The case against evolution

by George Barry O'Toole

But in demonstrating against the Neo-Lamarckians that somatic modifications unrepresented in the germ plasm could have no significance in the process of racial evolution, Weismann had proved too much. His argument was no less telling against Darwinism than it was against Lamarckism. Darwin’s “individual differences” or “slight variations,” now spoken of as fluctuations, were quite as unrepresented and unrecorded in the germ cells as Lamarck’s “acquired adaptations.” There can be no “summation of individual differences” for the simple reason that fluctuations have no germinal basis and are therefore uninheritable—“We must bear in mind the fact,” says Prof. Edmund Wilson, “that Darwin often failed to distinguish between non-inheritable fluctuations and hereditary mutations of small degree.” (Smithson. Inst. Rpt. for 1915, p. 406.) Fluctuations, as we have seen, are due to variability in the environmental conditions, e.g. in access to soil nutrients, etc. As an instance of fluctuational variation the seeds of the ragweed may be cited. Normally these seeds have six spines, but around this average there is considerable fluctuation in individual seeds, some having as many as nine spines and others no more than one. Yet the plants reared from nine-spine seeds, even when similarly mated, show no greater tendency to produce nine-spine seeds than do plants reared from one-spine seeds.

To meet the difficulty presented by the non-inheritability of the Lamarckian adaptation and the Darwinian fluctuation, De Vries substituted for them those rare and abruptly-appearing inheritable variations, which he called mutations[2] and regarded as elementary steps in the evolutionary process. This new version of transformism was announced by De Vries in 1901, and more fully explained in his “Die Mutations-Theorie” (Leipzig, 1902-1903). Renner has shown that De Vries’ new forms of Œnothera were cases of complex hybridization rather than real mutants, as the forms produced by mutation are now called. Nevertheless, the work of Morgan, Bateson, and others leaves little doubt as to the actual occurrence of factorial mutants, while Dr. Albert F. Blakeslee has demonstrated the existence of chromosomal mutants. When unqualified, the term mutant usually denotes the factorial mutant, which arises from a change in one or more of the concatenated genes (hereditary factors) of a single chromosome (nuclear thread) in the germinal (i.e. gametic) complex. All such changes are called factorial mutations. They are hereditarily transmissible, and affect the somatic characters of the race permanently, although, in rare cases, such as that of the bar-eyed Drosophila mutant, the phenomenon of reversion has been observed. The chromosomal mutant, on the contrary, is not due to changes in the single factors or genes, but to duplication of one or more entire chromosomes (linkage-groups) in the gametic complex. Like the factorial mutant, it produces a permanent and heritable modification. The increase in nuclear material involved in chromosomal mutation (i.e. duplication) seems to cause a proportionate increase in the cytoplasmic mass of the single somatic cells, which manifests itself in the phenotype as giantism. De Vries’ Œnothera gigas is a chromosomal mutant illustrative of this phenomenon. Besides the foregoing, there is the pseudomutant produced by the factorial recombination, which results from a crossover, i.e. an exchange of genes or factors between two germinal chromosomes of the same synaptic pair. This reciprocal transfer of genes from one homologous chromosome to another happens, in a certain percentage of cases, during synapsis. The percentage can be artificially increased by exposing young female hybrids to special conditions of temperature.

If these new mutant forms could be regarded as genuine new species, then the fact that such variations are heritable and come within the range of actual observation, would constitute the long-sought empirical proof of the reality of evolution. Consciously or subconsciously, however, De Vries recognized that this was not the case; for he refers to mutants as “elementary species,” and does not venture to present them as authentic organic species.

The factorial mutant answers neither the endurance test nor the intersterility test of a genuine species. It would, doubtless, be going too far to regard all such mutant forms as examples of germinal degeneracy, but it cannot be denied that all of them, when compared to the wild type, are in the direction of unfitness, none of them being viable and prosperous under the severe conditions obtaining in the wild state. Bateson, who seems to regard all mutant characters as recessive and due to germinal loss, declares: “Even in Drosophila, where hundreds of genetically distinct factors have been identified, very few new dominants, that is to say positive additions, have been seen, and I am assured that none of them are of a class which could be expected to be viable under natural conditions. I understand even that none are certainly viable in the homozygous state.” (Toronto Address, Science, Jan. 20, 1922, p. 59.) “Garden or greenhouse products,” says D. S. Jordan, “are immensely interesting and instructive, but they throw little light on the origin of species. To call them species is like calling dress-parade cadets ‘soldiers.’ I have heard this definition of a soldier, ‘one that has stood.’ It is easy to trick out a group of boys to look like soldiers, but you can not define them as such until they have ‘stood.’” (Science, Oct. 20, 1922.) In a word, factorial mutants, owing, as they do, their survival exclusively to the protection of artificial conditions, could never become the hardy pioneers of new species.

Bateson insists that the mutational variation represents a change of loss. “Almost all that we have seen,” he says, “are variations in which we recognize that elements have been lost.” (Science, Jan. 20, 1922, p. 59.) In his Address to the British Association (1914), he cites numerous examples tending to show that mutant characters are but diminutions or intensifications of characters pre-existent in the wild or normal stock, all of which are explicable as effects of the loss (total or partial) of either positive, or inhibitive (epistatic) hereditary factors (genes). One of these instances illustrating the subtractive nature of the factorial mutation is that of the Primula “Coral King,” a salmon-colored mutant, which was suddenly given off by a red variety of Primula called “Crimson King.” Such a mutation is obviously based on the loss of a germinal factor for color. The loss, however, is sometimes partial rather than total, as instanced in the case of the purple-edged Picotee sweet pea, which arose from the wholly purple wild variety by fractionation of the genetic factor for purple pigment. Even where the mutational variation appears to be one of gain, as happens when a positive character appears de novo in the phenotype, or when a dilute parental character is intensified in the offspring, it is, nevertheless, interpretable as a result of germinal loss, the loss, namely, total or partial, of a genetic inhibitor. Such inhibitive genes or factors are known to exist. Bateson has shown, for example, that the whiteness of White Leghorn chickens is due, not to the absence of color-factors, but to the presence of a genetic inhibitor—“The white of White Leghorns,” he says, “is not, as white in nature often is, due to the loss of the color elements, but to the action of something which inhibits their expression.” (Address to the Brit. Ass’n., Smithson. Inst. Rpt. for 1915, p. 368.) Thus the sudden appearance in the offspring of a character not visibly represented in the parents may be due, not to germinal acquisition, but the loss of an inhibitory gene, whose elimination allows the somatic character previously suppressed by it to appear. Hence Bateson concludes: “In spite of seeming perversity, therefore, we have to admit that there is no evolutionary change which in the present state of our knowledge we can positively declare to be not due to loss.” (Loc. cit., p. 375.)

Another consideration, which disqualifies the factorial mutant for the rôle of a new species, is its failure to pass the test of interspecific sterility. When individuals from two distinct species are crossed, the offspring of the cross is either completely sterile, as instanced in the mule, or at least partially so. But when, for example, the sepia-eyed mutant of the vinegar fly is back-crossed with the red-eyed wild type, whence it originally sprang, the product of the cross is a red-eyed hybrid, which is perfectly fertile with other sepia-wild hybrids, with wild flies, and with sepia mutants. This proves that the sepia-eyed mutant has departed, so to speak, only a varietal, and not a specific, distance away from the parent stock. Ordinary or factorial mutation does not, therefore, as De Vries imagined, produce new species. These mutants do, indeed, meet the requirement of permanent transmissibility, for their distinctive characters cannot be obliterated by any amount of crossing. Nevertheless, the factorial mutation falls short of being an empirical proof of evolution, because it is a varietal, and not a specific, change. In other words, factorial mutants are new varieties and not new species. Only a heritable change based on germinal acquisition of sufficient magnitude to produce gametic incompatibility between the variant and the parent type would constitute direct evidence of the transmutation of species, provided, of course, that the variant were also capable of survival under the natural conditions of the wild state.

In his Toronto address of December 28, 1921, Wm. Bateson announced the failure of De Vries’ Mutation Theory, when he said: “But that particular and essential bit of the theory of evolution, which is concerned with the origin and nature of species remains utterly mysterious. We no longer feel as we used to do, that the process of variation, now contemporaneously occurring, is the beginning of a work which needs merely the element of time for its completion; for even time cannot complete that which has not yet begun. The conclusion in which we were brought up that species are a product of a summation of variations ignored the chief attribute of species first pointed out by John Ray that the product of their crosses is frequently sterile in greater or less degree. Huxley, very early in the debate, pointed out this grave defect in the evidence, but before breeding researches had been made on a large scale no one felt the objection to be serious. Extended work might be trusted to supply the deficiency. It has not done so, and the significance of the negative evidence can no longer be denied....

“If species have a common origin where did they pick up the ingredients which produce this sexual incompatibility? Almost certainly it is a variation in which something has been added. We have come to see that variations can very commonly—I do not say always—be distinguished as positive and negative.... Now we have no difficulty in finding evidence of variation by loss, but variations by addition are rarities, even if there are any such which must be so accounted. The variations to which interspecific sterility is due are obviously variations in which something is apparently added to the stock of ingredients. It is one of the common experiences of the breeder that when a hybrid is partially sterile, and from it any fertile offspring can be obtained, the sterility, once lost, disappears. This has been the history of many, perhaps most, of our cultivated plants of hybrid origin.

“The production of an indubitably sterile hybrid from completely fertile parents which has arisen under critical observation is the event for which we wait. Until this event is witnessed, our knowledge of evolution is incomplete in a vital respect. From time to time such an observation is published, but none has yet survived criticism.” (Science, Jan. 20, 1922, pp. 58, 59.)

But what of the chromosomal mutant? For our knowledge of this type of mutation we are largely indebted to Blakeslee’s researches and experiments on the Jimson weed (Datura stramonium). According to Blakeslee, chromosomal mutants result from duplication, or from reduction, of the chromosomes, and they are classified as balanced or unbalanced types according as all, or only some, of the chromosomal linkage-groups are similarly doubled or reduced. If only one of the homologous chromosomes of a synaptic pair is doubled, the mutant is termed a triploid form. It is balanced when one homologous chromosome is doubled in every synaptic pair, but if one or more chromosomes be added to, or subtracted from, this balanced triploid complex, the mutant is termed an unbalanced triploid. When all the chromosomes of the normal diploid complex are uniformly doubled, we have a balanced tetraploid race. The subtraction or addition of one or more chromosomes in the case of a balanced tetraploid complex renders it an unbalanced tetraploid mutant. The retention in somatic cells of the haploid number of chromosomes characteristic of gametes and gametophytes gives a balanced haploid mutant, from which hitherto no unbalanced haploids have been obtained. The normal diploid type and the balanced tetraploid type are said to constitute an even balance, while balanced triploids and haploids constitute an odd balance. The odd balances and all the unbalanced mutants are largely sterile. Thus, for example, more than 80% of the pollen of the haploid mutant is bad. “The normal Jimson Weed,” says Blakeslee, “is diploid (2n) with a total of 24 chromosomes in somatic cells. In previous papers the finding of tetraploids (4n) with 48 chromosomes and triploids (3n) with 36 was reported, as well as unbalanced mutants with 25 chromosomes represented by the formula (2n + 1). The finding of two haploid or 1n plants, which we are now able to report, adds a new chromosomal type to the balanced series of mutants in Datura. This series now stands: 1n, 2n, 3n, 4n. Since a series of unbalanced mutants has been obtained from each of the other balanced types by the addition or subtraction of one or more chromosomes, it is possible that a similar series of unbalanced mutants may be obtainable from our new haploid plants, despite the great unbalance which would thereby result.” (Science, June 16, 1923, p. 646.) The haploid mutant, of which Blakeslee speaks, has, of course, 12 unpaired chromosomes in its somatic cells.