Chapter IV

CHARACTERS AS HEREDITARY AND ACQUIRED (_continued_).

(C.) _Experimental Evidence in favour of the Inheritance of Acquired Characters._

Notwithstanding the fact already noticed, that no experiments have hitherto been published with reference to the question of the transmission of acquired characters[63], there are several researches which, with other objects in view, have incidentally yielded seemingly good evidence of such transmission. The best-known of these researches--and therefore the one with which I shall begin--is that of Brown-Sequard touching the effects of certain injuries of the nervous system in guinea-pigs.

[63] The experiments of Galton and Weismann upon this subject are
nugatory, as will be shown later on. But since the above was
written an important research has been published by Mr.
Cunningham, of the Marine Biological Association. For a full
account I must refer the reader to his forthcoming paper in the
_Philosophical Transactions_. The following is his own
statement of the principal results:--

"A case which I have myself recently investigated
experimentally seems to me to support very strongly the theory
of the inheritance of acquired characters, I have shown that in
normal flat-fishes, if the lower side be artificially exposed
to light for a long time, pigmentation is developed on that
side; but when the exposure is commenced while the specimens
are still in process of metamorphosis, when pigment-cells are
still present on the lower side, the action of light does not
prevent the disappearance of these pigment-cells. They
disappear as in individuals living under normal conditions, but
after prolonged exposure pigment-cells reappear. The first fact
proves that the disappearance of the pigment-cells from the
lower side in the metamorphosis is an hereditary character, and
not a change produced in each individual by the withdrawal of
the lower side from the action of light. On the other hand, the
experiments show that the absence of pigment-cells from the
lower side throughout life is due to the fact that light does
not act upon that side, for, when it is allowed to act,
pigment-cells appear. It seems to me the only reasonable
conclusion from these facts is, that the disappearance of
pigment-cells was originally due to the absence of light, and
that this change has now become hereditary. The pigment-cells
produced by the action of light on the lower side are in all
respects similar to those normally present on the upper side of
the fish. If the disappearance of the pigment-cells were due
entirely to a variation of the germ-plasm, no external
influence could cause them to reappear, and, on the other hand,
if there were no hereditary tendency, the colouration of the
lower side of the flat-fish when exposed would be rapid and
complete."--_Natural Science_, Oct. 1893.

During a period of thirty years Brown-Sequard bred many thousands of guinea-pigs as material for his various researches; and in those whose parents had not been operated upon in the ways to be immediately mentioned, he never saw any of the peculiarities which are about to be described. Therefore the hypothesis of coincidence, at all events, must be excluded. The following is his own summary of the results with which we are concerned:--

1st. Appearance of epilepsy in animals born of parents which had
been rendered epileptic by an injury to the spinal cord.

2nd. Appearance of epilepsy also in animals born of parents which
had been rendered epileptic by section of the sciatic nerve.

3rd. A change in the shape of the ear in animals born of parents in
which such a change was the effect of a division of the cervical
sympathetic nerve.

4th. Partial closure of the eyelids in animals born of parents in
which that state of the eyelids had been caused either by section
of the cervical sympathetic nerve, or the removal of the superior
cervical ganglion.

5th. Exophthalmia in animals born of parents in which an injury to
the restiform body had produced that protrusion of the eyeball.
This interesting fact I have witnessed a good many times, and seen
the transmission of the morbid state of the eye continue through
four generations. In these animals, modified by heredity, the two
eyes generally protruded, although in the parents usually only one
showed exophthalmia, the lesion having been made in most cases only
on one of the corpora restiformia.

6th. Haematoma and dry gangrene of the ears in animals born of
parents in which these ear-alterations had been caused by an injury
to the restiform body near the nib of the calamus.

7th. Absence of two toes out of the three of the hind leg, and
sometimes of the three, in animals whose parents had eaten up their
hind-leg toes which had become anaesthetic from a section of the
sciatic nerve alone, or of that nerve and also of the crural.
Sometimes, instead of complete absence of the toes, only a part of
one or two or three was missing in the young, although in the
parent not only the toes but the whole foot were absent (partly
eaten off, partly destroyed by inflammation, ulceration, or
gangrene.)

8th. Appearance of various morbid states of the skin and hair of
the neck and face in animals born of parents having had similar
alterations in the same parts, as effects of an injury to the
sciatic nerve.

These results[64] have been independently vouched for by two of Brown-Sequard's former assistants--Dr. Dupuy, and the late Professor Westphal. Moreover, his results with regard to epilepsy have been corroborated also by Obersteiner[65]. I may observe, in passing, that this labour of testing Brown-Sequard's statements is one which, in my opinion, ought rather to have been undertaken, if not by Weismann himself, at all events by some of his followers. Both he and they are incessant in their demand for evidence of the transmission of acquired characters; yet they have virtually ignored the foregoing very remarkable statements. However, be this as it may, all that we have now to do is to consider what the school of Weismann has had to say with regard to these experiments on the grounds of general reasoning which they have thus far been satisfied to occupy.

[64] For Professor Weismann's statement of and discussion of these
results see _Essays_, vol. i. p. 313.

[65] _Oesterreichische medicinische Jahrbuecher_, 1875, 179.

In view of Obersteiner's corroboration of Brown-Sequard's results touching the artificial production and subsequent transmission of epilepsy, Weismann accepts the facts, but, in order to save his theory of heredity, he argues that the transmission may be due to a traumatic introduction of "some unknown microbe" which causes the epilepsy in the parent, and, by invading the ova or spermatozoa as the case may be, also produces epilepsy in the offspring. Here, of course, there would be transmission of epilepsy, but it would not be, technically speaking, an hereditary transmission. The case would resemble that of syphilis, where the sexual elements remain unaffected as to their congenital endowments, although they have been made the vehicles for conveying an organic poison to the next generation.

Now it would seem that this suggestion is not, on the face of it, a probable one. For "some unknown microbe" it indeed must be, which is always on hand to enter a guinea-pig when certain operations are being performed on certain parts of the nervous system, but yet will never enter when operations of any kind are being effected elsewhere. Moreover, Westphal has produced the epilepsy _without any incision_, by striking the heads of the animals with a hammer[66]. This latter fact, it appears to me, entirely abolishes the intrinsically improbable suggestion touching an unknown--and strangely eclectic--microbe. However, it is but fair to state what Weismann himself has made of this fact. The following is what he says:--

[66] _Loc. cit._

"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 centre of the pons and
medulla oblongata, identical with those produced by microbes in the
other cases.... Various stimuli might cause the nervous centres
concerned to develop 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 (viz. blows
on the head with a hammer); in Brown-Sequard's experiments, by the
penetration of microbes[67]."

[67] _Essays_, vol. i. p. 315.

But from this passage it would seem that Weismann has failed to notice that in "Westphal's case," as in "Brown-Sequard's experiments," the epilepsy was _transmitted to progeny_. That epilepsy may be produced in guinea-pigs by a method which does not involve any cutting (i.e. possibility of inoculation) would no doubt tend to corroborate the suggestion of microbes being concerned in its transmission when it is produced by cutting, _if in the former case there were no such transmission_. But as there _is_ transmission in _both_ cases, the facts, so far as I can see, entirely abolish the suggestion. For they prove that even when epilepsy is produced in the parents under circumstances which render "it obvious that the presence of microbes can have nothing to do with such an attack," the epileptiform condition is notwithstanding transmitted to the progeny. What, then, is gained by retaining the intrinsically improbable hypothesis of microbes to explain the fact of transmission "in Brown-Sequard's experiments," when this very same fact is proved to occur without the possibility of microbes "in Westphal's case"?

The only other objection with regard to the seeming transmission of traumatic epilepsy which Weismann has advanced is, that such epilepsy may be produced by two or three very different operations--viz. division of the sciatic nerves (one or both), an injury to the spinal cord, and a stroke on the head. Does not this show, it is asked, that the epileptic condition of guinea-pigs is due to a generally unstable condition of the whole nervous system and is not associated with any particular part thereof? Well, supposing that such is the case, what would it amount to? I cannot see that it would in any way affect the only question in debate--viz. What is the significance of the fact that epilepsy is _transmitted_? Even if it be but "a tendency," "a disposition," or "a diathesis" that is transmitted, it is none the less a case of transmission, in fact quite as much so as if the pathological state were dependent on the impaired condition of any particular nerve-centre. For, it must be observed, there can be no question that it is always produced by an operation of _some_ kind. If it were ever to originate in guinea-pigs spontaneously, there might be some room for supposing that its transmission is due to a congenital tendency running through the whole species--although even then it would remain unaccountable, on the ultra-Darwinian view, why this tendency should be congenitally _increased_ by means of an operation. But epilepsy does not originate spontaneously in guinea-pigs; and therefore the criticism in question appears to me irrelevant.

Again, it may be worth while to remark that Brown-Sequard's experiments do not disprove the possibility of its being some one nerve-centre which is concerned in all cases of traumatic epilepsy. And this possibility becomes, I think, a probability in view of Luciani's recent experiments on the dog. These show that the epileptic condition can be produced in this animal by injury to the cortical substance of the hemispheres, and is then transmitted to progeny[68]. These experiments, therefore, are of great interest--first, as showing that traumatic and transmissible epilepsy is not confined to guinea-pigs; and next, as indicating that the pathological state in question is associated with the highest nerve-centres, which may therefore well be affected by injury to the lower centres, or even by section of a large nerve trunk.

[68] _Les fonctions du Cerveau_, p. 102.

So much, then, with regard to the case of transmitted epilepsy. But now it must be noted that, even if Weismann's suggestion touching microbes were fully adequate to meet this case, it would still leave unaffected those of transmitted protrusion of the eye, drooping of the eyelid, gangrene of the ear, absence of toes, &c. In all these cases the facts, as stated by Brown-Sequard, are plainly unamenable to any explanation which would suppose them due to microbes, or even to any general neurotic condition induced by the operation. They are much too definite, peculiar, and localized. Doubtless it is on this account that the school of Weismann has not seriously attempted to deal with them, but merely recommends their repetition by other physiologists[69]. Certain criticisms, however, have been urged by Weismann against the _interpretation_ of Brown-Sequard's facts as evidence in favour of the transmission of acquired characters. It does not appear to me that these criticisms present much weight; but it is only fair that we should here briefly consider them[70].

[69] _Essays_, vol. i. p. 82.

[70] As Weismann gives an excellent abstract of all the alleged
facts up to date (_Essays_, vol. i. pp. 319-324), it is
needless for me to supply another, further than that which I
have already made from Brown-Sequard.

First, with regard to Brown-Sequard's results other than the production of transmitted epilepsy, Weismann allows that the hypothesis of microbes can scarcely apply. In order to meet these results, therefore, he furnishes another suggestion--viz. that where the nervous system has sustained "a great shock," the animals are very likely to bear "weak descendants, and such as are readily affected by disease." Then, in answer to the obvious consideration, "that this does not explain why the offspring should suffer from the same disease" as that which has been produced in the parents, he adds--"But this does not appear to have been by any means invariably the case. For 'Brown-Sequard himself says, the changes in the eye of the offspring were of a very variable nature, and were only occasionally exactly similar to those observed in the parents.'"

Now, this does not appear to me a good commentary. In the first place, it does not apply to the other cases (such as the ears and the toes), where the changes in the offspring, when they occurred at all, _were_ exactly similar to those observed in the parents, save that some of them occasionally occurred on the _opposite_ side, and frequently also on _both_ sides of the offspring. These subordinate facts, however, will not be regarded by any physiologist as making against the more ready interpretation of the results as due to heredity. For a physiologist well knows that homologous parts are apt to exhibit correlated variability--and this especially where variations of a congenital kind are concerned, and also where there is any reason to suppose that the nervous system is involved. Moreover, even in the case of the eye, it was always protrusion that was caused in the parent and transmitted to the offspring as a result of injuring the restiform bodies of the former; while it was always partial closure of the eyelids that was caused and transmitted by section of the sympathetic nerve, or removal of the cervical ganglia. Therefore, if we call such effects "diseases," surely it _was_ "the same disease" which in each case appeared in the parents and reappeared in their offspring. Again, the "diseases" were so peculiar, definite, and localized, that I cannot see how they can be reasonably ascribed to a general nervous "shock." Why, for instance, if this were the case, should a protruding eye never result from removal of the cervical ganglia, a drooping eyelid from a puncture of the restiform body, a toeless foot from either or both of these operations, and so on? In view of such considerations I cannot deem these suggestions touching "microbes" and "diseases" as worthy of the distinguished biologist from whom they emanate.

Secondly, Weismann asks--How can we suppose these results to be instances of the transmission of acquired characters, when from Brown-Sequard's own statement of them it appears that the mutilation itself was not inherited, but only its effects? Neither in the case of the sciatic nerve, the sympathetic nerve, the cervical ganglion, nor the restiform bodies, was there ever any trace of transmitted injury in the corresponding parts of the offspring; so that, if the "diseases" from which they suffered be regarded as hereditary, we have to suppose that a consequence was in each case transmitted without the transmission of its cause, which is absurd. But I do not think that this criticism can be deemed of much weight by a physiologist as distinguished from a naturalist. For nothing is more certain to a student of physiology, in any of its branches, than that negative evidence, if yielded by the microscope alone, is most precarious. Therefore it does not need a _visible_ change in the nervous system to be present, in order that the part affected should be functionally weak or incapable: pathology can show numberless cases of nerve-disorder the "structural" causes of which neither the scalpel nor the microscope can detect. So that, if any peculiar form of nerve-disorder is transmitted to progeny, and if it be certain that it has been caused by injury to some particular part of the nervous system, I cannot see that there is any reason to doubt the transmission of a nervous lesion merely on the ground that it is not visibly discernible. Of course there may be other grounds for doubting it; but I am satisfied that this ground is untenable. Besides, it must be remembered, as regards the particular cases in question, that no one has thus far investigated the histology of the matter by the greatly improved methods which are now at our disposal.

* * * * *

I have now considered all the criticisms which have been advanced against what may be called the Lamarckian interpretation of Brown-Sequard's results; and I think it will be seen that they present very little force--even if it can be seen that they present any force at all. But it must be remembered that this is a different thing from saying that the Lamarckian interpretation is the true one. The facts alleged are, without question, highly peculiar; and, on this account alone, Brown-Sequard's interpretation of them ought to be deemed provisional. Hence, although as yet they have not encountered any valid criticism from the side of ultra-Darwinian theory, I do not agree with Darwin that, on the supposition of their truth as facts, they furnish positive proof of the transmission of acquired characters. Rather do I agree with Weismann that further investigation is needed in order to establish such an important conclusion on the basis of so unusual a class of facts. This further investigation, therefore, I have undertaken, and will now state the results.

Although this work was begun over twenty years ago, and then yielded negative results, it was only within the last decade that I resumed it more systematically, and under the tutelage of Brown-Sequard himself. During the last two years, however, the experiments have been so much interrupted by illness that even now the research is far from complete. Therefore I will here confine myself to a tabular statement of the results as far as they have hitherto gone, on the understanding that, in so far as they are negative or doubtful, I am not yet prepared to announce them as final.

We may take Brown-Sequard's propositions in his own order, as already given on page 104.

1st. Appearance of epilepsy in animals born of parents which had
been rendered epileptic by an injury to the spinal cord.

2nd. Appearance of epilepsy also in animals born of parents which
had been rendered epileptic by section of the sciatic nerve.

I did not repeat these experiments with a view to producing epilepsy, because, as above stated, they had been already and sufficiently corroborated in this respect. But I repeated many times the experiments of dividing the sciatic nerve for the purpose of testing the statements made later on in paragraphs 7 and 8, and observed that it almost always had the effect of producing epilepsy in the animal thus operated upon--and this of a peculiar kind, the chief characteristics of which may here be summarized. The epileptiform habit does not supervene until some considerable time after the operation; it is then transitory, lasting only for some weeks or months. While the habit endures the fits never occur spontaneously, but only as a result of irritating a small area of skin behind the ear on the same side of the body as that on which the sciatic nerve had been divided. Effectual irritation may be either mechanical (such as gentle pinching), electrical, or, though less certainly, thermal. The area of skin in question, soon after the epileptiform habit supervenes, and during all the time that it lasts, swarms with lice of the kind which infest guinea-pigs--i.e. the lice congregate in this area, on account, I think, of the animal being there insensitive, and therefore not disturbing its parasites in that particular spot; otherwise it would presumably throw itself into fits by scratching that spot. On removing the skin from the area in question, no kind or degree of irritation supplied to the subjacent tissue has any effect in producing a fit. A fit never lasts for more than a very few minutes, during which the animal is unconscious and convulsed, though not with any great violence. The epileptiform habit is but rarely transmitted to progeny. Most of these observations are in accordance with those previously made by Brown-Sequard, and also by others who have repeated his experiments under this heading. I can have no doubt that the injury of the sciatic nerve or spinal cord produces a change in some of the cerebral centres, and that it is this change--whatever it is and in whatever part of the brain it takes place--which causes the remarkable phenomena in question.

3rd. A change in the shape of the ear in animals born of parents in
which such a change was the effect of a division of the cervical
sympathetic nerve.

4th. Partial closure of the eyelids in animals born of parents in
which that state of the eyelids had been caused either by section
of the cervical sympathetic nerve, or the removal of the superior
cervical ganglion.

I have not succeeded in corroborating these results. It must be added, however, that up to the time of going to press my experiments on this, the easiest branch of the research, have been too few fairly to prove a negative.

5th. Exophthalmia in animals born of parents in which an injury to
the restiform body had produced that protrusion of the eyeball....
In these animals, modified by heredity, the two eyes generally
protruded, although in the parents usually only one showed
exophthalmia, the lesion having been made in most cases only on one
of the corpora restiformia.

I have fully corroborated the statement that injury to a particular spot of the restiform body is quickly followed by a marked protrusion of the eyeball on the same side. I have also had many cases in which some of the progeny of parents thus affected have shown considerable protrusion of the eyeballs on both sides, and this seemingly abnormal protrusion has been occasionally transmitted to the next generation. Nevertheless, I am far from satisfied that this latter fact is anything more than an accidental coincidence. For I have never seen the so-called exophthalmia of progeny exhibited in so high a degree as it occurs in the parents as an immediate result of the operation, while, on examining any large stock of normal guinea-pigs, there is found a considerable amount of individual variation in regard to prominence of eyeballs. Therefore, while not denying that the obviously abnormal amount of protrusion due to the operation may be inherited in lesser degrees, and thus may be the cause of the unusual degree of prominence which is sometimes seen in the eyeballs of progeny born of exophthalmic parents, I am unable to affirm so important a conclusion on the basis supplied by these experiments.

6th. Haematoma and dry gangrene of the ears in animals born of
parents in which these ear-alterations had been caused by an injury
to the restiform body.

As regards the animals operated upon (i. e. the parents), I find that the haematoma and dry gangrene may supervene either several weeks after the operation, or at any subsequent time up to many months. When it does supervene it usually affects the upper parts of both ears, and may then eat its way down until, in extreme cases, it has entirely consumed two-thirds of the tissue of both ears. As regards the progeny of animals thus affected, in some cases, but by no means in all, a similarly morbid state of the ears may arise apparently at any time in the life-history of the individual. But I have observed that in cases where two or more individuals _of the same litter_ develop this diseased condition, they usually do so at about the same time--even though this be many months after birth, and therefore after the animals are fully grown. But in progeny the morbid process never goes so far as in the parents which have been operated upon, and it almost always affects the _middle_ thirds of the ears. In order to illustrate these points, reproductions of two of my photographs are appended. They represent the consequences of the operation on a male and a female guinea-pig. Among the progeny of both these animals there were several in which a portion of each ear was consumed by apparently the same process, where, of course, there had been no operation.

It should be observed that not only is a different _part_ of the ear affected in the progeny, but also a very much less _quantity_ thereof. Naturally, therefore, the hypothesis of heredity seems less probable than that of mere coincidence on the one hand, or of transmitted microbes on the other. But I hope to have fairly excluded both these alternative explanations. For, as regards merely accidental coincidence, I have never seen this very peculiar morbid process in the ears, or in any other parts, of guinea-pigs which have neither themselves had their restiform bodies injured, nor been born of parents thus mutilated. As regards the hypothesis of microbes, I have tried to inoculate the corresponding parts of the ears of normal guinea-pigs, by first scarifying those parts and then rubbing them with the diseased surfaces of the ears of mutilated guinea-pigs; but have not been able in this way to communicate the disease.

It will be seen that the above results in large measure corroborate the statements of Brown-Sequard; and it is only fair to add that he told me they are the results which he had himself obtained most frequently, but that he had also met with many cases where the diseased condition of the ears in parents affected the same parts in their progeny, and also occurred in more equal degrees. Lastly, I should like to remark, with regard to these experiments on restiform bodies, and for the benefit of any one else who may hereafter repeat them, that it will be necessary for him to obtain precise information touching the _modus operandi_. For it is only one very localized spot in each restiform body which has to be injured in order to produce any of the results in question. I myself lost two years of work on account of not knowing this exact spot before going to Paris for the purpose of seeing Brown-Sequard himself perform the operation. I had in the preceding year seen one of his assistants do so, but this gentleman had a much more careless method, and one which in my hands yielded uniformly negative results. The exact spot in question in the restiform body is as far forwards as it is possible to reach, and as far down in depth as is compatible with not producing rotatory movements.

7th. Absence of two toes out of the three of the hind leg, and
sometimes of the three, in animals whose parents had eaten up their
hind-leg toes which had become anaesthetic from a section of the
sciatic nerve alone, or of that nerve and also of the crural.
Sometimes, instead of complete absence of the toes, only a part of
one or two or three was missing in the young, although in the
parent not only the toes but the whole foot were absent.

As I found that the results here described were usually given by division of the sciatic nerve alone--or, more correctly, by excision of a considerable portion of the nerve, in order to prevent regeneration--I did not also divide the crural. But, although I have bred numerous litters from parents thus injured, there has been no case of any inherited deficiency of toes. My experiments in this connexion were carried on through a series of six successive generations, so as to produce, if possible, a cumulative effect. Nevertheless, no effect of any kind was produced. On the other hand, Brown-Sequard informed me that he had observed this inherited absence of toes only in about one or two per cent. of cases. Hence it is possible enough, that my experiments have not been sufficiently numerous to furnish a case. It may be added that there is here no measurable possibility of accidental coincidence (seeing that normal guinea-pigs do not seem ever to produce young with any deficiency of toes), while the only possibility of mal-observation consists in some error with regard to the isolation (or the tabulation) of parents and progeny. Such an error, however, may easily arise. For gangrene of the toes does not set in till some considerable time after division of the sciatic nerve. Hence, if the wound be healed before the gangrene begins, and if any mistake has been made with regard to the isolation (or tabulation) of the animal, it becomes possible that the latter should be recorded as an uninjured, instead of an injured, individual. On this account one would like to be assured that Brown-Sequard took the precaution of examining the state of the sciatic nerve in those comparatively few specimens which he alleges to have displayed such exceedingly definite proof of the inheritance of a mutilation. For it is needless to remark, after what has been said in the preceding chapter on the analogous case of epilepsy, that the proof would not be regarded by any physiologist as displaced by the fact that there is no observable deficiency in the sciatic nerve of the toeless young.

8th. Appearance of various morbid states of the skin and hair of
the neck and face in animals born of parents having had similar
alterations in the same parts, as effects of an injury to the
sciatic nerve.

I have not paid any attention to this paragraph, because the facts which it alleges did not seem of a sufficiently definite character to serve as a guide to further experiment.

On the whole, then, as regards Brown-Sequard's experiments, it will be seen that I have not been able to furnish any approach to a full corroboration. But I must repeat that my own experiments have not as yet been sufficiently numerous to justify me in repudiating those of his statements which I have not been able to verify.

The only other experimental results, where animals are concerned, which seemed to tell on the side of Lamarckianism, are those of Mr. Cunningham, already alluded to. But, as the research is still in progress, the school of Weismann may fairly say that it would be premature to discuss its theoretical bearings.

* * * * *

Passing now from experiments on animals to experiments on plants, I must again ask it to be borne in mind, that here also no researches have been published, which have had for their object the testing of the question on which we are engaged. As in the case of animals, therefore, so in that of plants, we are dependent for any experimental results bearing upon the subject to such as have been gained incidentally during the course of investigations in quite other directions.

Allusion has already been made, in my previous essay, to De Vries' observations on the chromatophores of algae passing from the ovum of the mother to the daughter organism; and we have seen that even Weismann admits, "It appears possible that a transmission of somatogenetic variation has here occurred[71]." It will now be my object to show that such variations appear to be sometimes transmitted in the case of higher plants, and this under circumstances which carry much less equivocal evidence of the inheritance of acquired characters, than can be rendered by the much more simple organization of an alga.

[71] _Examination of Weismannism_, p. 83.

I have previously mentioned Hoffmann's experiments on transplantation, the result of which was to show that variations, directly induced by changed conditions of life, were reproduced by seed[72]. Weismann, however, as we have seen, questions the _somatogenetic_ origin of these variations--attributing the facts to a _blastogenetic_ change produced in the plants by a direct action of the changed conditions upon the germ-plasm itself[73]. And he points out that whether he is right or wrong in this interpretation can only be settled by ascertaining whether the observable somatic changes occur in the generation which is first exposed to the changed conditions of life. If they do occur in the first generation, they are somatogenetic changes, which afterwards react on the substance of heredity, so as to transmit the acquired peculiarities to progeny. But if they do not occur till the second (or any later) generation, they are presumably blastogenetic. Unfortunately Hoffmann does not appear to have attended to this point with sufficient care, but there are other experiments of the same kind where the point has been specially observed.

[72] _Examination of Wiesmannism_, p. 93.

[73] _Ibid._ p. 153.

For instance, M. L. A. Carriere[74] gathered seed from the wild radish (_Raphanus Raphanistrum_) in France, and sowed one lot in the light dry soil near the Museum of Natural History in Paris, while another lot was sown by him at the same time in heavy soil elsewhere. His object was to ascertain whether he could produce a good cultivated radish by methodical selection; and this he did; in a wonderfully rapid manner, during the course of a very few generations. But the point for us is, that _from the first_ the plants grown in the light soil of Paris presented sundry marked differences from those grown in the heavy soil of the country; and that these points of difference had nothing to do with the variations on which his artificial selection was brought to bear. For while his artificial selection was directed to increasing the _size_ of the "root," the differences in question had reference to its _form_ and _colour_. In Paris an elongated form prevailed, which presented either a white or a rose colour: in the country the form was more rounded, and the colour violet, dark brown, or "almost black." Now, as these differences were strongly apparent in the first generation, and were not afterwards made the subject of selection, both in origin and development they must have been due to "climatic" influences acting on the somatic tissues. And although the author does not appear to have tested their hereditary characters by afterwards sowing the seed from the Paris variety in the country, or _vice versa_, we may fairly conclude that these changes must have been hereditary--1st, from the fact of their intensification in the course of the five sequent generations over which the experiment extended, and, 2nd, from the very analogous results which were similarly obtained in the following case with another genus, where both the somatogenetic and the hereditary characters of the change were carefully and specially observed. This case is as follows.

[74] _Origine des Plantes Domestiques, demontree par la culture du
Radis Sauvage_ (Paris, 1869).

The late Professor James Buckman, F.R.S., saved some seed from wild parsnips (_P. sativa_) in the summer of 1847, and sowed under changed conditions of life in the spring of 1848. The plants grown from these wild seeds were for the most part like wild plants; but some of them had "already (i.e. in the autumn of 1848) the light green and smooth aspect devoid of hairs which is peculiar to the cultivated plant; and among the latter there were a few with longer leaves and broader divisions of leaf-lobes than the rest--the leaves, too, all growing systematically round one central bud. The roots of the plant when taken up were observed to be for the most part more fleshy than those of wild examples[75]."

[75] _Journl. Agric. Soc._ 1848.

Professor Buckman then proceeds to describe how he selected the best samples for cultivation in succeeding generations, till eventually the variety which he called "The Student" was produced, and which Messrs. Sutton still regard as the best variety in their catalogue. That is to say, it has come true to seed for the last forty years; and although such great excellence and stability are doubtless in chief part due to the subsequent process of selection by Professor Buckman in the years 1848-1850, this does not affect the point with which we are here concerned--namely, that the somatogenetic changes of the plants in the first generation were transmitted by seed to the second generation, and thus furnished Professor Buckman with the material for his subsequent process of selection. And the changes in question were not merely of a very definite character, but also of what may be termed a very _local_ character--affecting only particular tissues of the soma, and therefore expressive of a high degree of _representation_ on the part of the subsequently developed seed, by which they were faithfully reproduced in the next generation.

Here is another case. M. Lesage examined the tissues of a large number of plants growing both near to, and remote from, the sea. He suspected that the characteristic fleshiness, &c. of seaside plants was due to the influence of sea-salt; and proved that such was the case by causing the characters to occur in inland plants as a result of watering them with salt-water. Then he adds:--

"J'ai reussi surtout pour le _Lepidium sativum_ cultive en 1888;
j'ai obtenu pour la meme plante des resultats plus nets encore dans
la culture de 1889, entreprise en semant les graines recoltees avec
soin des pots de l'annee precedente et traitees exactement de la
meme facon[76]."

[76] _Rev. Gen. de Bot._ tom. ii. p. 64.

Here, it will be observed, there was no selection; and therefore the increased hereditary effect in the second generation must apparently be ascribed to a continuance of influence exercised by somatic tissues on germinal elements; for at the time when the changes were produced no seed had been formed. In other words, the accumulated change, like the initial change, would seem to have been exclusively of somatogenetic origin; and yet it so influenced the qualities of the seed (as this was afterwards formed), that the augmented changes were transmitted to the next generation, part for part, as the lesser changes had occurred in the preceding generation. "This experiment, therefore, like Professor Buckman's, shows that the alteration of the tissues was carried on in the second generation from the point gained in the first. In both cases no germ-plasm (in the germ-cells) existed at the time during which the alterations arose, as they were confined to the vegetative system; and in the case of the parsnips and carrots, being biennials no germ-cells are produced till the second year has arrived[77]."

[77] I am indebted to the Rev. G. Henslow for the references to
these cases. This and the passages which follow are quoted from
his letters to me.

Once more, Professor Bailey remarks:--

"Squashes often show remarkable differences when grown upon
different soils; and these differences can sometimes be perpetuated
for a time by seeds. The writer has produced, from the same parent,
squashes so dissimilar, through the simple agency of a change of
soil in one season, that they might readily be taken for distinct
varieties. Peas are known to vary in the same manner. The seeds of
a row of peas of the same kind, last year gave the writer marked
variations due to differences of soil.... Pea-growers characterize
soils as 'good' and 'viney.' Upon the latter sort the plants run to
vine at the expense of the fruit, and their offspring for two or
three generations have the same tendency[78]."

[78] _Gardener's Chronicle_, May 31, 1890, p. 677.

I think these several cases are enough to show that, while the Weismannian assumption as to the seeming transmission of somatogenetic characters being restricted to the lowest kinds of plants is purely gratuitous, there is no small amount of evidence to the contrary--or evidence which seems to prove that a similar transmission occurs likewise in the higher plants. And no doubt many additional cases might be advanced by any one who is well read in the literature of economic botany.

It appears to me that the only answer to such cases would be furnished by supposing that the hereditary changes are due to an alteration of the residual "germ-plasm" in the wild seed, when this is first exposed to the changed conditions of life, due to its growth in a strange kind of soil--e.g. while germinating in an unusual kind of earth for producing the first generation. But this would be going a long way to save an hypothesis. In case, however, it should now be suggested, I may remark that it would be negatived by the following facts.[79]

[79] Since the above was written Professor Weismann has advanced, in
_The Germ-plasm_, a suggestion very similar to this. It is
sufficient here to remark, that nearly all the facts and
considerations which ensue in the present chapter are
applicable to his suggestion, the essence of which is
anticipated in the above paragraph.

In the first place, an endless number of cases might be quoted where somatogenetic changes thus produced by changed conditions of life are not hereditary. Therefore, in all these cases it is certainly not the "germ-plasm" that is affected. In other words, there can be no question that somatogenetic changes of the kinds above mentioned do very readily admit of being produced in the first generation by changes of soil, altitude, &c. And that somatogenetic changes thus produced should not always--or even generally--prove themselves to be hereditary from the first moment of their occurrence, is no more than any theory of heredity would expect. Indeed, looking to the known potency of reversion, the wonder is that in any case such changes should become hereditary in a single generation. On the other hand, there is no reason to imagine that the hypothetical germ-plasm--howsoever _unstable_ we may suppose it to be--can admit of being directly affected by a change of soil in a single generation. For, on this view, it must presumably be chiefly affected during the short time that the seed is germinating; and during that time the changed conditions can scarcely be conceived as having any points of attack, so to speak, upon the residual germ-plasm. There are no roots on which the change of _soil_ can make itself perceptible, nor any stem and leaves on which the change of _atmosphere_ can operate. Yet the changed condition's may produce hereditary modifications in any parts of the plant, which are not only precisely analogous to non-hereditary changes similarly produced in the somatic tissues of innumerable other plants, but are always of precisely the same kind in the same lot of plants that are affected. When all the radishes grown from wild seed in Paris, for instance, varied in the direction of rotundity and dark colour, while those grown in the country presented the opposite characters, we can well understand the facts as due to an entire season's action upon the whole of the growing plant, with the result that all the changes produced in each set of plants were similar--just as in the cases where similarly "climatic" modifications are not hereditary, and therefore unquestionably due to changed conditions acting on roots, stems, leaves, or flowers, as the case may be. On the other hand, it is not thus intelligible that during the short time of germination the changed conditions should effect a re-shuffling (or any other modification) of the "germ-plasm" in the seeds--and this in such a manner that the effect on the residual germ-plasm reserved for future generations is precisely similar to that produced on the somatic tissues of the developing embryo.

In the second place, as we have seen, in some of the foregoing cases the changes were produced months--and even years--before the seeds of the first germination were formed. Therefore the hereditary effect, if subsequent to the period of embryonic germination, must have been produced on germ-plasm as this occurs diffused through the somatic tissues. But, if so, we shall have to suppose that such germ-plasm is afterwards gathered in the seeds when these are subsequently formed. This supposition, however, would be radically opposed to Weismann's theory of heredity: nor do I know of any other theory with which it would be reconcilable, save such as entertain the possibility of the Lamarckian factors.

Lastly, in the third place, I deem the following considerations of the highest importance:--

"As other instances in which peculiar structures are now hereditary
may be mentioned aquatic plants and those producing subterraneous
stems. Whether they be dicotyledons or monocotyledons, there is a
fundamental agreement in the anatomy of the roots and stem of
aquatic plants, and, in many cases, of the leaves as well. Such has
hitherto been attributed to the aquatic habit. The inference or
deduction was, of course, based upon innumerable coincidences; the
water being supposed to be the direct cause of the degenerate
structures, which are hereditary and characteristic of such plants
in the wild state. M. Costantin has, however, verified this
deduction, by making terrestrial and aerial stems to grow
underground and in water: the structures _at once_ began to assume
the subterranean or aquatic type, as the case might be; and,
conversely, aquatic plants made to grow upon land _at once_ began
to assume the terrestrial type of structure, while analogous
results followed changes from a subterranean to an aerial position,
and _vice versa_."

This is also quoted from the Rev. Prof. Henslow's letters to me, and the important point in it is, that the great changes in question are proved to be of a purely "somatogenetic" kind; for they occurred "at once" _in the ready-grown plant_, when the organs concerned were exposed to the change from aquatic to terrestrial life, or _vice versa_--and also from a subterranean to an aerial position, or _vice versa_. Consequently, even the abstract possibility of the changed conditions of life having operated on the _seed_ is here excluded. Yet the changes are of precisely the same kind as are now _hereditary_ in the wild species. It thus appears undeniable that all these remarkable and uniform changes must originally have been somatogenetic changes; yet they have now become blastogenetic. This much, I say, seems undeniable; and therefore it goes a long way to prove that the non-blastogenetic character of the changes has been due to their originally somatogenetic character. For, if not, how did natural selection ever get an opportunity of making any of them blastogenetic, when every individual plant has always presented them as already given somatogenetically? This last consideration appears in no small measure to justify the opinion of Mr. Henslow, who concludes--"These experiments prove, not only that the influence of the environment is _at once_ felt by the organ; but that it is indubitably the _cause_ of the now specific and hereditary traits peculiar to normally aquatic, subterranean, and aerial stems, or roots[80]."

[80] It also serves to show that Weismann's newer doctrine of
similar "determinants" occurring both in the germ and in the
somatic tissues is a doctrine which cannot be applied to rebut
this evidence of the transmission of acquired characters in
plants. Therefore even its hypothetical validity as applied by
him to explain the seasonal variation of butterflies is
rendered in a high degree dubious.

He continues to furnish other instances in the same line of proof--such as the distinctive "habits" of insectivorous, parasitic, and climbing plants; the difference in structure between the upper and under sides of horizontal leaves, &c. "For here, as in all organs, we discover by experiment how easily the anatomy of plants can be affected by their environment; and that, as long as the latter is constant, so are the characters of the plants constant and hereditary."

[The following letter, contributed by Dr. Hill to _Nature_, vol. I.
p. 617, may here be quoted. C. Ll. M.

"It may be of interest to your readers to know that two guinea-pigs
were born at Oxford a day or two before the death Dr. Romanes, both
of which exhibited a well-marked droop of the left upper eyelid.
These guinea-pigs were the offspring of a male and a female
guinea-pig in both of which I had produced for Dr. Romanes, some
months earlier, a droop of the left upper eyelid by division of the
left cervical sympathetic nerve. This result is a corroboration of
the series of Brown-Sequard's experiments on the inheritance of
acquired characteristics. A very large series of such experiments
are of course needed to eliminate all sources of error, but this I
unfortunately cannot carry out at present, owing to the need of a
special farm in the country, for the proper care and breeding of
the animals.--LEONARD HILL.

"Physiological Laboratory, Univ. Coll. London, Oct. 18, 1894."]