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

northern forms all show a greater development of spines on the scales.

Whether this is an effect of colder temperature it is difficult to say. It

is possible that the difference is due to external conditions, of which

lower temperature of the water is the most obvious, and it may be that

these conditions have a greater effect on the male than on the female in

the Plaice.

Sexual differences in scales, which have a function in the relations of

the sexes, occur in a few other fishes, and these can be attributed with

good reason to mechanical stimulation. For example, in the Rajidae among

Elasmobranchs the males possess on each 'wing' or pectoral two series of

large, recurved, hooked spines. It has been stated, [Footnote: Darwin,

_Descent of Man_ (2nd edit., 1885), p. 331.] apparently by Yarrell, that

these spines are developed only in the breeding season. It is doubtful if

there is any marked breeding season in these fishes, but it is probable

that the spines are absent in the immature male, as it is known that in

_Raia clavata_ the adult male has sharp pointed teeth, while the young

male and the female at all ages have broad flat teeth. It is supposed that

the spines and perhaps the sharp teeth are used for holding the female,

but it seems equally probable that these structures are really used by the

males in fighting with each other. The habits of these marine fish have

not been much observed, but there is little reason to doubt that these

differences in scales and teeth correspond with differences of mechanical

stimulation. This does not at all imply that the scales and teeth

themselves have been produced by mechanical stimulation, or that the

difference between the dermal denticles of Elasmobranchs and the scales of

Teleosteans correspond to differences of stimulation. But the degree of

development of a structure whose presence is due to gametic factors may

very probably be modified by external stimulation, and the modification

may become hereditary. If the views here advocated are true, the two

processes mutation and modification must be always acting together and

affecting the development not only of the individual but of any organ or

structure. Thus the peculiarities of antlers in stags, it seems to me,

prove that the mechanical stimulation due to fighting was the cause of the

evolution of antlers, that without the habit of fighting in the males

antlers would not exist. At the same time each species of the _Cervidae_

has its special characters in the antlers, in shape and branching, and it

would be impossible to attribute these to differences in mode of fighting:

they are due to mutation.

In connexion with the metamorphosis of Amphibia the case of the Axolotl

has always been of very great interest. In the few small lakes near the

city of Mexico where it occurs it has never been known to undergo

metamorphosis but is aquatic throughout its life and breeds in that

condition. Yet in captivity by reducing the quantity of water in which it

is placed the young Axolotl can be forced to breathe air, and then it

undergoes complete metamorphosis to the abranchiate condition. The same

species in other parts of North America normally goes through the

metamorphosis, like other species of the Urodela. It is evident,

therefore, that the Mexican Axolotls, although they have been

perennibranchiate for a great number of generations, have not lost the

hereditary tendency to the metamorphosis which changes the larvae of

_Amblystoma_ elsewhere into an air-breathing terrestrial animal. This may

be regarded as evidence that the conditions of life which prevent the

metamorphosis in the Mexican Axolotl have produced no hereditary effect.

The fact, however, that Axolotls require special treatment to induce

metamorphosis seems to show that they have distinctly less congenital

tendency to metamorphosis than larvae of the same species, _Amblystoma

tigrinum_, in other parts of North America, and this difference must be

attributed to the inherited effect of the conditions. The most important

of these conditions seems to be abundance of oxygen in solution in the

water, and the next in importance abundance of food in the water. Recently

it has been shown that the metamorphosis may be induced by feeding

Axolotls on thyroid gland. But there is no reason to suppose that a

congenital defect of thyroid arising as a mutation was the original cause

of the neoteny, _i.e._ the peisistence of the larval or aquatic,

branchiate condition. Such a supposition would imply that the association

between Axolotls and the peculiar Mexican lakes, supplied with oxygenated

water by springs at the bottom, was purely accidental. Moreover, there is

no evidence that there is any deficiency of thyroid in the Axolotl. The

secretion of the thyroid gland is necessary for the normal growth and

development of all Vertebrates, and we are only beginning to understand

the effects of defect or excess of this secretion. There is nothing very

surprising in the fact that excess in the case of the Axolotl causes the

occurrence of the metamorphosis which had already in numerous experiments

been produced by forcing the animals to breathe air.

Metamorphosis, as in the development of gill arches and gill slits in the

embryos of Birds, Reptiles, and Mammals, exhibits a recapitulation of the

stages of evolution of certain organs. But in the case of other organs the

absence of recapitulation is remarkable by contrast. If, as I believe, the

development of lungs and disappearance of gills was directly due to the

necessity of breathing air, it is difficult to avoid the conclusion that

the terrestrial legs were originally evolved from some type of fishes'

fins by the use of the fins for terrestrial locomotion. Yet neither the

amphibian larva nor the embryo of higher Vertebrates develops anything

closely similar to a fin. There is no gradual change of a fin-like limb

into a leg, but the leg develops directly from a simple bud of tissue. The

larva of the Urodela is probably more primitive than the tadpole of the

Frogs and Toads, and in the former the legs develop while the external

gills are still large, long before the animal leaves the water.

It is possible that the limbs were transformed to the terrestrial type

before the animal itself became terrestrial, the habit of swimming having

been partly abandoned for that of crawling or walking at the bottom of the

water, and the tail being used merely for swimming to the surface to

obtain air. But the condition of the Dipnoi, which possess lungs but do

not walk on land, does not support this supposition, for they possess fins

which are either filamentous or fin-like, having a central axis with rays

on each side. There can be little doubt that the digits of the terrestrial

limb are homologous with endoskeletal fin-rays, but the evolution of the

axis of the limb is not to be ascertained either from development or

palaeontology. The absence of metamorphosis here may perhaps be due to the

fact that the lateral fins ceased to function in the earlier aquatic

stages, only the caudal fin being used for swimming. If this were the case

the absence of metamorphosis in the legs is itself an adaptation, the

disuse of the paired limbs in the larva having caused the earlier fin-like

stages of these limbs to disappear, while the terrestrial leg was

developed later by heredity, just as the legs have disappeared in the

larvae of many insects, though fully developed in the adult.

Metamorphosis of structure in Amphibia and in Flat-fishes corresponds to

the change of conditions of life in the free-living animal. In the case of

the eyes of the Cave-fishes the conditions in respect of absence of light

are constant throughout life, and we find only an embryonic development of

the eye taking place by heredity. The question arises whether, when there

is no embryonic recapitulation, it must be concluded that apparent

adaptations are due to mutation and not to function or external

conditions. One case of this kind is that of the limbs of Snakes, where,

if we except the vestiges of hind limbs in the Pythons, there is no trace

of limbs either in the embryo or after hatching. There are several similar

cases among Reptiles and Amphibia. The Slow-worm (_Anguis fragilis_) is

limbless, and so are the members of the sub-class Apoda among the

Amphibia. In these also rudiments of limbs are entirely absent in the

embryos or larval stages. Considering the recent evolution of Snakes as

compared with the origin of lungs and loss of gills and gill slits in

terrestrial Vertebrates in general, we have here a remarkable contrast

which shows in the first place the difference resulting when the change in

habits and conditions in the one case takes place from one stage of life

to another, and in the other case the new habits are constant throughout

life from the moment of hatching. It seems to me that in the present state

of our knowledge we cannot form a decisive opinion on the question whether

the absence of limbs in such cases is the result of mutation or of

disuse--that is, absence of functional stimulation.

The power of flight is an excellent example of adaptation. It has been

evolved independently in Pterodactyls, Bats, and Birds. In the two first

groups, and to a slight degree in the third, the expanse of the wing is

formed by an extension of the skin into a thin membrane, supported by the

fore-limbs. It is not necessary to argue in detail that the evolution of

this membrane and of the modifications of bones and muscles by which it is

supported and moved, can be satisfactorily explained on the theory that

modifications due to mechanical and functional stimulation are ultimately

inherited. In birds, however, the surface of the wing is supplied chiefly

by feathers, and consideration of the matter affords no reason for

supposing that the evolution of feathers was due to any external or

functional stimulation. It is often stated that the feathers of birds are

a modification of the epidermic scales of reptiles, but investigation does

not fully confirm this statement. The reptilian scales are retained on the

tarso-metatarsal region of the leg in the majority of birds, and it would

be expected, if the view just quoted were correct, that a transition from

scales to feathers would be visible at the ankle-joint. This, however, is

not the case. In fowls some breeds have scaly shanks and others feathered.

In those with scaly legs I have found cases in winch, in the chicks, there

were two or three very minute feathers, and I have examined these

microscopically by means of sections of the skin. The result was to show

that the minute feathers were not a prolongation of the tips or edges of

the scales, but arose from follicles between the scales. The scale is flat

and is a fold of the epidermis not arising from an invaginated follicle.

The feather, on the other hand, is a tubular structure arising from a

papilla at the base of a deep follicle extending inwards from the surface

of the skin. As the feather grows the papilla grows with it. This papilla

consists of vascular dermal, _i.e._ mesodermic tissue, and if the feather

is pulled out during growth bleeding occurs. The epidermic horny tube

splits posteriorly towards the apex of the feather, and is divided into

rachis and barbs, and thus the dermal tissue within, by this time dead and

dry, is exposed and is shed. Every feather is in fact an open wound, and

is perhaps the only other case, in addition to that of the antlers of

stags, in which vascular mesodermic tissue is normally shed in such

considerable quantities. When the development of the feather is complete,

growth gradually ceases, the proximal part of the feather remains tubular

and does not split, and the vascular tissue within dies, shrivels, and

dries up, forming the pith of the quill When the papilla recommences to

grow the old feather is pushed out, and this process causes the moult. It

would appear, therefore, that the feather must have been evolved, not by a

continuous modification from the scale but by a development of a new kind

between the scales. I have been unable to discover hitherto any evidence

suggesting an external stimulus which could cause this remarkable process

of development in feathers, or indicating that the function of flight

would involve such a stimulus. For the present, therefore, we must

conclude that feathers are not an adaptation, and not due to somatogenic

modification, but must be result of a gametogenic mutation.

Feathers, having been evolved, served in the wings and tail as important

organs of flight. There is reason to believe that, once present, the

growth of feathers was modified greatly by the degree of stimulation

applied to the papillae at roots by the movement and bending strain of the

feathers. The modification of the hones and of the wing, shoulders, and

sternum by the functional stimuli involved in flying are obviously

adaptations, and in my opinion are only to be explained as the hereditary

effects of functional stimulation, like all skeleto-muscular adaptations.

The strains produced in bones by muscular contraction produce hypertrophy

of the part of the bone to which the muscles are attached and thus we can

understand the origin of the carina of the sternum in flying birds, and

its absence in flightless forms. In bats and in pterodactyls also the

sternum is produced into a carina along the median line. The reduction of

the digits of the wing in birds to three, with the bones firmly united

together, would follow from their use in flight and their disuse as

digits, and it would seem, from the fact that the flight-feathers must

have been always on the posterior edge of the wing, and that the ulna is

larger than the radius, that the three digits which have persisted are the

3rd, 4th, and 5th, and not the 1st, 2nd, and 3rd as usually taught. A

comparison of the hind-limbs of birds with those of bats and pterodactyls

suggests strongly that the patagium flyers have arisen from arboreal or

climbing animals, while the birds arose from terrestrial forms which

acquired the bipedal habit, as certain reptiles have. An arboreal animal

would necessarily use all four limbs, as climbing animals actually do. The

wings of birds, on the other hand, would have arisen, from the endeavour

to increase speed by movements of the fore-limbs. The perching birds would

therefore have arisen by later adaptations after the power of flight had

been evolved.

Complete recapitulation does not occur in the development of the digits of

the wing. Only a rudiment of a fourth digit has been found in the

embryonic wing, not, as might be expected, rudiments of five digits of

which two disappear. The metacarpals are free, not united as in the adult,

and there are separate distal carpals, which in the adult are united with

the metacarpals. In other respects the modifications of wings and sternum

are so obviously adaptive that it is difficult to believe that the

reduction of digits was not due to disuse. This is another of those cases

in which the function to which structure is adapted is constant from the

beginning of independent life to the end, and there is some ground for

believing that in course of time in such cases embryonic recapitulation

may be much diminished or disappear. The period of time since birds were

first evolved is in all probability immensely greater than that which has

elapsed since the blind fish, _Amblyoysis_, was modified by cave-life, so

that we can understand why the eye is developed to a certain stage in the

embryo of the blind fish, although it lives in darkness all its life,

while embryonic recapitulation in the wing of the bird is very incomplete.

In another class of adaptations the embryonic or larval stage is adapted

to new conditions, while the adult condition is either less changed or not

changed at all. One of the most obvious examples of this is the allantois

in the Amniota. The embryos of Reptiles, Birds, and Mammals all develop

two embryonic or foetal membranes, the amnion and the allantois. Of the

function or origin of the amnion little is known: to state that it is

protective affords little explanation. It seems possible that it is merely

the mechanical result of the weight of the embryo and the development of

the allantois. The latter is a precocious hypertrophy of the cloacal

bladder found in Amphibia, with the function of embryonic respiration. In

the water the amphibian larva respires by means of gills and gill slits.

In adaptation to terrestrial life it is necessary, if the free aquatic

larval stage is to be eliminated, that the embryo should be able to

breathe air before hatching. Various Amphibia show how this requirement

was met in various ways. In the South American tree-frogs of the genus

_Nototrema_ the eggs are developed in a dorsal pouch of the skin of the

female, and within this pouch the respiration of the embryo is carried on

by a membranous expansion of the second and third external gills on each

side. In the Reptilia the bladder is expanded for the same function, and

absorbs oxygen and gives off carbon dioxide through the pores of the

shell. It is impossible to reconcile the conception of mutation with the

adaptive relation between this allantois and the expulsion of the egg

enclosed in a shell on land. The transition probably came about gradually

from the deposition of the eggs in moist places but not in water. In the

midwife toad (_Alytes obstetricans_) the male carries the eggs about

attached to his legs, respiration is effected by enlarged external gills,

and the larvae are hatched in water. In the ancestral reptiles external

gills may have helped at first, until by the enlargement of the bladder

they were rendered unnecessary. In all such cases the absorption of oxygen

must be regarded as the stimulus which caused the enlargement of the

respiratory membrane. As the allantois could not be absorbed or retracted

again into the abdomen, the umbilicus was evolved--that is to say, the

scar formed by the union of the folded edge between the body wall and

amnion surrounding the stalk of the allantois. It would he difficult for a

mutationist to explain how a mutation should affect the development of the

cloacal bladder to such an enormous degree, just when it was required for

embryonic respiration, and cause the sides of the body to unite ventrally

at the time of hatching, cutting off the allantois and the amnion.

T. H. Morgan [Footnote: _A Critique of the Theory of Evolution_, p.18.]

states that a mutation of gametic origin may affect any stage in the

development of the individual. This may be true when there are already

distinct stages in the life history. The more important question is

whether distinct stages can be caused by mutation. It is true that in

heterozygous individuals characters may develop more fully in the adult

stage than in the young. But when we find different stages evidently

adapted to different modes of life, it is impossible to explain them by

mutations affecting different stages of life. In such cases as the larval

stages of Insects we find the larvae have become adapted to new habits

while the adults have remained unchanged, or have evolved quite

independent adaptations. For example, the adults in the chief orders of

Insects have the typical three pairs of legs, while the maggots or grubs

of the Diptera or Hymenoptera have no legs at all, the caterpillars of

Lepidoptera have evolved pseudo-legs on the abdomen, and the larvae of

Coleoptera have the ordinary legs and no more. This is the reverse of

recapitulation: in the case of legless maggots, and caterpillars with

pro-legs, the adult is more similar to the ancestor than the larva. But

the same principle holds, that where functions and habits are different,

there organs are different. No mutationist has yet produced by breeding

experiments a caterpillar without the three pairs of thoracic legs and yet

developing into a moth that had normal three pairs. Morgan, with all his

mutations of the adult _Drosophila_, says nothing of mutants possessing

legs. The only rational conclusion is that legless larvae have lost the

disuse, since those larvae which are destitute of legs do not go in search

of food but either live in the midst of it or are fed by others, and that

the pro-legs of the caterpillar have been developed by the muscular action

of the insect in clinging to leaves. Here again the hormone theory,

although we cannot pretend to understand the matter completely, helps us

to form a conception of the process of heredity and evolution. The disuse

of legs in the larva affects the determinants, so that they remain

inactive in the presence of the hormones produced in the body generally in

this stage. In the adult stage activity of the legs produces hormones

which influence the same determinants in the gametes to develop legs, but

again in the presence of the different hormones which are present in the

body generally in the adult stage. As the habits of larva and adult became

more specialised and contrasted, the change became less and less gradual,

and the intermediate stage, not being adapted to any transitional mode of

life, became an inactive pupa in which the adult organs develop.

In conclusion I will briefly consider the attempts which have been made to

prove the influence of somatic modifications or characters on the gametes

by direct experiment. The method of Kammerer of inducing changes of habit

or structure by conditions, and then showing that the change is in some

degree inherited, has already been mentioned. One obvious criticism of

this evidence is that it seems to prove too much, for it is difficult to

believe that a change produced in individuals would show so much

hereditary effect in their immediate offspring. Two other methods are

conceivable by which the influence of somatic hormones might be evident.

One of these is to graft ovaries or testes from one animal into another

which possesses a certain somatic character, and then to see if the

offspring produced from these gonads shows any trace of the character of

the foreign soma in which it was nourished. C. C. Guthrie [Footnote:

_Journ. Exper. Zool._ (1908), v.] claimed to have done this in his

experiments on hens. He grafted the ovaries of two Black Leghorn pullets

into two White pullets of the same breed, and vice versa. The black and

the white birds bred true when mated to cocks of their own colour. The

black hen with white ovary mated with black cock produced four black

chicks and two black chicks with white legs, the white hen with black

ovary mated with white cock produced some white chicks, some black and

some white with black spots. This is held to prove that the transplanted

ovaries were functional, because they produced evidence of the character

originally belonging to them. On the other hand, the black hen with white

ovary mated with white cock produced nine white chicks, and eleven chicks

which were white spotted with black, and the white hen with black ovary

mated with black cock produced not black chicks but white chicks spotted

with black. This was held to prove that the somatic characters of the

"foster mothers" were transmitted.

Davenport repeated Guthrie's experiments on different fowls, grafting the

ovary from a cinnamon-coloured hen into a white hen, and mating her with a

cinnamon-coloured cock. The chicks were exactly similar to those obtained

from crossing such a cock with a normal white hen, and Davenport concludes

that the engrafted ovary was not functional but had degenerated. It is

known to be almost if not quite impossible to remove the ovary completely

from a hen, owing to its close attachment over the great post-caval vein.

At the same time it is difficult to see how Guthrie could have obtained

black and spotted chicks from a white hen mated with, a white cock if the

grafted ovary from a black hen had not been functional. One point which

Guthrie does not mention, and of which apparently he was not aware, is

that the white of the White Leghorn is dominant to colour, the

heterozygotes not being pure white but white with spots. Thus when he

mated a black cock with a white hen with grafted ovary and obtained

spotted chicks, this would have been the result if the original white

ovary was functional. None of his results prove conclusively the influence

of the soma of the hen into which ovaries were grafted, but would all be

explained if some eggs were derived from the part of the original ovary

not removed in the operation, and others from the grafted ovary.

The grafting of ovaries in Mammals has often been tried, but very rarely

with success. The introduced ovary usually dies and is absorbed. C. Foa

[Footnote: _Arch. Ital. de Bid._ (1901), Tome xxxv.] states that he made

bilateral grafts of ovaries from newborn rabbits into adult rabbits, and

two months after the operation one of the operated females was fecundated

and produced five normal young. In other cases he placed ovaries from

new-born young in positions far from the normal position, such as the

space between the uterus and bladder, and in one case the female so

treated became pregnant, and when killed had a single embryo in one uterus

and no trace of the original ovaries in the normal position. But Foa was

not investigating the influence of somatic characters on ova in the

grafted ovaries, and does not even mention the characters or breed of the

rabbits he used or of the young which were produced from the grafted

ovaries. Castle [Footnote: W. E, Castle and J. C. Phillips, _On Germinal

Transplantation in Vertebrates_, Pub. Carnegie Institution in Washington

(1911), No. 144.] carried out seventy-four transplantations of ovaries

principally in guinea-pigs. Out of all these only one grafted female

produced young. In this case the ovaries of two different black

guinea-pigs about one month old were grafted into an albino female about

five months old. After recovery the grafted female was kept with an albino

male. She produced six young in three pregnancies, first two, then one,

and lastly died with three foetus in the uteri. All these were black, with

some red hairs among the black. One of the first two young had a white

forefoot. In this case black is dominant, and therefore there is nothing

extraordinary in the offspring from a black grafted ovary being black. The

presence of red hairs and a white foot is no evidence of the influence of

the foster soma, but is due to imperfect dominance. When the same male was

mated with a normal black female the offspring were black with red hairs

interspersed.

All these experiments are open to the following criticism. It has been the

main argument of this volume that there are two distinct kinds of

characters in all organisms--namely, those of somatogenic origin and those

of gametogenic origin. Theory supposes that somatic modifications by means

of hormones affect the determinants in the gametes. But it is obvious that

the black and white of Leghorn fowls and of guinea-pigs are gametogenic

characters, and are strongly established in the gametes of their

respective varieties. It is not even certain that the black or white hair

or feathers are giving off special hormones which would or could influence

the gametes. The hormone theory only postulates such influence from

hormones issuing from tissues modified by external stimuli. It is quite

certain that the black colour in Leghorns or guinea-pigs is not due to any

external stimulus or influence. The experiments therefore are entirely

irrelevant to what has been called the inheritance of acquired characters.

All that they can be said to prove is that an albino soma does not convert

ingrafted ova of black race into ova carrying the albino character.

It is probably impossible to prove experimentally the influence of a

modified soma in one generation. I have endeavoured to find a case which

would not be open to the above criticism--that is, to find a character

which could be considered somatogenic and which was absent in a closely

allied variety. Most of the characters in domesticated varieties are

obviously gametogenic mutations, but the lop-ear in rabbits may be, partly

at least, somatogenic. Since many breeds have upright ears, we cannot say

that disuse of the external ear has produced lop-ears in domesticated

rabbits generally, but in lop-eared breeds the ears are much enlarged; and

though this may be gametogenic, the increased weight may have been the

cause of the loss of the power to erect the ears. I therefore tried

grafting ovaries from straight-eared females into lop-eared individuals.

The operation was perfectly successful in seven specimens--that is to say,

they recovered completely and lived for many months, up to a year or more

afterwards, but none of them became pregnant. When killed no trace of

ovary was in any of them; in every case it had been completely absorbed,

and the uteri and vagina were diminished in size and anaemic. For grafting

I used ovaries from young rabbits of various ages from seven days to six

weeks or more, but all were equally unsuccessful. Satisfactory evidence by

direct experiment of the inheritance of somatogenic modifications due to

external stimuli cannot be said to have been yet produced, and, as I have

shown, such evidence from the nature of the case must be very difficult to

obtain. The indirect evidence, however, which has been considered in this

volume is too strong to be ignored--namely, the case of Japanese

long-tailed fowls, that of colour on the lower sides of Flat-fishes, and

the similarity of the congenital development of the antlers in stags, to

the generally admitted effects of mechanical stimulation and injury on the

skin and superficial bones of Mammals.

The general conclusions which are logically to be drawn from our present

knowledge with regard to the problems of heredity and evolution in animals

are in my opinion as follows:--

1. All attempts to explain adaptation by gametogenic mutations, or changes

in gametic factors or 'genes,' have completely failed, as Bateson himself

has admitted.

2. The facts discovered concerning mutations and Mendelian heredity

harmonize with the nature of the majority of specific and varietal

characters, and with the diagnostic characters of many larger divisions in

classification.

3. Some of the most striking cases of adaptation, such as the organs of

respiration and circulation in terrestrial Vertebrates, and the asymmetry

of Flat-fishes, are developed in the individual by a metamorphosis which

is generally regarded as a recapitulation of the ancestral evolution. No

cases of mutation or gametogenic variation hitherto described exhibit a

similar metamorphosis or recapitulation.

4. Secondary sexual characters, usually in the male sex, correspond in

their development with the development of maturity and functional activity

in the gonads, and it has been proved that the latter influence the former

by means of 'hormones' or internal secretions. The evidence concerning sex

and sex-linked characters and the localisation of their factors in the

chromosomes of the gametes has no bearing on the action of hormones.

5. The facts concerning the action of hormones are beyond the scope of

current conceptions of the action of factors or genes localised in the

gametes and particularly in the chromosomes. According to these

conceptions, characters are determined entirely by the genes in the

chromosomes, whereas in certain cases the development of organs or

characters depends on a chemical substance secreted in some distant part

of the body.

6. It was formerly stated that no process was known or could be conceived

by which modifications produced in the soma by external stimuli could

affect the determinants in the gametes in such a way that the

modifications would be inherited. The knowledge now obtained concerning

the nature and action of hormones shows that such a process actually

exists, and in modern theory real substances of the nature of special

chemical compounds take the place of the imaginary gemmules of Darwin's

theory of pangenesis or the 'constitutional units' of Spencer.

7. The theory of the heredity of somatogenic modifications by means of

hormones harmonises with and goes far to explain the facts of

metamorphosis and recapitulation in adaptive characters, and also the

origin of secondary sexual characters, their correlation with the

periodical changes in the gonads and the effects of castration. At the

same time there are some somatic sex-characters, _e.g._ in insects and

birds, which do not appear to be correlated with changes in the gonads,

and which are probably gametogenic, not somatogenic in origin.

8. The theory of the heredity of somatogenic modifications is not in

opposition to the mutation theory. The author's view is that are two kinds

of variation in evolution, one somatogenic and due to external stimuli,

acting either directly on passive tissues or indirectly through function,

and the other gametogenic and due to changes in the chromosomes of the

gametes which are spontaneous and not in any way due to modifications of

the soma. Adaptations are due to somatogenic modifications, non-adaptive

diagnostic characters to gametogenic mutations. It is a mistake to attempt

to explain all the results of evolution by a principle. There are two

kinds of congenital, constitutional or hereditary characters in all

organisms, namely, the adaptive and the non-adaptive, and every distinct

type in classification exhibits a combination of the two. To assert that

all characters are adaptive is as erroneous as to state that all

characters are blastogenic mutations, and therefore in their origin

non-adaptive.

9. Finally it may be urged, although the question has not been directly

discussed in this volume, that no biologist is justified in the present

state of knowledge in dogmatically teaching the lay public that

gametogenic characters are alone worthy of attention in questions of

eugenics and sociology. Hereditary or constitutional factors are of course

of the highest importance, but there exists very good evidence that

modifications due to external stimulus do not perish with the individual,

but are in some degree handed on to succeeding generations, and that good

qualities and improvement of the race are not exclusively due to mutations

which are entirely independent of external stimuli and functional

activity. It is important to produce good stock, but it is also necessary

to exercise and develop the moral, mental, and physical qualities of that

stock, not merely for the benefit of the individual, but for the benefit

of succeeding generations and to prevent degeneration.

INDEX

_Abraxas groussularioun_ and _lacticolor_

Adaptations, origin of; evolution of

_Agonus entaphractus_

Albinism

Allantois

Allurements

_Alytes obstetricans_

_Amblyopsis_, eyes of

_Amblystoma tigrinum_

Amnion

_Anableps tetrophthalmus_

_Anas boscas_, crosses of

_Anas tristis_, crosses

Ancel and Bouin

_Anguis fragilis_

_Antilocapra_

_Antirrhinum_, crossing of

Antlers of stags

Ants, heredity of sex in

Aphidae, heredity of sex in

Apoda

Axolotl, albino; metamorphosis; influence of thyroid feeding

Barred plumage in fowls

Basoh

Bateson

Bees, heredity of sex in

Bernard, Claude

Berthold, A. A.

Biedl and Konigstein

Bionomies

Blindness in cave animals

_Bombyx mori_

Boring, Miss

Born and Fränkel

Brachydactyly

Bresslau

Brown-Séquard

Bühler

_Cambarus_, males of

Capons

Castle, experiments in grafting; on sex

Castration; in ducks; of frog; of Lepidoptera

Cats, heredity of colour in

Cave animals, absence of pigment

Cephalopoda

Cetacea, absence of scrotum

Chelonia

_Chologaster agassixii_

Chromosomes; in mutations

_Clevelandia_

_Colaptes_

Colour-blindness; heredity of

Colours, origin of, in domesticated breeds

Comb of fowls, uselessness of

Corpora lutea, evolution of; in viviparous lower vertebrates; origin of

_Corystes cassivelaunus_

Courtship, organs of

Criss-cross inheritance

Crossing over

Cryptorchidism

Cuttle-fishes

Cyclostomes, absence of corpora lutea in

Cytology

Cytoplasm, in heredity

_Dafila acuta_ crosses

_Daphnia_, heredity of sex in

Darwin

_Dasyurus_; corpora lutea; lactation

Davenport

Determinants

Determination of sex

Dipnoi, fins

Dog-fishes, oviparous and viviparous

Dominant characters, origin of

Doncaster; on heredity in cats

_Drosophila_, blind mutation, heredity of sex, mutations

Ducks, crosses of

Dutch rabbit

Earthworms, sex in

Eclipse plumage

Eigenmann

Eimer

Elasmobranchs; corpus luteum in

Elephants, testes

Eugenics

Eunuch

Evolution, evidence of

Factors, origin of

Feathers, evolution of

Flat-fishes, mutations of

Flight, evolution of

Flounder

Foa, on lactation; on grafting

ovaries

Foges

Fowls, castration of; origin of breeds

Fractionation of Mendelian factors

Fränkel

Frog, thumb-pad

_Gallus bankiva_

Gates, Dr. R. Ruggles

Geddes and Thomson

Gemmules

Genital ducts

_Gigas, Oenothera_

_Gillichthys

Gipsy moth

Goltz and Ewald

Gonads, hormones of

Goodale, H. D.

Grafting, of ovaries or testes

Graves' disease

Gudernatsch

Guthrie, C. C.

Gynandromorphism

Haemophilia

Hanau

Hegner

Herdwick sheep, castration in

Heredity; and sex

Hermaphroditism

Hill, J. P.

Horns

Houssaye

_Inachus scorpio_

Insects, heredity of sex in

Interstitial cells

Intromittent organs

Japanese long-tailed fowls; artificial treatment of

Kammerer

Kellog

Kopec

Lactation, dependence on stimulation, in males; regulation of

_Laevifolia, Oenothera_

Lamarck

Lamarckian theory

Lane-Claypon, Miss; and Starling, on ovaries of rabbit

Larvae of insects

_Lata, Cenothera_

Leghorn, White

Lemon-dab

Leopold and Ravana

Lepidoptera, castration in

_Leptinotarsa_

_Limantria dispar_

Limon

Linnæus

Lode

Loeb, on "blind fish; on blindness in cave animals;

on tadpoles and thyroid

Lop-eared rabbits, grafting experiments

Lotsy, Professor; on crossing

Lutein, of corpora lutes

Male characters in female

Mallard crosses

Mammary glands; origin of rudimentary in male

Marshall; and Jolly

Marsupials, relation of foetus to pouch; scrotum of

Masked crab

Meisenheimer; thumb-pad of frog

_Mendel's Principles of Heredity_

Mendelism; and castration

Menstruation

Metamorphosis; in Flat-fishes; causes of; and hormones;

and diagnostic characters

Michaux,

Midwife toad,

Milk glands,

Mole, eyes of,

Monotremata, origin of milk glands,

Morgan, T. H., on blindness in cave animals, on mutations, on sex:,

on sex-linked heredity, on sexual dimorphism in _Drosophila_,

on variation,

Mutations, in antlers,

Natural selection,

Nuptial plumage,

Nussbaum,

_Nyssia zonaria_

O'Donoghue, development of milk glands,

_OEnothera_, mutations, _grandiflora_, lata_, _Lamarckiana_,

Onagra, species of,

_Origin of Species_, Darwin's,

_Ornithorhyncus_, corpus luteum

Orthogenesis,

Otariidae, scrotum,

Ovaries, position of,

Ovary, in birds,

Ovulation,

Pangenesis,

Parthenogenesis,

Parturition,

Pearson, Karl,

Pheasant, male, gynandramorphism in

Phillips, John C.,

_Philosophie Zoologique_

Phoeidae, testes,

_Physiology of Reproduction_,

Picotee Sweet Pea,

Pigeons,

Pigment, absence in cave animals,

Pile fowls,

Pintail duck, crosses,

Plaice,

_Pleuronectes flesus_,

_glacialis_,

_platesca_,

Plymouth Rock fowl,

Pole-dab,

Poll,

Preformation,

_Problems of Genetics_,

Prong buck,

Pro-oestrus,

_Proteus_, eyes of,

Prototheria, milk glands in,

Rabbits, lactation in,

Recapitulation, absence of, and mutations,

Reptiles, corpora lutea in,

Reversal, in Flat-fishes,

_Rhinoderma darwinii_,

Ribbert,

Rieger,

Rodents, testes,

Romanes, GJ

Röntgen rays, effect on testes,

Rose comb, in fowls,

Rotifers, heredity of sex in,

_Rubricalyx, Oenothera_,

_Rubrinervis, Oenothera_,

_Sacculina_,

Salamanders, transplantation of eye,

Sandes,

Schuster, Edgar,

Scrotum, origin, of,

Sea-horse,

Secondary sexual characters,

Selheim,

_Semilata, Oenothera_,

Sertoli's cells,

Sex, chromosomes; Mendelian theory of,

Sex-Linked heredity,

_Sexual Dimorphism_,

Sexual dimorphism, in Rajidae, in Plaice,

Shattock and Seligmann,

Silkworm,

Silky fowl, plumage of,

Sirenia, absence of scrotum,

Slow-worm,

Smith, Geoffrey,

Snakes, absence of limbs,

Sociology,

Somatic sexual characters,

Species, conception of, origin of, characters of, sterility and hybridism,

Spermatogenesis, in man,

Starling and Lane-Claypon, on lactation,

Steinach, heredity of milk glands,

Sternum, carina of,

Swallows,

Sweet Pea,

Swifts,

Tadpoles, effect of thyroid in

Tandler and Gross

Taxonomies

Teleosteans; corpora lutea in; ovarian follicles

Testes, descent of

Tetraploidy

Thayer

Thumb-pad of frog

Thyroid-gland feeding

Tortoise-shell colour in cats

Tosa fowls, Japanese

Transplantation of gonads

_Typhiogobius_

Uhlenhuth

Urodela, larva

Variations

_Vespa vulgaris_; _germanica_

Vries, De

Wallart

Wasps; heredity of sex in

Weapons, organs used as

Weismann

Whale, paddle of

White Leghorn, crosses

Wilson, E. B.

Wing, development of

Winiwarter, von

Witch

Wood, T. B., on crossing of sheep

Woodland, W.

Woodpecker

X chromosome

_Zeugopterus_

_Zoaea_

End of Project Gutenberg's Hormones and Heredity, by J. T. Cunningham