Professor T. H. Morgan informs us [Footnote: A Critique of the Theory of Evolution (Oxford Univ. Press, 1916), p. 60] that within five or six years in laboratory cultures of the fruit-fly, Drosophila ampelophila, arose over a hundred and twenty-five new types whose origin was completely known. The first of these which he mentions is that of eye colour, differing in the two sexes, in the female dark eosin, in the male yellowish eosin. Another mutation was a change of the third segment of the thorax into a segment similar to the second. Normally the third segment bears minute appendages which are the vestiges of the second pair of wings; in the mutant the wings of the third segment are true wings though imperfectly developed. A factor has also occurred which causes duplication of the legs. Another mutation is loss of the eyes, but in different individuals pieces of the eye may be present, and the variation is so wide that it ranges from eyes which until carefully examined appear normal, to the total absence of eyes. Wingless flies also arose by a single mutation. These were found on mating with normal specimens to be all recessive characters, thus agreeing with Bateson's views. The next one described is dominant. A single male appeared with a narrow vertical red bar instead of the broad red normal eye. When this male was bred with normal females all the eyes of the offspring were narrower than the normal eye, though not so narrow as in the abnormal male parent. It may be pointed out that this is scarcely a sufficient proof of dominance. If the mutation were due to the loss of one factor affecting the eye, the heterozygote carrying the normal factor from the mother only might very well develop a somewhat imperfect eye.
Morgan arranges the numerous mutations observed in Drosophila in four groups, corresponding in his opinion to the four pairs of chromosomes occurring in the cells of the insect. After the meiotic or reduction divisions each gamete of course contains in its nucleus four single chromosomes. One of the four pairs consists of the sex-chromosomes. All the factors of one group are contained in one chromosome, and it is found in experiments that the members of each group tend to be inherited together—that is to say, if two or more enter a cross together, in other words, if a specimen possessing two or more mutations is crossed with another in which they are absent, they tend to segregate as though they were a single factor. This fact agrees with the hypothesis that the factors in such a case are contained in a single chromosome which segregates from the fellow of its pair in the reduction divisions. Exceptions may occur, however, and these are explained by what is called 'crossing over.' When one chromosome of a pair, instead of being parallel to the other in the gametocyte, crosses it at a point of contact, then when the chromosomes separate, part of one chromosome remains connected with the part of the other on the same side and the two parts separate as a new chromosome, so that two factors originally in the same chromosome may thus come to lie in different chromosomes. In consequence of this, two or more factors which are usually 'coupled' or inherited together may come to appear in different individuals.
Morgan emphasises the statement that a factor does not affect only one particular organ or part of the body. It may have a chief effect in one kind of organ, e.g. the wings or eyes, but usually affects several parts of the body. Thus the factor that causes rudimentary wings also produces sterility in females, general loss of vigour, and short hind legs.
The facts to which I shall refer concerning Oenothera are for the most part quoted on the authority of Dr. Ruggles Gates, and taken from his book The Mutation Factor in Evolution (London, 1915). The occurrence of mutations in Oenothera was first noticed by De Vries, the Dutch botanist, in the neighbourhood of Amsterdam in 1886. He found a large number of specimens of Oenothera Lamarckiana growing in an abandoned potato-field at Hilversum, and these plants showed an unusual amount of variation. He transplanted nine young plants to the Botanic Garden of Amsterdam, and cultivated them and their descendants for seven generations in one experiment. Similar experiments have been made by himself and others. The large majority of the plants produced from the Oe. Lamarckiana by self-fertilisation were of the same form with the same characters, but a certain percentage presented 'mutations'—that is, characters different from the parent form, and in some cases identical with those of plants occurring occasionally among those growing wild in the field where the observations began. Nine of these mutants have been recognised and defined, and distinguished by different names. The characters are precisely described and in many cases figured by Gates in the volume cited above. The first mutant to be recognised—in 1887—was one called lata. It must be explained that the young plant of Oenothera has practically no stem, but a number of leaves radiating in all directions from the growing point which is near the surface of the soil. The plant is normally biennial, and in the first season the internodes are not developed. This first stage is called the 'rosette.' From the reduced stem are afterwards developed one or more long stems with elongated internodes, bearing leaves and flowers. In the mutation lata the rosette leaves are shorter and more crinkled than those of Lamarckiana, and the tips of the leaves are very broad and rounded. The stems of the mature plant are short and usually more or less decumbent with irregular branches. The flower-buds are peculiarly stout and barrel-shaped, with a protrusion on one side. The seed-capsules are short and thick, containing relatively few seeds, and the pollen is wholly or almost wholly sterile.
It is to be noted here, a fact emphasised by DeVries in his earliest publications on the subject, that in nearly all, if not all cases, a mutation does not consist in a peculiarity of a single organ, but in an alteration of the whole plant in every part. In this respect mutations as observed in Oenothera seem to be in striking contrast to the majority of Mendelian characters. Mutation in fact seems to be a case of what the earlier Darwinians called correlation, while Mendelian characters may apparently be separated and rejoined in any combination. For example, in breeds of fowls any colour or any type of plumage may be obtained with single comb or with rose comb. In my own experiments on fowls the loose kind of plumage first known in the Silky fowl, which is white, could be combined with the coloured plumage of the type known as black-red. At the same time it must be borne in mind that since the factor, whether a portion of a chromosome or not, is transmitted in heredity as a part of a single cell, the gamete, and since every cell of the developed individual is derived by division from the single zygote cell formed by the union of the two gametes, the factor or determinant must be contained in every cell of the soma, except in cases where differential division, or what is called somatic segregation, takes place. Thus the factor which causes the comb to be a rose comb in a fowl must be present in the cells that produce the plumage or the toes or any other part of the body. Morgan, as mentioned above, finds in Drosophila that factors do affect several parts of the body. It is, however, curious to consider that the factor which produces intense pigmentation of the skin and all the connective tissue in the Silky fowl has no effect on the colour of the plumage in that breed, which is a recessive white. The plumage is an epidermic structure, and therefore distinct from the connective tissue, but it is difficult to understand why a pigment factor though present in every cell has no effect on epidermic cells.
The Mendelians, when the mutations of Oenothera were first described, endeavoured to show that they were merely examples of the segregation of factors from a heterozygous combination. They suggested in fact that Oenothera Lamarckiana was the result of a cross, or repeated crosses, between plants differing in many factors, that the numerous mutations were similar to the variety of different types which are produced by breeding together the grey mice arising from a cross between an albino and a Japanese waltzing mouse in Darbishire's experiment. Since that time, however, the natural distribution and the cultural history of Oenothera has been very thoroughly worked out. Oenothera Lamarckiana is the common Evening Primrose of English gardens. The species of the sub-genus Onagra to which Lamarckiana belongs were originally confined to America (Canada, United States, and Mexico), but Lamarckiana itself has never been found there in a wild state. Attempts, however, to produce it by crossing of other forms have not succeeded, and a specimen has been discovered at the Muséum d'Histoire Naturelle at Paris, collected by Michaux in North America about 1796, which agrees exactly with the Oenothera Lamarckiana naturalised or cultivated in Europe. The plant was first described by Lamarck from plants grown in the gardens of the Muséum d'Histoire Naturelle, under the name OE. grandiflora, which had been introduced by Solander from Alabama, but Seringe subsequently decided that Lamarck's species was distinct from grandiflora, and named it Lamarckiana. Gates states that Michaux was in the habit of collecting seeds with his specimens, and that it is therefore highly probable that Lamarck's specimens were grown directly from seeds collected in America by Michaux. Gates considers that the suggestion of the hybrid origin of Lamarckiana in culture is thus finally disposed of. By the year 1805, Lamarckiana was apparently naturalised and flourishing on the coast of Lancashire, and in 1860 it was brought into commerce, probably from these Lancashire plants, by Messrs, Carter. The cultures of De Vries are descended from these commercial seeds, but the Swedish race of Lamarckiana, as well as those of English gardens, differ in several features and must have come from another source or been modified by crossing with grandiflora. This last remark is quoted from Gates, but it seems improbable that the Dutch plants should be derived from those of Lancashire, and those of English gardens from a different source. The fact seems to be, according to other parts of Gates's volume, that there are various races of Lamarckiana in English gardens and in the Isle of Wight, as well as in Sweden, etc., and that these races differ from one another less than the mutants of De Vries and his followers.
An important point about these mutations is that their production is a constant feature of Lamarckiana. Whenever large numbers of the seeds of this plant are grown, a certain proportion of the plants developed present these same mutations; not always all of them—some may be absent in one culture, present in another, but four of them are fairly common and of constant occurrence. The total proportion of mutant plants compared with the normal was 1.55 per cent. in one family, 5.8 per cent. in another. It would appear therefore, supposing that mutations arose subsequently in the same determinate way from previous mutations, that evolution, though in a number of divergent directions from one ancestral form, would proceed along definite lines, and that there would be nothing accidental about it. We should thus arrive at a demonstration of what Eimer called orthogenesis, or evolution in definite directions.
The mutation lata cannot be said to breed true, as the pollen is almost entirely sterile. It has therefore been propagated by crossing with Lamarckiana pollen, with the result that both forms are obtained with lata varying in proportion from 4 per cent. to 45 per cent.
Rubrinervis is a mutation from Lamarckiana, chiefly distinguished by red midribs in the leaves and red stripes on the sepals. When propagated from self-fertilised seed it produced about 95 per cent. of offspring with the same characters, and the remaining 5 per cent. mutants, one of which was laevifolia which had been found by De Vries among plants growing wild at Hilversum. Gates obtained a single plant among offspring of rubrinervis in which the sepals were red throughout, and to this he gave the name rubricalyx. When selfed this plant gave rise to both rubricalyx and rubrinervis, and in the second generation when the rubricalyx was selfed again the numbers of the two were approximately 3 to 1. Rubricalyx is therefore a dominant heterozygote, and this fact was further confirmed in the third generation when a selfed plant gave 200 offspring all rubricalyx, the mother plant having evidently been homozygous for the red character. In this case, therefore, we have what Bateson was seeking, the origin of a new dominant character under observation, the original mutation having arisen in a single gamete of the zygote which gave rise to the plant. It is claimed by mutationists that mutations are not new combinations or separations of Mendelian unit characters already present, but are themselves new characters, though not always necessarily, as in the case of rubricalyx, new unit characters in the Mendelian sense.
Perhaps the most interesting of the researches on the phenomena of mutation are those concerning the relation of the characters to the chromosomes of the cell, in which Gates has been a pioneer and one of the most industrious and successful investigators. The behaviour of the chromosomes in meiosis or reduction division both in the pollen mother-cells and in the megaspore mother-cells which give rise to the so-called embryo-sac are fully described by Gates. Here it is only necessary to refer to the abnormalities in the reduction division which are related to mutation, and the results of these abnormalities in the number of chromosomes. The original number of chromosomes in OEnothera is 14. In the mutation lata this has become 15, and also in another mutation called semilata. The chromosomes before the reduction division are arranged in pairs, each pair consisting, it is believed, of one paternal and one maternal chromosome. One of each pair goes into one daughter-cell and the other into the other, but not all maternal into one and all paternal into the other. Thus each daughter-cell after the first or heterotypic division in normal cases contains 7 chromosomes. A second homotypic division takes place in which each chromosome splits into two as in somatic divisions, and thus we have 4 gametes with 7 chromosomes each. Now when lata is produced it is believed that in the heterotypic division one pair passes into one daughter-cell instead of one chromosome of the pair into each daughter-cell, the other pairs segregating in the usual way. We thus have one daughter-cell with 8 chromosomes and the other with 6. This 6+8 distribution has actually been observed in the pollen mother-cell in rubrinervis. When a gamete with 8 chromosomes unites in fertilisation with a normal gamete with 7 the zygote has 15. The lata mutants having an odd chromosome are almost completely male-sterile, and their seed production is also much reduced: but this partial sterility cannot be attributed entirely to the odd chromosome because semilata, which has also 15 chromosomes, does not show the same degree of sterility.
Other cases occur in which the number of chromosomes in the somatic cells is double the ordinary number—namely, 28—and others in which the number is 21. The normal number in the gamete, 7, is considered the simple or haploid number, and therefore the number 28 is called tetraploid. This doubling of the somatic number of chromosomes is now known in a number of plants and animals. It occurs in the OEnothera mutant gigas. The origin of it has not been clearly made out, but it must result either from the splitting of each chromosome or from the omission of the chromosome reduction. In many cases the more numerous chromosomes are individually as large as those in normal plants, and consequently the nucleus is larger, the cell is larger, and the whole plant is larger in every part. But giantism may occur without tetraploidy, and vice versa. In the OEnothera gigas the rosette leaves are broadly lanceolate with obtuse or rounded tips, more crinkled than in Lamarckiana, petioles shorter. The stem-leaves are also larger, broader, thicker, more obtuse, and more crinkled than in Lamarckiana. The stem is much stouter, almost double as thick, but not taller because the upper internodes are shorter and less numerous. It is difficult to avoid the conclusion that the stouter character of the organs in this plant is causally connected with the increased number of chromosomes. Where the number of cells formed is approximately similar, as in two allied forms of plant in this case, the greater size of the cells would naturally give a stouter habit, but it is clear that large cells do not necessarily mean greater size. The cells of Salamander and Proteus are the largest found among Vertebrates, but those Amphibia are not the largest Vertebrates. It is curious to note how different are these discoveries concerning differences in the number of chromosomes from the conception of Morgan that a mutation depends on a factor situated in a part of one chromosome.
More copious details concerning mutations will be found in the publications cited. The question to be considered here is how far the claim is justified that the facts of this kind hitherto discovered afford an explanation of the process of evolution. It seems probable that mutations are of different kinds, as exemplified in Oenothera by gigas and rubricalyx respectively, the former producing only sterile hybrids, the latter behaving exactly like a Mendelian unit. There can be little doubt that, as Bateson states, numerous forms recognised as species or varieties in nature differ in the same way as the races or breeds of cultivated organisms which differ by factors independently inherited. There are facts, however, which prove that all species are not sterile inter se, and that their characters when they are hybridised do not always segregate in Mendelian fashion. John C. Phillips, [Footnote: Journ. Exper. Zool., vol. xviii., 1915.] for example, crossed three wild species of duck, Anas boscas (the Mallard) with Dafila acuta (the Pintail) and with Anas tristis. In the former cross he states that except for one or two characters there seemed to be no more tendency to variation in the F2 generation than in the F1. An F1 Pintail-Mallard [female] was mated with a wild Pintail [male]. According to Mendelian expectation the offspring of this mating should have been half Pintail and half Pintail-Mallard hybrids, but Phillips states that on casual inspection the plumage of all the males appeared pure Pintail although the shape was distinctly Mallard-like. The statement is, however, open to criticism. The question is, what were the unit characters in the parent species? If the unit characters were very small and numerous, an individual in which all the characters of the Pintail existed together among the offspring of the hybrid mated with pure Pintail would be rare in proportion to the individuals presenting other combinations. Of the F2's obtained from crossing Anas tristis [male] with Anas boscas [female] Phillips obtained 23 females and 16 males. The females were all alike and similar to F1 females. Of the males one was a variate specially marked, about half-way between the F1 type and the Mallard parent. This, according to Phillips, was a segregate. The rest showed a range of variation but no distinct segregation.
It is somewhat surprising that Mendelian experts, who seem to believe that species are distinguished by Mendelian characters, have not made systematic experiments on the crossing of species in order to prove or disprove their belief.
For my own part I cannot help thinking that the origin of varieties in species in a domesticated or cultivated state is in a sense pathological. Such variation doubtless occurs in nature, but not with such luxuriance. The breeds of domestic fowls differ so greatly that Bateson and others refuse to believe that they have all arisen from the single species Gallus bankiva. It seems to me from the evidence that there cannot be any doubt that they have so arisen. One fact that impresses my mind is that if we consider colour variations in domesticated animals, we find that a similar set of colours has arisen in the most diverse kinds of animals with sometimes certain markings or colours peculiar to one group, e.g. dappling in horses, wing bars in pigeons. Thus in various kinds of Mammals and Birds we have white and black, red or yellow, chocolate with various degrees of dilution, and piebald combinations. Why should forms originally so different, as the cat with its striped markings and the rabbit with no markings at all, give rise to the same colour varieties? It seems probable that the reason is that the original form had the small number of pigments which occur mixed together in very small particles, and that in the descendants the single pigments have separated out, with increase or decrease in different cases. It is true that historical evidence tends to show that the greatest variations, such as albinism in one direction or excess of pigment in the other in the Sweet Pea, were the first to arise (see Bateson, Presidential Address to British Association, Australia, 1914, Part I.), and the splitting appears often to be intentionally produced by crossing these extreme variations with the original form, but the possibility remains that the conditions of domestication, abundant food, security and reduced activity, lead to irregularity in the process of heredity. In any case the mere separation among different individuals of factors originally inherited together in one complex does not account for the origin of the complex or of the factors. This is somewhat the same idea as that of Bateson when he states that it is easy to understand the origin of a recessive character but difficult to conceive the origin of a dominant.
The point, however, which I desire most to emphasise is that the investigations we have been discussing are concerned with variations which have no relation whatever to adaptation, and afford no explanation of the evolution of adaptations. These variations perform no function in the life of the individual, have no relation to external conditions, either in the sense of being caused by special conditions or fitting the individual to live in special conditions. A still more important fact is that they do not explain the origin of metamorphosis. They do not arise by a metamorphosis: in the case of the rose comb of fowls the chick is not hatched with a single comb which gradually changes into a rose comb, but the rose comb develops directly from the beginning. Mutationists and Mendelians do not seem in the least to appreciate the importance of metamorphosis or of development generally in considering the relation of the mutations or factors which they study to evolution in general, because they have not grasped the fact that there are two kinds of characters to be explained, adaptational and non-adaptational. T. H. Morgan, for example, [Footnote: A Critique of the Theory of Evolution, p. 67 (Princeton, U.S.A., and London, 1916).] describes a mutation in Drosophila consisting in the loss of the eyes, and triumphantly remarks: 'Formerly we were taught that eyeless animals arose in caves. This case shows that they may also arise suddenly in glass milk-bottles by a change in a single factor.' As it stands the statement is perfectly true, but it is obvious that the writer does not believe that the darkness of caves ever had anything to do with the loss of eyes. It is almost as though a man should discover that blindness in a certain case was due to a congenital, i.e. gametic, defect, and should then scoff at the idea that any person could become blind by disease. Some of those who specialise in the investigation of genetics seem to give inadequate consideration to other branches of biology. It is a well-established fact that in the mole, in Proteus, and in Ambtyopsis (the blind fish of the Kentucky caves), the eyes develop in the embryo up to a certain stage in a perfectly normal way and degenerate afterwards, and that they are much better developed in the very young animal than in the adult. Does this metamorphosis take place in the blind Drosophila of the milk-bottle? The larva of the fly is, I believe, eyeless like the larvae of other Diptera, but Morgan says nothing of the eye being developed in the imago or pupa and then degenerating. There is therefore no relation or connexion between the mutation he describes and the evolution of blindness in cave animals. It is a truth, too often insufficiently appreciated by biologists, that sound reasoning is quite as important in science as fact or experiment. Loeb [Footnote: The Organism as a Whole, p. 319 (New York and London, 1916).] also endeavours to prove that the blindness of cave animals is no evidence of the influence of darkness in causing degeneration of the eyes. He refers to experiments by Uhlenhuth, who transplanted eyes of young Salamanders into different parts of their bodies where they were no longer connected with the optic nerves. These eyes underwent a degeneration which was followed by a complete regeneration. He showed that this regeneration took place in complete darkness, and that the transplanted eyes remained normal when the Salamanders were kept in the dark for fifteen months. Hence the development of the eyes does not depend on the influence of light or on the functional action of the organs. But it must be obvious to any biologist who has thoroughly considered the problem, that this experiment has little to do with the question of the cause of blindness in cave animals. No one ever supposed that cave fishes became blind in fifteen months, or in fifteen years. The experiment cited merely proves that in the individual the embryonic or young eye will continue developing by heredity even after it is transplanted and in the absence of light. But the eye of the Mammal normally develops in the uterus in the absence of light.
In his remarks concerning Typhlogobius, a blind fish on the coast of southern California, Loeb seems to be mistaken with regard to the facts. He states that this fish lives 'in the open, in shallow water under rocks, in holes occupied by shrimps.' According to Professor Eigenmann the same species of shrimp is found all over the Bay of San Diego, and is accompanied by other genera of goby, such as Clevelandia and Gillichthys, which have eyes; but these fishes live outside the holes, and only retreat into them when frightened, while the blind species is found only at Point Loma, and never leaves the burrows of the shrimp. It would appear, therefore, that Typhlogobius lives in almost if not quite complete darkness, instead of being, as Loeb states, 'blind in spite of exposure to light,' while the closely allied forms which are exposed to light are not blind.
Loeb states, on the authority of Eigenmann, that all those forms which live in caves were adapted to life in the dark before they entered the cave, because they are all negatively heliotropic and positively stereotropic, and with these tropisms would be forced to enter a cave whenever they were put at the entrance. Even those among the Amblyopsidae which live in the open have the tropisms of the cave dweller. But these latter are not blind, and the argument only tends to show that the blind fish Amblyopsis entered the caves before it was blind. Nocturnal animals generally must be said to be negatively heliotropic, but these usually have larger and more sensitive eyes than the diurnal.
It is said, however, that Chologaster agassizii, which is not blind, lives in the underground streams of Kentucky and Tennessee, but I think it is open to doubt whether it is a species entirely confined to darkness.
Another point which Loeb omits to mention is the absence of pigment in cave animals, especially Vertebrates such as Amblyopsis and Proteus. If absence of light is not the cause of blindness in these cases, how is it that the blindness is always associated with absence of pigment, since we know that the latter in Fishes and Amphibia is due to the absence of light? It has been shown that Proteus when kept in the light develops some amount of pigment, although it does not become pigmented to the same degree as ordinary Amphibia. We have here, I think, an example of the essential difference between mutations and somatic modifications. Absence of the gametic factor or factors for pigmentation results in albinism, and no amount of exposure to light produces pigmentation in albinos, e.g. albino Axolotls which are well known in captivity. Absence of light, on the other hand, prevents the development of pigment. The question therefore is whether the somatic modification is inherited. The fact that Proteus does not rapidly become as deeply coloured when exposed to light as ordinary Amphibia shows that the gametic factors for pigmentation have been modified as well as the somatic tissues.
Loeb attributes the blindness of cave fishes to a disturbance in the circulation and mutation of the eyes originally occurring as a mutation. But how could an explanation of this kind be applied to the case of Anableps tetrophthalmus, in which each eye is divided by a partition of the cornea and lens into an upper half adapted for vision in air and a lower half for vision in water? This fish lives in the smooth water of estuaries in Central America, and swims habitually with the horizontal partition of the lens level with the surface of the water. It is impossible to understand in this case, firstly, how a mutation could cause the eyes to be divided and doubly adapted to two different optic conditions, and, secondly, how at the same time a convenient 'tropism' should occur which caused the animal to swim with its eyes half in and half out of water. Are we to suppose that the upper half of the body or eye had a positive heliotropism and the lower half a negative heliotropism? The fact is that the fish swims at the surface in order to watch for and feed on floating particles. The tropism concerned is the food tropism, but what is gained by calling the search for food common to all active animals a tropism, and how is the search for food before the food is perceptible to the senses, before it can act as a stimulus on a food-sensitive substance in the body, to be compared to a tropism at all?
Loeb undertakes to prove that the organism as a whole acts automatically according to physicochemical laws. But he misses the question of evolution altogether. For example, he quotes Gudernatsch as having proved that legs can be induced to grow in tadpoles at any time, even in very young specimens, by feeding them with thyroid gland. Loeb writes: 'The earlier writers explained the growth of the legs in the tadpole as a case of an adaptation to life on land. We know through Gudernatsch that the growth of the legs can be produced at any time by feeding the animal with the thyroid gland.' Obviously he thinks that these two propositions are contradictory to each other, whereas there is no contradiction, between them at all. Loeb actually supposes that the thyroid is the cause of the development of the legs. Logically, if this were the case it would follow that if we fed an eel or a snake with thyroid it would develop legs like those of a frog, and if a man were injected with extract of the testes of a stag he would develop antlers on his forehead. It will be obvious to most biologists that the thyroid, whether that of the tadpole itself or that which is supplied as food, only causes the development of legs because the hereditary power to develop legs is already present. The question is how this hereditary power was evolved. Legs are an adaptation to life on land. What we have to consider and to investigate is whether the legs arose as a gametic mutation or as a direct result of locomotion on land.
The general result of clinical and experimental evidence is to show that the hormone of the thyroid is necessary to normal development. The arrest of development in cretinous children is due to some deficiency of thyroid secretion, and is counteracted by the administration of thyroid extract. Excess of the secretion produces a state of restlessness and excitement associated with an abnormally rapid rate of metabolism and protrusion of the eye-balls (Graves' disease). The physiological text-books, however, say nothing of precocity of development in children as a result of hyperthyroidism. This, however, is undoubtedly what occurs in the case of tadpoles. The legs would naturally develop at some time or other, after a prolonged period of larval life. Feeding with thyroid causes them to develop at once. I have repeated Gudernatsch's experiment with the following results:—
This year I had a considerable number of tadpoles of the common English frog, which were hatched between March 26 and March 29. On April 12, when they had all passed the stage of external gills and developed internal gills and opercula, I divided them into two lots, one in a shallow pie-dish, the other in a glass cylinder. To one lot I gave a portion of rabbit's thyroid, to the other a piece of rabbit's liver. They fed eagerly on both. Afterwards I obtained at intervals of a week or so the thyroid of a sheep. I have seen no precise details of Gudernatsch's method of feeding tadpoles, but my own method was simply to put a piece of thyroid into the water containing the tadpoles and leave it there for several days, then to take it out and put in another piece, changing the water when it seemed to be getting foul.
April 22. Noticed that the non-thyroid tadpoles were larger than those fed on thyroid. Changed the former into the pie-dish and the latter into the glass jar, to make sure that the difference in size was not due to larger space.
May 3. Only eighteen of the non-thyroid tadpoles surviving, owing to the water having become foul, but these are three times as large as those fed on thyroid. In the latter no trace of hind-legs was visible, but the abdominal region was much emaciated and contracted, while the head region was broader.
May 4. Noticed minute white buds of hind-legs in the thyroid-fed tadpoles.
May 6. A number of the thyroid-fed were dying, and the skin and opercular membranes were swollen out away from the tissues beneath.
Largest normal tadpole, 2.7 cm. long.
body, 1.0 "
tail, 1.7 "
Largest thyroid-fed tadpole, 1.1 cm. long.
body, 0.5 "
tail, 0.6 "
May 10. A great number of the thyroid-fed dead and the rest dying, lying at the bottom motionless. They now had the tail much shorter, and the fore-legs showing as well as the hind, but the latter not very long, and without joints or toes.
Period from first feeding with thyroid, thirty days. I now decided to feed the controls with thyroid, expecting that as they were large and vigorous they would have strength enough to complete the metamorphosis and become frogs.
May 15. Fed the controls with thyroid for first time.
The smallest of them was in total length 1.7 cm.
body, 0.7 "
tail, 1.0 "
The largest measured was in total length 2.2 "
body, 0.8 "
tail, 1.4 "
May 25. All but two of the tadpoles dead. The tails were only half the original length, all had well-developed hind-legs, some with toes, but the fore-legs were beneath the opercula, not projecting from the surface.
Smallest total length, 1.2 cm.
body, 0.5 "
tail, 0.7 "
Largest total length, 1.8 "
body, 0.7 "
tail, 1.1 "
These last measurements were made after the tadpoles had been preserved in spirit, and were therefore doubtless somewhat less than in the fresh condition. Making allowance for this it is evident that the tails had undergone reduction as part of the metamorphosis, but the body was also shorter. There is some reason therefore for concluding that actual reduction in size of body occurs as the result of metamorphosis induced by thyroid feeding. As in the other case the skin and opercular membranes were distended by liquid beneath them.
The total period of the change in this second experiment was ten days.
I conclude that the amount of thyroid eaten was so excessive as to cause pathological conditions as well as precocious metamorphosis, so that the animals died without completing the process.
On June 10 I still had four tadpoles which had never had thyroid, but only pieces of meat, earthworm, or fish. These were very much larger than any of the others, were active and vigorous, and the largest one showed small rudiments of hind-legs, the others none at all.
CHAPTER VII
Metamorphosis And Recapitulation
As one of the most remarkable examples of metamorphosis and recapitulation in connexion with adaptation we will consider once more the case of the Flat-fishes which I have already mentioned in an earlier chapter. These fishes offer perhaps the best example of the difference between gametogenic mutations and adaptive modifications. In several species specimens occur occasionally in which the asymmetry is not fully developed. [Footnote: See 'Coloration of Skins of Fishes, especially of Pleuronectidae,' Phil. Trans. Royal Soc., 1894.] These abnormalities are most frequent in the Turbot, Brill, Flounder, and Plaice. The chief abnormal features are pigmentation of the lower side as well as of the upper, the eye of the lower side, left or right according to the species, on the edge of the head instead of the upper side, and the dorsal fin with its attachment ceasing behind this eye, the end of the fin projecting freely forwards over the eye in the form of a hook. Such specimens have been called ambicolorate, but it is an important fact that they are also ambiarmate—that is to say, the scales or tubercles which in the normal Flat-fish are considerably reduced or absent on the lower side, in these abnormal specimens are developed on the lower side almost as much as on the tipper. Minor degrees of the abnormality occur: in Turbot with the hook-like projection of the dorsal fin the lower side of the head is often without pigment, while the rest of the lower side is pigmented. Less degrees of pigmentation of the lower side occur without structural abnormality of the eye and dorsal fin.
There is no evidence that these abnormalities are due to abnormal conditions of life. One specimen of Plaice of this type was kept alive in the aquarium, and it lay on its side, buried itself in the sand, and when disturbed swam horizontally, like a normal specimen. The abnormalities are undoubtedly mutations of gametic origin. The development of one of these abnormal specimens from the egg has not to my knowledge been traced, but there is no reason to suppose that the fish develops first into the normal asymmetrical condition and then changes gradually to the abnormal condition described. On the contrary, everything points to the conclusion that the abnormality is an arrest or incomplete occurrence of the normal process of development, i.e. of the normal metamorphosis. T. H. Morgan, in a volume published some years ago, [Footnote: Evolution and Adaptation.] put forward the extraordinary view that the Pleuronectidae arose from symmetrical fishes by a mutation which was entirely gametogenetic and entirely independent of habits or external conditions, and then finding itself with two eyes on one side of its head, and no air-bladder, adopted the new mode of life, the new habit of lying on the ground on one side in order to make better use of its asymmetrically placed eyes. According to this view habits have been adapted to structure, not structure to habits. We are thus to believe that Amphibia came out of the water and breathed air because by an accidental mutation they possessed lungs and a pulmonary circulation capable of atmospheric respiration. Such is the result of applying conclusions derived from phenomena of one kind to phenomena of a totally different kind. One of the chief differences between structural features and correlations which are adaptive from those which are not is the process of metamorphosis, where we see the structure changing in the individual life history as the mode of life changes. The egg of the Flat-fish develops into a symmetrical pelagic larva similar to that of many other marine fishes. The larva has an eye on each side of its head and swims with its plane of symmetry in a vertical position: it has also colour on both sides equally. When the skeleton begins to develop the transformation takes place: the eye of one side, left in some species, right in others, moves gradually to the edge of the head and then on to the other side. The dorsal fin extends forward, preserving its original direction, and so passes between the eye that has changed its position and the lower side of the fish, on which that eye was originally situated. In some cases this extension of the fin takes place earlier and the eye passes beneath the base of the fin to reach the other side. Any one who takes the trouble to make himself acquainted with the facts will see that the three chief features of the Pleuronectid—namely, the position of the eyes, the extension of the dorsal and ventral fins, and the absence of pigment from the lower side—are not structurally correlated with one another at all as changes in different parts of the organism in a mutation are said to be, but are all closely related to their functions in the new position of the body. A mutation consisting in general asymmetry would be comprehensible, but the head of the Pleuronectid is not asymmetrical in a general sense, but only so far as to allow of the changed position of the eyes. The posterior end of the skull is as symmetrical as in any other fish, and in some cases the mouth and jaws are also symmetrical, entirely unaffected by the change in the position of the eyes. In other cases the jaws are asymmetrical in a direction opposite to that of the eyes, there is no change of position but a much greater development of the lower half of the jaws, reduction, with absence of teeth, of the upper half. In the latter case the fish feeds on worms and molluscs living on the ground and seized with the lower half of the jaws, in the former the food consists of small fish swimming above the Flat-fish and seized with the whole of the jaws (Turbot, Halibut, etc.).
I contend, then, that the mode in which the normal Flat-fish develops is quite different from that in which mutations arise. T. H. Morgan [Footnote: A Critique of the Theory of Evolution (1916), p. 18.] states that a variation arising in the germ-plasm, no matter what its cause, may affect any stage in the development of the next individuals that arise from it. In certain cases this is true, that is to say, when there are very distinct stages already. For example, a green caterpillar becomes a white butterfly with black spots. A mutation might affect the black spots, an individual might be produced which had two spots on each wing instead of one, and no sign of this mutation would be evident in the caterpillar. But my contention is that when this mutation occurred, the original condition of one spot would not be first developed and then gradually split into two. Morgan proceeds to state clearly what I wish to insist upon concerning mutations. He writes that in recent times the idea that variations are discontinuous has become current. Actual experience, he tells us, shows that new characters do not add themselves to the line of existing characters, but if they affect the adult characters, they change them without as it were passing through and beyond them.
Now in the case of the ancestors of the Flat-fish the adult and the larva must have had the same symmetry with regard to eyes and colour and the dorsal fin terminated behind the level of the eyes. Thus the variations which gave rise to the Flat-fish were not discontinuous but continuous. In each individual development now, not merely hypothetically in the ancestor, the condition of the adult arises by an absolutely continuous change of the eyes, fins, and colour. Such a continuous change cannot be explained by a discontinuous variation, i.e. a mutation. The abnormalities above mentioned on the other hand, although they doubtless arise from the same kind of symmetrical larva as the normal Flat-fish, and develop by a gradual and continuous process, do not presumably pass through the condition of the normal adult Flat-fish and then change gradually into the condition we find in them. As compared with the normal Flat-fish they arise by a discontinuous variation, they are mutations, whereas the normal Flat-fish as compared with its symmetrical ancestor arises by a continuous change.
In order to make my meaning clear I must point out that I have been using the word continuous in a different sense from that in which it is used by other biologists, Bateson for example. The word has been applied previously to variations which form a continuous series in a large number of individuals, each of which differs only slightly from those most similar to it. No two individuals are exactly alike, and thus such continuous variations are universal. According to the theory of natural selection the course of evolutionary change in any organ or character would form a similar continuous series, the mean of each generation differing only by a small difference from that of the preceding. According to the modern mutationists such small differences are to be called fluctuations, and have no effect on evolution at all, are not even hereditary, are not due to genetic factors in the gametes. Discontinuous variations, on the other hand, are as a rule differences in an individual from the normal type and from its parents of considerable degree, and are conspicuous: these are what are called mutations.
The mutationists and Mendelians have not shown how the essential characteristics of mutations are to be reconciled with the facts of metamorphosis, or with recapitulation in development which is so often associated with metamorphosis. T. H. Morgan is the only mutationist, so far as my reading has gone, who has attempted to do this, and he seems to me to have failed to understand the difficulties or even the nature of the problem. He points out that the embryos of Birds and Mammals have gill slits representing the same structures as those of the adult Fish, but the young stage of the Fish also possessed gill slits, therefore it is 'more probable that the Mammal and Bird possess this stage in their development simply because it has never been lost.' He concludes therefore that the gill slits of the embryo Bird represent the gill slits of the embryo Fish, and not the adult gill slits of the Fish, which have been in some mysterious way pushed back into the embryo of the Bird.
Morgan evidently does not realise that the Birds and Reptiles must have been derived from Amphibia, and that the embryo Reptile or Bird with gill slits and gill arches is merely a tadpole enclosed in an egg shell. The Frog in its adult state differs much from a Fish, while the larva in its gill arches and gill slits resembles a Fish. Morgan contends that the new characters do not add themselves to the end of the line of already existing characters. But in the case of the Frog this is exactly what they have done. The existing characters were in this case the gill arches and slits. Those who believe in recapitulation do not suppose that the animal had to live a second life added on to the life of its ancestors and that the new characters appeared in the second life. They believe that in the ancestor a certain character or general structure of body when developed persisted without change throughout life like the gill arches and slits in a Fish. At some stage of life before maturity this character underwent a change, and in the descendants the development of the original character and the change were repeated by heredity. There is no 'mysterious pushing back of adult characters into the embryo,' although it is possible or even probable that in some cases the change gradually became earlier in the life history: it is the new character which is pushed back, not the adult character of the ancestor.
It is perfectly true, as Morgan says, that new characters which arise as discontinuous variations—in other words, those kinds of variation which are called mutations—do not add themselves to the line of already existing characters, but 'change the adult characters without as it were passing through and beyond them.' The mutations which Morgan describes in his own experiments on Drosophila illustrate this in every case. In no case is the original organ or character, e.g. wings, of the normal Fly first developed and then changed by a gradual continuous process into the new character. It might perhaps be said that this took place in the pupa, but that seems impossible, for the complete wing is not fully developed in the pupa. The same truth is equally apparent in the mutations described in OEnothera. It follows, therefore, that none of the evolutionary changes which have produced what are called recapitulations can have been due to changes of that kind which is known as mutation.
The abnormalities in Pleuronectidae to which I have referred are of the kind usually regarded as due to arrested development. But closer consideration gives rise to doubt concerning the validity of this explanation. It might be supposed that the attached base of the dorsal fin is unable to extend forward because the eye on the edge of the head is in the way, but if the metamorphosis is arrested, why should the fin grow forward in a free projection? I have described a very abnormal specimen of Turbot in a paper communicated to the Zoological Society of London, [Footnote: Proc. Zool Soc., 1907.] and in that paper have discussed other possible explanations of these mutations. In the specimen to which I refer the pigmentation instead of being present on both sides was reversed: the lower side was pigmented from the posterior end to the edge of the operculum (Plate II, fig. 2), while the upper side was unpigmented excepting a scattering of minute black specks and a little pigment on the head (Plate II., fig. 1).
[Illustration: PLATE II, Fig. 1 and Fig. 2,
Abnormal Specimen Of Turbot]
I have suggested that the explanation here is that in the zygote the primordia of a normal body and a reversed head have been united together. We may suppose that different parts of the body are represented in the gametes by different determinants or factors, and therefore it is possible that these factors may be separated. In the specimen we are considering the body is normal or nearly so, with the pigmentation on the left side, which is normal for the Turbot, while the head has both eyes with some pigment on the right side and the left side unpigmented. Reversed specimens occasionally occur in many species of Pleuronectidae, and if the determinants for a reversed head and a normal body were united in one zygote, the curious abnormality observed might be the result. It is just a possibility that if this fish which was only 4.4 cm. long had lived to adult size, the upper side would have become pigmented under the influence of light, while the strong hereditary influence would have prevented the disappearance of the pigment from the lower side. In that case the adult condition would have been similar to that of ordinary ambicolorate specimens, but reversed, with eyes on the right side instead of the left. Other explanations of the more frequent ambicolorate mutation are possible: the body may consist of two left sides instead of a left and right, joined on to a normal head. But the first suggestion seems the more probable, as two rights or two lefts would not be symmetrical. Supposing the head and body not properly to belong to each other, one being reversed and one normal, we can in a way understand why the dorsal fin does not form the usual connexion with the edge of the head, because the determinants would not be in the normal intimate relation to each other. In thus writing of reversed and normal it must be understood that the former word does not mean merely turned over, for in that case right side of the body would be joined to the left side of the head, and the dorsal fin would be next to the ventral side of the head, which is not the case. What is meant is that a left side of the body which is normally pigmented is joined to a left side of the head which instead of having both eyes has neither, the two eyes being on the right side of the head which is joined to the right side of the body, and this is normal and unpigmented. The dorsal fin belonging to the normal sinistral body would therefore have a congenital tendency in the metamorphosis to unite with the head on the outer side of the original lower or right eye after it has moved to the left side. Actually, however, in this abnormal specimen it finds itself on the outer side of the left eye which has passed to the right side, and it has no tendency to unite with this part of the head. At the same time it has no tendency to bend over at an angle to reach the outer side of the right eye, and therefore it grows directly forward without attachment to the head at all.
It will be seen, therefore, that what is changed in relative position in these mutations is not the actual parts of the body, but merely the characters of those parts. In a sinistral Flat-fish, whether it is normally sinistral like the Turbot or abnormally like a 'reversed' Flounder, the viscera are in the same position as in a dextral specimen: the liver is on the left side, the coils of the intestine on the right. Thus in a reversed or sinistral Flounder, which is normally dextral, the left side which is uppermost is still the left side, but it has colour and two eyes, whereas in the normal specimen the right side has these characters and not the left. Thus we are forced to conceive of the determinants in the chromosomes of the fertilised ovum which correspond to the two sides of the body, as entirely distinct from the determinants which cause the condition or 'characters' of the two sides, unless indeed we suppose that determinants of right side with eyes and colour occur in some gametes and of right side without eyes and colour in others, and vice versa, and that homozygous and heterozygous combinations occur in fertilisation. On this last hypothesis the mutation here considered might be a heterozygous specimen, with the dextral condition dominant in the head and the sinistral in the body. Or it might be somehow due to what Morgan and his colleagues have called crossing over in the segregation of heterozygous chromosomes, so that a part corresponding to a sinistral body is united with a part corresponding to a dextral head.
My conclusion from the evidence is that any process of congenital development may in particular zygotes exhibit a mutation, a departure from the normal. We need not use the term heredity at all, or if we do, must remember that in the present argument it does not refer to any transmission from the parent. The factors in the gametes of the normal Flat-fish egg cause the normal metamorphosis to take place after the larval symmetry has lasted a certain time. In occasional individuals the factors whatever they are, portions of the chromosomes or arrangement of the chromosomes or anything else, are different from those of the normal egg, and in consequence the abnormalities above described are developed. But the chief fact which I cannot too strongly emphasise is that the development of the abnormality from the symmetrical larva is direct, whether it is merely an arrest of development or an abnormal combination of reversed and normal parts. The abnormal development is not due to a change occurring after the normal asymmetry has been developed. These abnormalities are true mutations.
The evolution of the normal Flat-fish, on the other hand, was obviously due to a change of a different kind. Here we are dealing with the change from a symmetrical fish to the asymmetrical. Judging from what takes place in other mutations, it was quite possible for asymmetry to have developed directly from the egg, in consequence of some difference in the chromosomes of the nucleus. It has been shown that placing a fish egg for a short time in MgCl[2] [Footnote: Stockard, Arch. Eut. Mech., xxiii. (1907).] causes a cyclopean monstrosity to be developed in which the two eyes are united into one: but the two eyes do not develop separately first and then gradually approach each other and unite, the development of the optic cups is different from the first. In the normal Flat-fish the evolution that has occurred is the original development of the symmetrical fish, and the subsequent continuous gradual change in eyes, fin, and colour to the adult Flat-fish as we see it. All the evidence accumulated by the experiments and observations of mutationists and Mendelians goes to prove that this change is of an entirely different kind from those variations which are described as mutations, or as loss or addition of genetic factors.
This being the case, we have to inquire what is the explanation of the evolution of the normal metamorphosis.
The important fact is that the original symmetrical structure of the larva and the asymmetrical structure of the adult Flat-fish correspond to the different positions of the body of the fish in relation to the vertical, the horizontal ground at the bottom of the water, and incidence of light. The larva swims with its plane of symmetry vertical like most other fishes; its locomotion requires symmetrical development of muscles and fins; the two sides being equally exposed to light, it requires an eye on each side, and the pigment on each side is also related to the equal exposure to light. The adult lying with one side on the ground has its original plane of symmetry horizontal and parallel to the ground, and only the other side exposed to light, and on this side only eyes and colour, i.e. pigment. The change of structure corresponds with the change of habit. It consists in the change of position of the lower eye, the extension of the dorsal fin forwards, and the disappearance of pigment from the lower side. In the actual metamorphosis these changes take place as the skeleton develops, before the hard bones are fully formed, while the fish is still small, but the young Turbot reaches a much larger size before metamorphosis is complete, namely, about one inch in length, than the young Plaice or Flounder. It is of little importance to consider whether at the beginning of the evolution the change of position occurred late or early in life. It may have become earlier in the course of the evolution. The important matter is to consider the evidence in support of the conclusion that the relation to external conditions has been the cause of the evolutionary change. We have already seen that the nature of the change and the relation of the change of structure to the change of conditions necessarily tend to the inference that the latter is the cause of the former. But we have to consider the particular changes in detail.
To take first the loss of pigmentation from the lower side. I have shown experimentally that exposure of the lower sides of Flounders to light reflected upwards from below causes development of pigment on the lower side. At the same time the experiments proved that the loss of pigment in the fish in the natural state and the development of it under exposure to light were not merely direct results of the presence or absence of light in the individual, for in some cases the young fish were placed in the apparatus before the pigment had entirely disappeared from the lower side, and the metamorphosis went on, the lower side becoming quite white, and the pigment only developed gradually after long exposure to the light. In the principal experiment four specimens were placed in the apparatus on September 17, 1890, when about six months old and 7 to 9 cm. in length. One of these died on July 1, 1891, and had no pigment on the lower side. The other three all developed pigment on that side. In one it was first noticed in April 1891, and in the following November the fish was 22 cm. long and had pigmentation over the greater part of the lower side (Plate III.). Microscopically examined, the pigmentation was found to consist of black and orange chromatophores exactly similar to those of the upper side. Some hundreds of young Flounders were reared at the same time under ordinary conditions and none of them developed pigment.
It is clear, therefore, that exposure of the lower side to light and reduction of the amount of light falling on the upper side (for the tops of the aquaria used were covered with opaque material) does not cause the two sides to behave in the same way in respect of pigment, as they would if the normal condition of the fish was merely due to the difference in the exposure to light of the two sides in the individual life. There is a very strong congenital or hereditary tendency to the disappearance of pigment from the lower side, and this is only overcome after long exposure to the light. On the other hand, if the disappearance of the pigment were due to a mutation, were gametogenic and entirely independent of external conditions, there would be no development of pigment after the longest exposure. To prove that an inherited character is an acquired character is quite as good evidence as to show that an acquired character is inherited. The latter kind of evidence is very difficult to get, for the effect of conditions in a single lifetime is but slight, and is not likely to show a perceptible inherited effect. The theory that adaptations are due to the heredity of the effects of stimulation assumes that the same stimulus has been acting for many generations.
[Illustration: PLATE III - Flounder, Showing Pigmentation Of Lower Side
After Exposure To Light]
It is necessary, however, to consider how far the conclusions drawn from these experiments are contradicted by the mutations occurring in nature, some of which have already been mentioned. We will consider first ambicolorate specimens. If the absence of pigment from the lower side in normal Flat-fishes is due to the absence of light, how is it that the pigmentation persists on the lower side of ambicolorate specimens, which is no more exposed to light than in normal specimens? The answer is that in the mutants the determinants for pigmentation are united with the determinants for the lower side of the fish. My view is that the differentiation of these determinants for the two sides was due in the course of evolution to the different exposure to light, was of somatic origin, but once the congenital factors or determinants were in existence they were liable to mutation, and thus in the ambicolorate specimens there is a congenital tendency to pigmentation on the lower side, which would only be overcome by exclusion of light for another series of generations.
Mutations also occur in which part or whole of the upper side is white and unpigmented. Several such specimens are mentioned in the memoir by myself and Dr. MacMunn in the Phil. Trans. already cited, one being a Sole which was entirely white on the lower side, and also on the upper, which was pigmented only over the head region from the free edge of the operculum forwards. Since the upper sides in these specimens are fully exposed to light in the natural state and yet remain unpigmented, it would appear impossible to believe that the action of light was the cause of the development of pigment on the lower sides of normal specimens in my experiments. To some it may be so, but in my own opinion the one fact is as certain as the other. I believe the two facts can be reconciled. I had one specimen of Plaice in the living condition which had the middle third of its upper surface white, and the whole of the lower side white as usual. This specimen was kept for 4-1/2 months with its lower surface exposed to light and the upper side shaded. At the end of that period there were numerous small patches of pigment scattered over the lower side principally in the regions of the interspinous bones, above and below the lateral line. In the area of the upper side, which was originally unpigmented, there were also numerous small pigment spots. I believe, therefore, that in this case there were determinants for absence of pigment not only on the lower side but on part of the upper side also, and that so long as light was excluded from the lower side the patch on the upper side remained unpigmented in sympathy. When the congenital tendency of the determinants on the lower side was overcome by the action of light, the white patch on the upper side also began to develop pigment.
Lastly, I may refer again to the specially abnormal Turbot mentioned above. In this case the lower side was over the greater part pigmented and the upper side white, and this would appear to contradict the conclusion just drawn concerning the piebald Plaice. But this Turbot was only 4.4 cm. long, and is the only case known to me where so much of the lower side was pigmented with the upper side almost entirely white. The theory of sympathy or correlation might apply here since the lower side of the head was unpigmented, but from the small size of the specimen and the amount of pigment on the lower side, it seems to me most probable that if the specimen had lived to be adult the upper side would have developed pigment under the action of light and the specimen would have become ambicolorate.
When we compare the results reached by the mutationists with those obtained by the Mendelians we find that they tend to two different conceptions of the relation between the gametes and the organism developed from them. The effect of a change in the determinants of the gametes according to the mutationists is evident in every part of the plant. A factor in Mendelian experiments usually affects only one organ or one part of the organism. The factor for double hallux in fowls, for instance, may coexist with single comb or rose comb. The general impression produced on the mind by study of Mendelian phenomena is that the organism is a mosaic of which every element corresponds to a separate element in the chromosomes. Thus we know that what we call a single factor may cause the whole plumage of a fowl to have the detached barbs, which constitutes the Silky character, but we also know that an animal may be piebald, strongly pigmented in one part and white or unpigmented in another. So we find in these Flat-fish mutations mosaic-like forms which evidently result from mosaic-like factors in the gametes, or in the chromosomes of the gametes.
Experimental evidence concerning the movement of the lower eye to the upper side and of the forward extension of the dorsal fin has not been obtained, though years ago I made some attempts, at the suggestion of Mr. G. J. Romanes, to obtain such evidence with regard to the eye by keeping young Flounders, already partially metamorphosed, in a reversed position. I did not succeed in devising apparatus which would keep the young fish alive in the reversed position for a sufficiently long time. We can only consider, therefore, whether those other changes can reasonably be attributed to the conditions of life. Anatomical investigation shows that the bony interorbital septum composed principally of the frontal bones, which in symmetrical fish passes between the eyes, is still between the eyes in the Flat-fish, but has been bent round through an angle of 90 degrees on the upper side, while in the lower side a new bony connexion has been formed on the outer side of the eye which has moved from the lower side. This connexion is due to a growth from the prefrontal backwards to join a process of the frontal, and is entirely absent in symmetrical fishes. It is along this bony bridge that the dorsal fin extends. The origin of the eye muscles and of the optic nerves is morphologically the same as in symmetrical fishes. On the theory of modification by external stimuli we must naturally attribute the dislocation of the eye of the lower side to the muscular effort of the fish to direct this eye to the dorsal edge, but something may also be due to the pressure of the flat ground on the eye-ball. There is little difficulty in attributing the bending of the interorbitl septum to pressure of the lower eye-ball against it, pressure which is probably due partly if not chiefly to the action of the eye muscles. The formation of the bony bridge outside the dislocated eye is more difficult to explain, as I have never had the opportunity to study the relation of this bridge to the muscles. It is worth mentioning that in the actual development of Turbot and Brill the metamorphosis takes place to a considerable degree while the young fish is pelagic, before the habit of lying on the ground is assumed, but of course this is no evidence that the change was not originally caused by the habit of lying on the ground.
With regard to the extension of the dorsal fin there is no difficulty in discovering a stimulus which would account for it. Symmetrical fishes propel themselves chiefly by the tail; in shuffling over the ground or swimming a little above it. Flat-fishes move by means of undulations of the dorsal and ventral fins. Increased movement produces hypertrophy, and according to the theory here maintained, not merely enlargement of parts existing, but phylogenetic increase in the number of such parts, here fin rays and their muscles. In Flat-fishes the dorsal and ventral fins extend along the whole length of the dorsal and ventral edges: the dorsal from the head, in some cases from a point anterior to the eyes, to the base of the tail, the ventral from the anus, which is pushed very far forward, to the base of the tail, and in some species of Solidae these fins are confluent with the caudal fin.
Formerly it was dogmatically maintained that the effect of an external stimulus on somatic organs or tissues could have no influence on the determinants in the chromosomes of the gametes to which the hereditary characters of the organism were due. As we have tried to show, this dogma is no longer credible in face of the discoveries concerning hormones. The hormone theory supposes that the somatic modifications due to external stimuli—in the case of the Flat-fish the disappearance of pigment from the lower side, the torsion of the orbital region of the skull, and the extension of the dorsal fin—modify the hormones given off by these parts, increasing some and decreasing others, and that these changes in the hormones affect the determinants, whatever they are, in the gametocytes within the body.
Here arises an interesting question—namely, how does the hormone theory explain the phenomenon of metamorphosis any better than the mutation theory? It might be agreed that if the determinants are stimulated or deprived of stimulation, the effect of the change should logically show itself from the beginning of development, and that therefore the process of metamorphosis or indirect development does not support the hormone theory any more than the theory of gametogenic mutations. This objection may be answered in the following way. The reason why the determinants give rise to the original structure first and then change it into the new structure is probably the same as that which causes secondary sexual characters to develop only at the stage of puberty. By the hypothesis the new habits and new stimuli begin to act at some stage after the complete development of the original structure of the body. The differences in the original hormones of the modified parts are therefore acting simultaneously with the hormones, that is, the chemical substances derived from all other parts of the body in its fully developed condition. It is very probable that in the early stages of development the metabolism of the body would be considerably different from that of the adult stage, and the same combination of hormones would not be present. We may suppose, therefore, that the determinants of the zygote have acquired a tendency to produce the increases and decreases of tissue which constitute a certain modification, e.g. the change in the position of the eyes in a Flat-fish, but the stimulus which caused this tendency has always acted when the adult combination of hormones was present. In consequence of this the developed tissues do not undergo the inherited modification until the adult combination is again present. In this way we can form a definite conception of the reason why an adaptive modification is inherited at the same stage in which it was produced, just as the antlers of a stag are only developed when the hormone of the mature testis is present. At the same time it is probable that the age at which the inherited development takes place tends to become earlier in later generations, to occur in fact as soon as the necessary hormone medium is present.
The diagnostic characters, of some of the species of Pleuronectidae have been mentioned in an earlier part of this volume, in order to point out that they have no relation to differences of habit or external conditions. Here it is to be pointed out that there is no evidence that they arise by metamorphosis. The scales, for example, afford distinct and constant diagnostic characters both of species and genera, but their peculiarities have not been found to arise by modification of a primitive form. The rough tubercles of the Flounder, and the scattered thornlike tubercles of the Turbot, develop directly, not by the continuous modification of imbricated scales. There is, however, one scale-character among the Pleuronectidae which appears to stand in direct contradiction to the conclusions drawn by me concerning scales in general. It not only develops by a gradual change, but it is a secondary sexual character developing in the males only at maturity. The character was described by E. W. L. Holt in specimens of the Baltic variety of the Plaice, Pleuronectes platessa, [Footnote: Journ. Mar. Biol. Assn., vol iii. (Plymouth, 1893-95.)] and consists in the spinulation of the posterior edges of the scales, especially on the upper side, in mature males. The same condition, but to a much slighter degree, was afterwards shown by myself to occur constantly in Plaice from the English Channel and North Sea. [Footnote: Ibid., vol. iv. p. 323.] It occurs also in P. glacialis, the representative of the Plaice in more northern seas. I have shown that the spinules develop in the mature males not as a modification of the scale, but as separate calcareous deposits the bases of which afterwards become united to the scale. It would seem that the development of this character is dependent on the hormone from the mature testis, and in order to conform with the arguments used by me in other cases, the spinulation should have some definite function in relation to the habits of the sexes, and this function should involve some kind of external stimulation restricted to the mature male. So far, however, no evidence whatever of such function or such stimulation has been discovered. It is possible that the case differs from other secondary sexual characters as the antlers of stags in one respect, namely, that the Dab (P. limanda), the Sole, and other species of Solea. and several other Pleuronectidae have what are called etenoid scales—that is, scales furnished with spines on the posterior edge—and since the ordinary scales of the Plaice are reduced, the spinulation of scales in the mature male Plaice is not a new character but the retention of a primitive character. Then the question would remain why the scales in the mature female and immature male have degenerated, or rather why the primitive character develops only in the mature stage of the male.