygous—that is, the red eye is due to one red-eye factor, not two. When the F1 are bred together, half the female gametes carry one X red chromosome, the other half one X white chromosome; half the male gametes carry one X red chromosome, the other half one Y white chromosome. The fertilisations are therefore one X red X red, one X red X white, one X red Y white, and one X white Y white. These last are the white-eyed males. The two different crosses are represented diagrammatically below, the dark rod representing the X red chromosome, the clear rod the X white chromosome, and the bent clear rod the Y white chromosome.

According to Morgan, the heredity of colour-blindness in man is to be explained exactly in the same way as that of white eye in Drosophila. A colour-blind man married to a normal (homozygous) woman transmits the peculiarity to half his grandsons and to none of his grand-daughters. Colour-blind women are rare, but in the few cases known where such women have married normal husbands the defect has appeared only in the sons, as in the second of the diagrams below.

Parents Red-eyed male White-eyed female
XR XR x XW YW

F1 Red-eyed male Red-eyed female
XR XW XR YW

F2 Red-eyed male Red-eyed male Red-eyed female White-eyed female
XR XR XW XR XR YW XW YW
Homozygous. Heterozygous. Heterozygous. Homozygous.

White-eyed male Red-eyed female
XW XW x XR YW

F1 Red-eyed male White-eyed female
XW XR XW YW

F2 White-eyed male Red-eyed male White-eyed female Red-eyed female
XW XW XR XW XW YW XR YW
Homozygous. Heterozygous. Homozygous. Heterozygous.

It must be explained that according to this theory the normal male is always heterozygous, because the Y chromosome never carries any other factor except that for sex; it is thus of no more importance than the absence of an X chromosome which occurs in those cases where the male has one sex-chromosome and the female two. According to the researches of von Winiwarter [Footnote: 'Spermatogénèse humaine,' Arch. de Biol., xxvii., 1912.] on spermatogenesis in man, the latter is actually the case in the human species. This investigator found that there were 48 chromosomes in the female cell, 47 in the male; after the reduction divisions the unfertilised ova had 24 chromosomes, half the spermatids 24 and half 23, so that sex is determined in man by the spermatozoon.

Morgan believes that the heredity of haemophilia (the constitutional defect which prevents the spontaneous cessation of bleeding) follows the same scheme, and also at least some forms of stationary night-blindness— that is, the inability to see in twilight.

We may mention a few other in animals, referring the reader for a fuller account to the works cited. One example in the barred character of the feathers in the breed of fowls called Plymouth Rock. In this the female is heterozygous for sex as in Abraxas grossulariata, and the barred character is sex-linked. When a barred hen is crossed with an unbarred cock all the male offspring are barred, all the females plain. On the other hand, if a barred cock is crossed with an unbarred hen, the barred character appears in all the offspring, both and females. The female thus transmits the character only to her sons. If we represent the barred character by B, and its absence by b, we can represent the heredity as follows:—

BARRED FEMALE WITH UNBARRED MALE

B female b male X b male b male

Bb male bb female

Barred male. Unbarred female.
Heterozygous. Homozygous.

B male B male X b female b male

B male b female b male b male

Barred female. Barred male.
Heterozygous. Heterozygous.]

This case is thus exactly similar to that of Abraxas grossulariata and A. lacticolor. The barred character like grossulariata is dominant, the unbarred recessive, and to explain the results it is necessary to assume that the female is not only heterozygous for the barred character, but also for sex, with the female sex-factor dominant. The recessive character in this case is linked to the female sex chromosome, or, as Bateson described it, the dominant character is repelled by the sex-factor. We may make a diagram of the kind given by Morgan if we use a rod of different shape for the female-producing sex-chromosome, and use the black rod for the dominant character:—

BARRED female x unbarred male
BX uY uX uX
| \/ |
| /\ |
BX uX uY uX
BARRED male unbarred female
Heterozygous Homozygous

BARRED male x unbarred female
BX BX uX uY
| \/ |
| /\ |
BX uX BX uY
BARRED male BARRED female
Heterozygous Heterozygous

Another case is that of tortoise-shell, i.e. black and yellow cats. The tortoise-shell with very rare exceptions is female, the corresponding male being yellow, without any black colour. Doncaster found that a yellow male mated to a black female produced black male offspring and tortoise-shell females. When a black male is mated to a yellow female, the female kittens are tortoise-shell as before, but the males yellow. The Mendelian hypothesis which explains these results is that the male is always heterozygous, or has only one colour factor whether yellow or black, and transmits these colours only to his daughters, while the female has two colour factors, either BB, YY, or BY. Thus the crosses are:—

YELLOW male x BLACK female
YO male BB female
| \/ |
| /\ |
YB female BO male
Tortoise-shell female BLACK male

BLACK male x YELLOW female
BO male YY female
| \/ |
| /\ |
BY female YO male
Tortoise-shell female YELLOW male

The sex must be determined therefore by the spermatozoa, as in the case of colour-blindness, etc., in man, and the colour factor must always be in the female-producing sperm.

SEXUAL DIMORPHISM

It is obvious from the above facts that however interesting and important sex-linked heredity may be, it is not the same thing as the heredity of secondary sexual characters, and does not in the least explain sexual dimorphism. In the first place, the term sex-linked does not mean occurring always exclusively in one sex, but the direct contrary— transmitted by one sex to the opposite sex—and in the second place there is no suggestion that the development of the character is dependent in any way on the presence or function of the gonad. The problem I am proposing to consider is what light the facts throw on the origin of the secondary sexual characters in evolution. In endeavouring to answer this question there are only two alternatives: either the characters are blastogenic— that is, they arise from some change in the gametocytes occurring somewhere in the succession of cell-divisions of these cells—or they arise in the soma and are impressed on the gametocytes by the influence of the soma within which these gametocytes are contained—that is to say, they are somatogenic. That characters do originate by the first of these processes may be considered to be proved by recent researches, and such characters are called mutations. There can be little doubt that the so- called sex-linked characters, of which examples have been given above, have originated in this way, and that their relation to sex is part of the mutation. According to T. H. Morgan, it is simply due to the fact that the determinants for such characters are situated in the sex-chromosome. Morgan, however, also states that a case of true sexual dimorphism arose as a mutation in his cultures of Drosphilia. The character was eosin colour in the eye instead of the red colour of the eye in the original fly. In the female this was dark eosin colour, in the male yellowish eosin. But this case differs from the characters particularly under consideration here in two points: (1) there is no suggestion that it was adaptive, (2) or that it was influenced by hormones from the gonads.

No character whose development is dependent in greater or less degree on the stimulation of some substance derived from the gonads can have originated as a mutation, because the term mutation means a new character which develops in the soma as a result of the loss or gain of some factor or determinant in the chromosomes. To say that certain mutations consist of new factors which only the development of characters in the soma when the part of the soma concerned is stimulated by a hormone, is a mere assertion unsupported at present by any evidence. As an example of the way in which Mendelians misunderstand the problem to be considered, I may refer to Doncaster's book, The Determination of Sex [Footnote: Camb. Univ. 1914, p. 99.] in which he remarks: 'It follows that the secondary sexual characters cannot arise simply from the action of hormones; they must be due to differences in the tissues of the body, and the activity of the ovary or testis must be regarded rather as a stimulus to their development than as their source of origin.' This seems to imply a serious misunderstanding of the idea of the action of the hormones from the gonads and of hormones in general. No one would suggest that the hormones from the testis should be regarded as in any sense the origin of the antlers of a stag. If so, why should not antlers equally develop in the stallion or in the buck rabbit, or indeed in man? How far Doncaster is right in holding that the soma is different in the two sexes is a question already mentioned, but it is obvious that in each individual the somatic sexual characters proper to its species are present potentially in its constitution by heredity—in other words, as factors or determinants in the chromosomes of the zygote from which it was developed; but the normal development of such characters in the individual soma is either entirely dependent on the stimulus of the hormone of the gonad or is profoundly influenced by the presence or absence of that stimulus. The evidence, as we have seen, proves that, at any rate in the large number of cases where this relation between somatic sex-characters and hormones produced by the reproductive organs exists, the characters are inherited by both sexes. In one sex they are fully developed, in the other rudimentary or wanting. But the sex, usually the female, in which they are rudimentary or wanting is capable of transmitting them to offspring, and also is capable of developing them more or less completely when the ovaries are removed, atrophied or diseased. If we state these facts in the terms of our present conceptions of chromosomes and determinants or factors, we must say that the factors for these characters are present in the chromosomes of both male and female gametes. The question then is, how did these factors arise? If they were mutations not caused by any influence from the exterior, what is the reason why these particular characters which alone have an adaptive relation to the sexual or reproductive habits of the animal are also the only characters which are influenced by the hormones of the reproductive organs? The idea of mutations implies neither an external relation nor an internal relation in the organ or character; but these characters have both, the external relation in the function they perform in the sexual life of the individual, the internal relation in the fact that their development is affected by the sexual hormones. There is no more striking example of the inadequacy of the current conceptions of Mendelism and mutation to cover the of bionomics and evolution.

The truth is that facts and experiments within a somewhat narrow field have assumed too much importance in recent biological research. No increase in the number of facts or experimental results of a particular class will compensate for the want of sound reasoning and a comprehensive grasp of the phenomena to be explained. The coexistence of the external and the internal relation in the characters we are considering suggests that one is the cause of the other, and as it is obvious that the relation for instance of a stag's antlers to a testicular hormone could not very well be the cause of the use of the antlers in fighting, the reasonable suggestion is that the latter is the cause of the former. We have already seen that the development and shedding of the antler are processes of essentially the same kind physiologically, or pathologically, as these which can be and are occasionally produced in the individual soma by mechanical stimulus and injury to the periosteum. The fact that a hormone from the testis affects the development of the antler, as well as our knowledge of hormones in general, suggests a special theory of the heredity of somatic modifications due to external stimuli. Physiologists are apt to look for a particular gland to produce every internal secretion. But the fact that the wall of the intestine produces secretion, which carried by the blood causes the pancreas to secrete, shows that a particular gland is not necessary. There is nothing improbable in supposing that a tissue stimulated to excessive growth by external irritation would give off special substances to the blood. We know that living tissues give off products, and that these are not merely pure CO2 and H2O, but complicated compounds. The theory proposed by me in 1908 was that we have within the gonads numerous gametocytes whose chromosomes contain factors corresponding to the different parts of the soma, and that factors or determinants might be stimulated by products circulating in the blood and derived from the parts of the soma corresponding to them. There is no reason to suppose that an exostosis formed on the frontal bone as a result of repeated mechanical stimulation due to the butting of stags would give off a special hormone which was never formed in the body before, but it would probably in its increased growth give off an increased quantity of intermediate waste products of the same kind as the tissues from which it arose gave off before. These products would act as a hormone on the gametocytes, stimulating the factors which in the next generation would control the development of the frontal bone and adjacent tissues.

The difficulty of this theory is one which has occurred to biologists who have previously made suggestions of a connexion between hormones and heredity—namely, how hormones or waste products from one part of the body could differ from these from the same tissue in another part of the body. If there were no special relation, hypertrophy of bone on one part of the body such as the head, would merely stimulate the factor for the whole skeleton in the gametocytes, and the result would merely be an increased development of the whole skeleton. On the other hand, we have the evident fact that a number of chromosomes formed apparently of the same substance, by a series of equal chromosome divisions determine all the various special parts of the complicated body. This is not more difficult to understand than that every part of the body should give off special substances which would have a special effect on the corresponding parts of the chromosomes. We know that skin glands in different parts of the body produce special odours, although all formed of the same tissue and all derived from the epidermis. It seems not impossible that bones of different parts of the body give off different hormones. If the factors in the gametes were thus stimulated they would, when they developed in a new individual, product a slightly increased development of the part which was hypertrophied in the parent soma. No matter how slight the degree of hereditary effect, if the stimulation was repeated in every generation, as in the case of such characters as we are considering it undoubtedly was, the hereditary effect would constantly increase until it was far greater than the direct effect of the stimulation. We may express the process mathematically in this way. Suppose the amount of hypertrophy in such a case as the antlers to be x, and that some fraction of this is inherited. Then in the second generation the same amount of stimulation together with the inherited effect would produce a result equal to x+x/n. The latter fraction being already hereditary, a new fraction x/n would be added to the heredity in each generation, so that after m generations the amount of hereditary development would be x+mx/n. If n were 1000, then after 1000 generations the inherited effect would be equal to x. This, it is true, would not be a very rapid increase. But it is possible that the fraction x/n would increase, for the heredity might very well consist not only in a growth independent of stimulation, but in an increasing response to stimulation, so that x itself might be increasing, and the fraction x/n would become larger in each generation. The death and loss of the skin over the antler, originally duo to the laceration of the skin in fighting, has also become hereditary, and it is certainly difficult to conceive the action of hormones in this part of the process. All we can suggest is that the hormone from the rapidly growing antler, including the covering skin, is acting on the corresponding factor in the gametocytes for a certain part of every year, and then, when the skin is stripped off, the hormone disappears. The factor then may be said to be stimulated for a time and then the stimulus suddenly ceases. The bone also begins to die when the skin and periosteum is stripped off, and the hormone from this also ceases to be produced.

The annual shedding and recrescence of the antler, however, is only to be understood in connexion with the effect of the testicular hormone. According to my theory there are two hormone actions, the centripetal from the hypertrophied tissue to the corresponding factor in the gametocytes, and the centrifugal from the testis to the tissue of the antler or other organ concerned. The reason why the somatic sexual character does not develop until the time of puberty, and develops again each breeding season in such cases as antlers, is that the original hypertrophy due to external stimulation occurred only when the testicular hormone was circulating in the blood. The factor in the gametocytes then in each generation acted upon by both hormones, and we must suppose that in some way the result was produced that the hereditary development of the antler in the soma only took place when the testicular hormone was present. It is to be remembered that we are unable at present to form a clear conception of the process of development, to understand how the simple fertilised ovum is able by cell-division and differentiation to develop into a complicated organism with organs and characters predetermined in the single cell which constitutes the ovum. If we accept the idea that characters are represented by particular parts of the chromosomes, according to Morgan's scheme, our theory of development is the modern form of the theory of preformation. When in the course of development the cells of the head from which the antlers arise are formed, each of these cells must be supposed to contain the same chromosomes as the original ovum from which the cells have descended by repeated cell-division. The factors in these chromosomes corresponding to the forehead have been stimulated while in the parent animal by hormones from the outgrowth of tissue produced by external mechanical stimulation, while at the same time they were permeated by the testicular hormone produced either by the gametocytes themselves or by interstitial cells of the testis. When the head begins to form in the process of individual development, the factors, according to my theory, have a tendency to form the special growth of tissue of which the incipient antler consists, but part of the stimulus is wanting, and is not completed until the testicular hormone is produced and diffused into the circulation—that is to say, when the testes are becoming mature and functional.

I do not claim that this theory in complete—it is impossible to understand the process completely in the present state of knowledge—but I maintain that it is the only theory which affords any explanation of the remarkable facts concerning the influence of the hormones from the reproductive organs on the development of secondary sexual characters, while at the same time explaining the adaptive relation of these characters or organs to the sexual habits of the various species. On the mutation hypothesis, adaptation is purely accidental. T. H. Morgan considers that the appearance of two slightly different shades of eye colour in male and female in a culture of a fruit-fly in a bottle is sufficient to settle the whole problem of sexual dimorphism, and to supersede Darwin's complicated theory of sexual selection. The possibility of a Lamarckian explanation he does not even mention. He would doubtless assume that the antlers of stags arose as a mutation, without explaining how they came to be affected by the testicular hormone, and that when they arose the stags found them convenient as fighting weapons. But the complicated adaptive relations are not to be disposed of by the simple word mutation. The males have sexual instincts, themselves dependent on the testicular hormone, which develop sexual jealousy and rivalry, and the Ruminants fight by butting with their heads because they have no incisor teeth in the upper jaw, or tusks, which are used in fighting in other species. Doubtless, mutations have occurred in antlers as in other characters; in fact all hereditary characters are subject to mutation. This in the most probable explanation, not only of the occasional occurrence of hornless individual stags, but of the differences between the antlers of different species, for there is no reason to believe that the special character of the antler in each species is adapted to a special mode of fighting in each species.

The different structure of the horns of the Bovine and Ovine Ruminants is, in my view, the result of a different mode of fighting. If we suppose that the fighting was slower and less fierce in the Bovidae, so that the skin over the exostosis was subject to friction but not lacerated, the result would be a thickening of the horny layer of the epidermis as we find it, and the fact that the skin and periosteum are not destroyed explains why the horns are not shed but permanent.

There is a tendency among Mendelians and mutationists to overestimate the importance of experiments in comparison with reasoning, either inductive or deductive. Bateson, however, has admitted that Mendelian experiments and observations on mutation have not solved the problem of adaptation. It seems to be demanded, nevertheless, that characters must be produced experimentally and then inherited before the hereditary influence of external stimuli can be accepted. Kammerer's experiments in this direction have been sceptically criticised, and it must be granted that the evidence he has published is not sufficient to produce complete conviction. But experiments of this kind are from the nature of the case difficult if not impossible. There is, however, another method—namely, to take a character which is certainly to some extent hereditary, and then to ascertain by experiment if it is 'acquired.' If it be proved that a hereditary character was originally somatogenic, it follows that somatogenic characters in time become hereditary. This is the reasoning I have used in reference to my experiments on the production of pigment on the lower sides of Flat-fishes, and I obtained similar evidence with regard to the excessive growth of the tail feathers in the Japanese Tosa-fowls, [Footnote: 'Observations and Experiments on Japanese Long-tailed Fowls,' Proc. Zool. Soc., 1903.] which is a modification of a secondary sexual character. In these fowls the feathers of the tail in the hens are only slightly lengthened.

I learned from Mr. John Sparks, who himself brought specimens of the breed from Japan, that the Japanese not only keep the birds separately on high perches in special cages, but pull the tail feathers gently every morning in order to cause them to grow longer. One question which I had to investigate on my specimens, hatched from eggs obtained from Mr. Sparks, was the relation of the growth of the feathers to the moult which occurs in ordinary birds. My experiment consisted in keeping two cocks, A and B, the first of which was left to itself, while in the second the feathers were gently pulled by stroking between the finger and thumb from the base outwards. The feathers in the tail were seven pairs of rectrices, two rows of tail coverts, anterior and posterior, four or five pairs in each row, a number of transition feathers: all these were steel-blue, almost black; in front of them on the saddle were a number of reddish yellow, very slender saddle hackles.

In September 1901, when the birds ware just over three months old, the adult feathers of the tail were all growing. The growing condition can be distinguished by the presence of a horny tubular sheath extending up the base of the feather for about one inch. When growth ceases this sheath is shed. In cock A growth continued till the end of the following March, when the longest feathers, the central rectrices, 2 feet 4-1/2 inches long. One of the feathers—namely, one of the anterior tail coverts—was accidentally pulled out on 11th February 1902, when it was 15-1/4 inches long and had nearly ceased to grow and formed its quill, and it immediately began to grow again and continued to grow till the following September, when it was accidentally broken off at the base: it was then 18 inches (44.5 cm.) long.

The effect of stroking in cock B was to pull out from time to time one of the growing feathers. Of the original feathers, one, the left central posterior covert, continued to grow till 13th July 1902, when it was 2 feet 9-1/2 inches long without the part contained in the follicle. All the feathers pulled out immediately commenced to grow again, except the last two pulled out 27th May and 13th July, which did not grow again till the following moulting season, in September.

The first right central rectrix in cock B was accidentally pulled out on 13th April 1902, when it was 2 feet 9-7/8 inches long. Its successor began to grow immediately, and in course of time pieces of it were broken off accidentally without injury to the base in the socket, which continued to grow until 16th June 1905, when it torn out of its socket. The total length of the feather with the pieces previously broken off, which were measured and preserved, was 11 feet 5-1/2 inches. It therefore continued to grow without interruption for three years and two months at an average rate of 3.6 inches per month.

In cock A only four of the short outer rectrices were moulted in the beginning of September 1902: the longer feathers—namely, central rectrices and tail coverts—which ceased to grow naturally in the spring of 1902, were not moulted till the beginning of October. This shows the great importance of pulling out the feathers as soon as they show signs of ceasing to grow, in order to obtain the abnormally long feathers. The central rectrices continued to grow till the beginning of September 1903, when that of the left side was 3 feet 6 inches long, that of the right about an inch shorter. The coverts had ceased to grow of their own accord some time before this, and the central ones of the posterior row were about 3 feet long.

As it seemed possible that there was some natural congenital difference in growth of feathers between cocks A and B, I commenced early in March 1903 to pull and stroke the feathers of the left side only in cock A, leaving those of the right side untouched. On 30th July on the left side the central rectrix and the first and second posterior coverts were still growing, on the right side the central rectrix was also growing, but the first and second posterior coverts had ceased growth and formed their quills. The first posterior covert on the left or pulled side was 3 inches longer than that of the right. The second posterior covert on the left side was still longer. The first and second posterior coverts of left side did not cease growth till 26th August. On 2nd September the left central rectrix was almost at the end of its growth, the right had ceased to grow a little before. The left was about an inch longer than the right. Thus both in length in duration of growth the feathers of the pulled side were longer than those of the right, and this was the result of treatment continued only six months, and commenced some months after the feathers had begun to grow. I have no doubt, however, that the pulling out of the feather as soon as it shows signs of forming quill, so that its successor at once grows again, is even more important in producing the great length of feather than the stroking of the feather itself.

In this case, then there is no doubt (a) that the long-tailed birds are artificially treated with the utmost care and ingenuity by the Japanese, who produced them; (b) that the mechanical stimulus in my experiments did cause the feathers to grow for a longer period and attain greater length; (c) that the tendency to longer growth is, even when no treatment is applied, distinctly inherited. It is a legitimate and logical conclusion that the inherited tendency is the result of the artificial treatment. No other breed of fowls shows such excessive growth of tail feathers. It may be admitted that individuals differ considerably in their congenital tendency to greater growth, i.e. greater length of the tail feathers, but according to my views this is not contradictory to the main conclusion, for every hereditary character shows individual variation.

It may be pointed out here that on the Lamarckian theory the conception of adaptations is not teleological: they do not exist for a certain purpose, but are the result of external stimulations arising from the actions and habits of the organism. The latter conception is the more general, for cases of somatic sexual characters exist which cannot be said to have a use or function. For example, the comb and wattles of Gallus are sexually dimorphic, being in the original species larger in the cock than in the hen. There is no convincing evidence that these appendages are either for use or ornament. They are, in fact, a disadvantage to the bird, being used by his adversary to take hold of when he strikes. The first thing that happens when cocks fight is the bleeding and laceration of the comb, as they peck at each other's heads. This laceration of the skin is, in my view, the primary cause of the evolution of these structures, leading to hypertrophy. But in this, as in other cases, the hereditary result is regular, constant, and symmetrical, while the immediate effect on the individual is doubtless irregular.