Essays Upon Heredity and Kindred Biological Problems

Appendix III. Adaptations in Plants213

It is well known that Christian Conrad Sprengel was the first to recognise that the forms and colours of flowers are not due to chance, that they are not the mere sport of nature, and that they are not made for the enjoyment of man, but that their purpose is to attract insects for the performance of cross-fertilization. It is also well known that this discovery—which was made at the end of the last century, and which caused much excitement at that time—was completely forgotten, and was brought to light again by Charles Darwin when attacking the same problem.

In his work entitled ‘The Solution of Nature’s Secret in the Structure and Fertilization of Flowers’ (‘Das entdeckte Geheimniss der Natur im Bau und der Befruchtung der Blumen’), published at Berlin, in 1793, Sprengel showed, in several hundred cases, that the peculiarities in the structure and colours of flowers were calculated to attract insects, and to ensure the fertilization of the flowers by their instrumentality. But it was due to his successor in this line of investigation that the whole significance of the cross-fertilization effected by insects was made clear. Darwin214 showed that in many cases, although not in all, the intention of nature was to avoid self-fertilization, and he showed that stronger and more numerous descendants are produced after cross-fertilization.

After Darwin, several investigators, such as Kerner, Delpino and Hildebrand, have paid further attention to the subject, but it has been especially studied in a most thorough manner by Hermann Müller215. He looked at the subject from more than one point of view, and showed by direct observation the species of insects which effect cross-fertilization in various species of our native flowers: he also studied the structure of insects in relation to that of flowers, and attempted to establish the mutual adaptations which exist between them. In this way he succeeded in throwing much light upon the process of transformation in many species of flowers, and in proving that certain insects, although unconsciously, are, as it were, breeders of certain forms of flowers. He not only distinguished the disagreeably smelling, generally inconspicuous flowers (‘Ekelblumen’) produced by Diptera which live on putrid substances, and the flowers which are produced by butterflies; but he also distinguished the flowers bred by saw-flies, by Fossoria, and by bees. He even believes that in certain cases (Viola calcarata) he can prove that a flower which owed its original form to being bred by bees, was afterwards adapted to cross-fertilization by butterflies, when it had migrated into an Alpine region where the latter insects are far more abundant than the former.

Although there must of course be much that is hypothetical in the interpretations of the different parts of flowers offered by Hermann Müller, the majority of these explanations are certainly correct, and it is of the greatest interest to be able to recognise the adaptive character of details, even when apparently unimportant, in the structure and colours of flowers.

Sachs has offered a very convincing explanation as to the meaning of leaf-veining, and of its significance in relation to the functions of leaves216. He shows that the venation of a leaf is in every case exactly adapted for the fulfilment of its purpose. It has, in the first place, to conduct the nutrient fluid in both directions, and in the second place to support the thin layers of assimilating chlorophyll cells, and to stretch them out so as to expose as large a surface as possible to the light; lastly, it has to toughen the leaf as a protection against being torn. He shows in a very convincing manner that the whole diversity of leaf venation can be understood from these three principles. Here, again, we meet with purposeful arrangements in a class of structures in which it was formerly thought that there was only a chaos of accidental forms, or, as it were, the mere sport of nature with form.

Appendix IV. On the supposed transmission of acquired characters217

When I previously maintained that the proofs of the transmission of artificially produced diseases are inconclusive, I had in mind the only experiments which, as far as I am aware, can be adduced in favour of the transmission of acquired characters; viz. the experiments of Brown-Séquard218 on guinea-pigs. It is well known that he produced artificial epilepsy in these animals by dividing certain parts of the central and also the peripheral nervous system. The descendants of the animals which acquired epilepsy sometimes inherited the disease of their parents.

These experiments have been since repeated by Obersteiner219, who has described them in a very exact and entirely unprejudiced manner. The fact itself cannot be doubted: it is certain that some of the descendants of animals in which epilepsy has been artificially produced, have also themselves suffered from epilepsy in consequence of the disease of their parents. This fact may be accepted as proved, but in my opinion we have no right to conclude from it that acquired characters can be transmitted. Epilepsy is not a morphological character; it is a disease. We could only speak of the transmission of a morphological character, if a certain morphological change which was the cause of epilepsy had been produced by the nervous lesion, and if a similar change had re-appeared in the offspring, and had produced in them also the symptoms of epilepsy. But that this really occurs is utterly unproved; and is even highly improbable. It has only been proved that many descendants of artificially epileptic parents are small, weakly, and very soon die; and that others are paralysed in various parts of the body, i. e. in one or both of the posterior or anterior extremities; while others again exhibit trophic paralysis of the cornea leading to inflammation and the formation of pus. In addition to these symptoms, the descendants in very rare cases exhibit upon the application of certain stimuli to the skin, a tendency towards those tonic and clonic convulsions together with loss of consciousness which constitute the features of an epileptic attack. Out of thirty-two descendants of epileptic parents only two exhibited such symptoms, both of them being very weakly, and dying at an early age.

These experiments, although very interesting, do not enable us to assert that a distinct morphological change is transmitted to the offspring after having been artificially induced in the parents. The injury caused by the division of a nerve is not transmitted, and the part of the brain corresponding to that which was removed from the parent is not absent from the offspring. The symptoms of a disease are undoubtedly transmitted, but the cause of the disease in the offspring is the real question which requires solution. The symptoms of epilepsy are by no means invariably transmitted; they are in fact absent from the great majority of cases, and the very small proportion in which they do occur, exhibit the symptoms of other diseases in addition to those of epilepsy. The offspring are either quite healthy (thirteen out of thirty cases) or they suffer from disturbances of the nervous system, such as the above-mentioned motor and trophic paralysis,—symptoms which are not characteristic of epilepsy: however in some of the latter epilepsy is also present.

If therefore we wish to express the matter correctly we must not state that epilepsy is transmitted to the offspring, but we must express the facts in the following manner:—animals which have been rendered epileptic by artificial means, transmit to some of their offspring a tendency to suffer from various nervous diseases, viz. from motor paralysis, to a less degree from sensory, and to a high degree from trophic paralysis; in rare cases, when the symptoms of paralysis are very marked, epilepsy is also transmitted.

If we now remember that a considerable number of diseases are already known to be caused by the presence of living organisms in the body, and that these diseases may be transmitted from one organism to another in the form of germs, ought we not to conclude from the above-mentioned facts, that the symptoms are due to an unknown microbe which finds its nutritive medium in the nervous tissues, rather than to suppose that they are due to morphological changes, such as a modification of the histological or molecular structure of certain parts of the nervous system? At all events, it would be more difficult to understand the transmission of such a structural change, than the passage of a bacillus into the sperm- or germ-cell of the parent. There is no ascertained fact which supports the former assumption, but it is very probable that the transmission of syphilis, small-pox and tuberculosis220 is to be explained by the latter method, although the bacilli have not yet been detected in the reproductive cells. Furthermore, this method of transmission has been rigidly proved in the case of the muscardine disease of the silkworm. At all events we can understand in this way how it happened that the offspring of artificially epileptic guinea-pigs were affected with various forms of nervous disease, a fact which would be quite unintelligible if we assume the occurrence of a true hereditary transmission of a morphological character, such as a pathological change in the structure of some nervous centre.

The manner in which artificial epilepsy becomes manifest after the operation, is also in favour of the explanation offered above. In the first place epilepsy does not result from any one single injury to the nervous system, but it may follow from a variety of different injuries. Brown-Séquard produced it by removing a portion of the grey matter of the brain, and by dividing the spinal cord, although the disease also resulted from a transverse section through half of the latter organ, or from the section of its anterior or posterior columns alone, or from simply puncturing its substance. The most striking effects appeared to follow when the spinal cord was injured in the region between the eighth dorsal and the second lumbar vertebrae, although the results were sometimes also produced by the injury of other parts. Epilepsy also followed the division of the sciatic nerve, the internal popliteal, and the posterior roots of all nerves which pass to the legs. The disease never appears at once, but only after the lapse of some days or weeks, and, according to Brown-Séquard, it is impossible to conclude that the disease will not follow the operation until after six or eight weeks have passed without an epileptic attack. Obersteiner did not witness in any case the first symptoms of the disease for several days after the division of the sciatic nerve. After the operation, sensibility decreases over a certain area on the head and neck, on the same side as the injury. If the animal be pinched in this region (which is called the epileptic area, ‘zone epileptogène’) it curves itself round towards the injured side, and violent scratching movements are made with the hind leg of the same side. After the lapse of several days or even weeks, these scratching movements which result from pinching in the above-mentioned area, form the beginning of a complete epileptic attack. Hence the changes immediately produced by the division of a nerve are obviously not the direct cause of epilepsy, but they only form the beginning of a pathological process which is conducted in a centripetal direction from the nerve to some centre which is apparently situated in the pons and medulla oblongata, although, according to others221, it is placed in the cortex of the cerebrum. Nothnagel222 considers that certain changes, the nature of which is still entirely unknown, but which may be histological or perhaps solely molecular in character, must be produced, leading to an increased irritability of the grey matter of the centres concerned.

Nothnagel thinks it possible or even probable that in those cases in which the division of nerves is followed by epilepsy, a neuritis ascendens—an inflammation passing along the nerves in a central direction—is the cause of the changes suggested by him in the epileptic centre. All our knowledge of bacteria and of the pathological processes induced by them, seems to indicate that such a neuritis ascendens, as is assumed by Nothnagel, would render important support to the hypothesis that the artificial epilepsy is due to infection. But when we further consider that the offspring of artificially epileptic animals may themselves become epileptic, although in most cases they suffer from a variety of other nervous diseases (in consequence of trophic paralysis), I hardly see how the facts can be rendered intelligible except by supposing that in these cases of what I may call traumatic epilepsy, we are dealing with an infectious disease caused by microbes which find their nutritive medium in the nervous tissues, and which bring about the transmission of the disease to the offspring by penetrating the ovum or the spermatozoon.

Obersteiner found that the offspring were more frequently diseased when the mother was epileptic, rather than the father. This is readily intelligible when we remember that the ovum contains an immensely larger amount of substance than the spermatozoon, and can therefore be more frequently infected by microbes and can contain a greater number of them.

Of course, I do not mean to assert that epilepsy always depends upon infection, or upon the presence of microbes in the nervous tissues. Westphal produced epilepsy in guinea-pigs by striking them once or twice sharply upon the head: the epileptic attack took place immediately and was afterwards repeated. It is obvious that the presence of microbes can have nothing to do with such an attack, but the shock alone must have caused morphological and functional changes in the centres of the pons and medulla oblongata, identical with those produced by microbes in the other cases. Nothnagel also distinctly expresses the opinion that epilepsy ‘does not depend upon one uniform and invariable histological change, but that the symptoms which constitute the disease may in all probability be caused by various anatomical alterations, provided that they take place in parts of the pons and medulla which are morphologically and physiologically equivalent223.’ Just as a sensory nerve produces the sensation of pain under various stimuli, such as pressure, inflammation, infection with the poison of malaria, etc., so various stimuli might cause the nervous centres concerned to develope the convulsive attack which, together with its after-effects, we call epilepsy. In Westphal’s case, such a stimulus would be given by a powerful mechanical shock, in Brown-Séquard’s experiments, by the penetration of microbes.

However, quite apart from the question of the validity of this suggestion, we can form no conception as to the means by which an acquired morphological change in certain nerve-cells—a change which is not anatomical, and probably not even microscopical, but purely molecular in nature—can be possibly transferred to the germ-cells: for this ought to take place in such a manner as to produce in their minute molecular structure a change which, after fertilization and development into a new individual, would lead to the reproduction of the same epileptogenic molecular structure of the nervous elements in the grey centres of the pons and medulla oblongata as was acquired by the parent. How is it possible for all this to happen? What substance could cause such a change in the resulting offspring after having been transferred to the egg or sperm-cell? Perhaps Darwin’s gemmules may be suggested; but each gemmule represents a cell, while here we have to do with molecules or groups of molecules. We must therefore assume the existence of a special gemmule for each group of molecules, and thus the innumerable gemmules of Darwin’s theory must be imagined as increased by many millions. But if we suppose that the theory of pangenesis is right, and that the gemmules really circulate in the body, accompanied by other gemmules from the diseased parts of the brain, and that some of these latter pass into the germ-cells of the individual,—to what strange results would the further pursuit of this idea lead? What an incomprehensible number of gemmules must meet in a single sperm- or germ-cell, if each of them is to contain a representative of every molecule or group of molecules which has formed part of the body at each period of ontogeny. And yet such is the unavoidable consequence of the supposition that acquired molecular states of certain groups of cells can be transmitted to the offspring. This supposition could only be rendered intelligible by some theory of preformation224, such as Darwin’s pangenesis; for the latter theory certainly belongs to this category. We must assume that each single part of the body at each developmental stage is, from the first, represented in the germ-cell as distinct particles of matter, which will reproduce each part of the body at its appropriate stage as their turn for development arrives.

I will only briefly indicate some of the inevitable contradictions in which we are involved by such a theory. One and the same part of the body must be represented in the germ- or sperm-cell by many groups of gemmules, each group corresponding to a different stage of development; for if each part gives off gemmules, which ultimately reproduce the part in the offspring, it is clear that special gemmules must be given off for each stage in the development of the part, in order to reproduce that identical stage. And Darwin quite logically accepts this conclusion in his provisional hypothesis of pangenesis. But the ontogeny of each part is in reality continuous, and is not composed of distinct and separate stages. We imagine these stages as existing in the continuous course of ontogeny; for here, as in all departments of nature, we make artificial divisions in order to render possible a general conception, and to gain fixed points in the continuous changes of form which have in reality occurred. Just as we distinguish a sequence of species in the course of phylogeny, although only a gradual transition, not traversed by sharp lines of demarcation, has taken place, so also we speak of the stages of ontogeny, although we can never point out where any stage ends and another begins. To imagine that each single stage of a part is present in the germ, as a distinct group of gemmules, seems to me to be a childish idea, comparable to the belief that the skull of the young St. Laurence exists at Madrid, while the adult skull is to be found in Rome.

We are necessarily driven to such conceptions if we assume that the transmission of acquired characters takes place. A theory of preformation alone affords the possibility of an explanation: an epigenetic theory is utterly unable to render any assistance in reaching an interpretation. According to the latter theory, the germ does not contain any preformed gemmules, but it possesses, as a whole, such a chemical and molecular constitution that under certain circumstances, a second stage is produced from it. For example, the two first segmentation spheres may be regarded as such a second stage; these again possess such a constitution that a certain third stage, and no other, can arise from them, forming the four first segmentation spheres. At each of these stages the spheres produced are peculiar to a distinct species and a distinct individual. From the third stage a fourth arises, and so on, until the embryo is developed, and still later the mature animal which can reproduce itself. No one of the parts of such an animal was originally present as distinct parts in the egg from which it was developed, however minute we may imagine these parts to be. If now an inherited peculiarity shows itself in any organ of the mature animal, this will be the consequence of the preceding developmental stages, and if we were able to investigate the molecular structure of all these stages as far back as the egg-cell, we should trace back to the latter some minute difference of molecular constitution which would distinguish it from any other egg-cell of the same species, and was destined to be the cause of the subsequent appearance of the peculiarity in the mature animal. It is only by the aid of some such hypothesis that we can conceive the cause of hereditary individual differences and the tendencies towards hereditary diseases. Hereditary epilepsy would be intelligible in this way, that is, when the disease is congenital and not due to the presence of microbes, as is presumably the case with artificially induced epilepsy.

The question now arises as to whether we can conceive the communication of such traumatic and therefore acquired epilepsy to the germ-cells. This is obviously impossible under the epigenetic theory of development described above. In what way can the germ-cells be affected by molecular or histological changes in the pons varolii and medulla oblongata? Even if we assume, for the sake of argument, that the central nervous system exercises trophic influences upon the germ-cells, and that such influences may consist of something more than variations in nutritive conditions, and may even include the power of altering the molecular constitution of the germ-plasm in spite of its usual stability; even if we concede these suppositions, how is it conceivable that the changes produced would be of the exact nature and in the exact direction necessary in order to confer upon the germ-plasm the molecular structure of the first ontogenetic stage of an epileptic individual? How can the last ontogenetic stage of the ganglion cells in the pons and medulla of such an individual, stamp upon the germ-plasm in the germ-cells of the same animal—not indeed the peculiar structure of the stage itself—but such a molecular constitution as will ensure the ultimate appearance of epilepsy in the offspring? The theory of epigenesis does not admit that the parts of the full-grown individual are contained in the germ as preformed material particles, and therefore this theory cannot allow that anything is added to the germ-plasm; but in accepting the above-made supposition, we are compelled to assume that the molecular structure of the whole of the germ-plasm is changed to a slight extent.

Nägeli is quite right in maintaining that the solid protoplasm alone, as opposed to the fluid part, i.e. that part of the protoplasm which has passed into solution, can act as the bearer of hereditary tendencies. This appears to be undoubtedly proved by the fact that the amount of material provided by the male parent for the development of an embryo is in almost all animals far smaller than the amount provided by the female parent.

In Mammalia the share contributed by the father probably only forms about one hundred-billionth part of that contributed by the mother, and yet nevertheless the influence of the former in heredity is on an average equal to that exerted by the latter225. Now, from the point of view of epigenesis, no molecule of the brain of an epileptic animal can reach the germ-cell except in a state of solution, and therefore no direct increase in the germ-plasm can be referred to such molecules, quite apart from the fact that such addition, even if possible, could not be of any value, because the last stage of the epileptic tendency must be represented in the nerve-cells and nerve-fibres of the diseased brain, while the first stage ought to be represented in the germ-cell.

It may be safely asserted that according to the theory of epigenesis the germ-cells cannot be influenced except as regards their nutrition. Nutritive changes may be imagined to occur through the varying trophic influence of the nervous system upon the sexual organs, but the structure of the germ-plasm cannot be altered by mere nutritive changes, or at all events it cannot be altered in that distinct and definite direction which is required by the supposed transmission of acquired epilepsy.

Thus the transmission of artificially produced epilepsy can neither be explained upon the epigenetic theory, nor upon the theory of preformation; it can only be rendered intelligible if we suppose that the appearance of the disease in the offspring depends upon the introduction and presence of living germs, viz. of microbes. The supposed transmission of this artificially produced disease is the only definite instance which has been hitherto brought forward in support of the transmission of acquired characters. I believe that I have shown that such support is deceptive, not because there is any uncertainty about the fact of the transmission itself, but because it is a transmission which cannot depend upon heredity, and is in all probability due to infection.