How sad is my condition!
My grandsire’s gift for writing well
Has gone to some lost polar cell
And so I write this doggerel,
I cannot do much better.”
These kinds of variation, however, in so far as they fall within the range of actual observation, are confined within the limits of the organic species. Intra-specific variation, however, will not suffice. To account for the adaptive modifications superimposed upon underlying structural identity, Transformism is obliged to assume the possibility of trans-specific variation. Yet in none of the foregoing processes of variation do we find a valid factual basis for this assumption.
Factorial mutation, for instance, waiving its failure to produce naturally-viable forms, or to meet the physiological sterility test of a new species, admits of interpretation as a change of loss due to the “dropping out” of a gene from the germinal complex. Bateson’s conception of evolution as a process consisting in the gradual loss of inhibitive genes, whose elimination releases suppressed potentialities, seems rather incredible. Many will be inclined to see in Castle’s facetious epigram a reductio ad absurdum of Bateson’s suggestion; for, according to the latter’s view, as the Harvard professor remarks, we should have to regard man as a simplified amœba. Certainly, it seems nothing short of a contradiction to ascribe the progressive complication of the phenotype to a simplification of the genotype by loss.
On the other hand, not only is there no experimental evidence of a germinal change by positive acquisition, that is, by the addition of genes, but it is hard to conceive how such a change could come about. “At first,” admits Bateson, “it may seem rank absurdity to suppose that the primordial form or forms of protoplasm could have contained complexity enough to produce the divers types of life.” “But,” he asks, “is it easier to imagine that these powers could have been conveyed by extrinsic addition? Of what nature could these additions be? Additions of material can not surely be in question. We are told that salts of iron in the soil may turn a pink hydrangea blue. The iron cannot be passed on to the next generation. How can iron multiply itself? The power to assimilate iron is all that can be transmitted. A disease-producing organism like the pebrine of silkworms can in a very few cases be passed on through the germ cells. But it does not become part of the invaded host, and we can not conceive it taking part in the geometrically ordered processes of segregation. These illustrations may seem too gross; but what refinement will meet the requirements of the problem, that the thing introduced must be, as the living organism itself is, capable of multiplication and of subordinating itself in a definite system of segregation?” (Heredity, Smithson. Inst. Rpt. for 1915, p. 373.)
Nor can we agree with Prof. T. H. Morgan’s contention that the foregoing difficulty of Bateson has been solved by the discovery of the chromosomal mutation. All unbalanced chromosomal mutants are subnormal in their viability and vitality, not to speak of their marked sterility. Haploidy represents a regressive, rather than a progressive, step. The triploid mutant is sterile. The tetraploid race of Daturas is inferior in fertility to the normal diploid plant. The origin of balanced tetraploidy from diploidy must be presumed, since it has never been observed. Moreover, tetraploidy represents only quantitative, and not qualitative, progress. The increased mass of the nucleus produces an enlargement of the cytoplasm, the result of which is giantism. This effect, however, is not specific; for giant and normal races possessing each the same number of chromosomes are known to exist in nature. Hence giantism may be due to other causes besides chromosomal duplication. The only effect of this doubling is a reinforcement and intensification of the former effect of the genetic factors, their specificity remaining unchanged. Double doses are substituted for single doses of the factors, but nothing really new is added. Morgan himself recognizes that this mere repetition of identical genes is insufficient, and that their multiplication must be qualitative as well as numerical, to answer the specifications of a progressive step in evolution. Hence he suggests that the chromosomal mutation is subsequently supplemented by appropriate factorial mutation. Once this supposition is made, however, all the objections we have mentioned in connection with factorial mutation (e.g. the subnormality of its products, its intra-specific nature, etc.) return to plague the speculator, and, in addition to these, he is confronted with the new difficulty of explaining how the redundance of duplicate genes can be removed and replaced by coördinate differentiation in their respective specificities. Now we have no factual evidence whatever of such a solidaric redifferentiation of the germinal factors, that would modify harmoniously the composition and rôle of each and every gene in the factorial complex. Nor is there any possibility whatever of accounting for this telic superregulation of the germinal regulators upon a purely mechanistic basis. How can the ultimate chemical determinants of heredity be thus redetermined? Consequently, although there is gametic incompatibility between diploid races and the tetraploid races, which are said to have arisen from the former, we are not, nevertheless, warranted, by what has been experimentally verified, in regarding tetraploid races as new species, or as progressive steps in the process of organic evolution.
To conclude, therefore, we have experimental verification of the efficacy of the similifying process said to have been at work in evolution, namely, inheritance. The same, however, cannot be said of the correlative diversifying process of trans-specific variation, which is said to have superficially modified old structures into new species. The latter process, accordingly, is but a pure postulate of science known to us only through the effect hypothetically assigned to it, namely, the adaptive modification.