Science in Christian Perspective



The Nature of the Gene and the Theory of Evolution
Graduate Student UCLA

From: JASA 6 (September 1954): 2-4.

The theory of evolution today is based on the natural selection of gene mutations as the mechanism for the changes it requires. Other theories in the past have been discarded for la& of evidence though some people still cling to them. Lamarckism, the use and disuse theory, is one example.' Some feel so many occurrences in the normal gene relationships are chance that it is easy to imagine the probability of favorable changes that can lead to evolutionary progression. For instance, the various gene combinations such as yellow and green seed color in the pea, are random occurrences dependent upon just which, parental chromosomes unite in the cross fertilization of hybrids, and also dependent upon random shifts of particular genes between chromosomes in crossing-over. (In the formation of sex gamets each of the normal pair of chromosomes split and come to lie alongside of each other. This bundle is halved and then each half is halved by two successive cell divisions, giving four cells with one chromosome of each kind in them. These are the haploid sex cells. The genes that lie in the same chromosome are, of course, inherited as a group. It sometimes happens, however, that a certain percentage of the chromosomes exchange parts of their length when they separate in the halving process, due to their intertwining. This is crossing-over. In man, sex is determined by which sex chromosome of the male, X or Y, chances to unite with the female X chromosome. In all of these chance occurrences, the gene itself and the spacial orientation of it along the chromosome rema:in the same. Variety is possible from this sort of mendelizing but no progression from an evolutionary point of view. The garden Dahlia is, functionally, an autotetraploid, that is, it has four of each kind of gene instead of two as in the more usual diploid plants. In certain crosses between magenta and ivory colored flowers, pigmented by cyanin and apigenin respectively, it was noticed that anthocyanin production was suppressed in the presence of flavone. Further investigations showed that interaction occurred in the production of all four of the pigments responsible for flower color in Dahlia. In other words, there was competition between these pigments in their parallel production from a common, limited source or intermediate; and this competition was proportional to the dosage and competitive value of the flower color genes governing the synthetic processes. When much anthocyanin was produced, there was less flavone; when much butein, less anthocyanin and/or flavone; and so on.2 A new color variety in Dahlia does not then mean a new gene but merely a new gene combination.

Now, what are genes, these units that are so important in fashioning our bodies from a single cell and enabling it to function as a living entity? Biochemically a gene is a large protein molecule associated with desozyribonucleic acid, and capable of autocatalytic or self -duplicating properties. The nature of the gene biologically is inferred from defects in organisms lacking the normal gene or possessing a mutant form of it.

A pyrimidine synthesizing gene in Neuros,pora, a mold found on bread, has three different mutant alleles or forms. One allele is unable to grow without a supplement of pyrimidine in the culture medium, irrespective of the temperature at which the plant is grown. Two other alleles will grow without a pyrimidine supplement at 25'C, but need it at 35'C. One of them shows normal growth, the other subnormal. 3

Hydrolyzed nuclei acid required for
            half maximal growth. (mg/ml/)
Mutant at      250C at 350C
pyr-3a 37301 3.3      3.15
pyr-3b 37815 0.0      2.4
Pyr-3c 67602 0.38    2.3

From experiments such as this one, the unitary principle of gene action is postulated. Haldane says, "roughly speaking we may say that each gene is responsible, not for a unit character, such as a form or color, but for a unit biochemical process In general, when a gene is responsible for a step in a synthesis, it probably acts by catalyzing the synthesis of an enzyme. Besides controlling catalysis, genes may control membrane permeability, and doubtless many other biochemical processes."4 Carr says, "Often several different varients (alleles) of one gene can be accumulated, and these seem to affect the same biochemical or morphological process, but by different degrees, confirming our suspicion that we have then a graded series of upsets of a single mechanism".5 Beadle says, "The numeroys instances in which a single gene substitution in an organism results in a block in a single metabolic step have led to the hypothesis that many or all genes have single primary functions".6 Cases are known where a single gene mutant affects many different processes and forms but are traceable to a single defect. One -example of this is the vestigal gene in Drosophila. The main effect it produces is the typical reduced wing; but it also causes the scutellar bristles to point forward and upward, prolongs the time of development, decreases viability, makes wings divergent, and causes rudimentation of balancers. These effects can be interpreted as a lack of some growth substance. The bristle effect may be a secondary one.7

Whether the gene effect is due to the spacial orientation of regionally differentiated chromatin, as Goldschmidt thinks, or to the primary action of localized segments of the chromosome though modified by position effects is still an open question.

Goldschmidt believes that the similarities between point mutations and position effects are most logically interpreted as the same The properties of so-called genes are those of small chromosome segments which function differently when the order of their architecture is changed. Visible changes of order are ordinary position effects, and invisible changes of order are ordinary point mutations. The existence of such an architectural mutant effect neither presupposes nor proves the existence of a non-mutated gene. Most geneticists speak of the demonstration of a gene, when only a mutant locus has been found. The overlapping sections of the position effect are in favor of the assumption that the normal action is not the function of a gene, but of a segment of undefined length, possibly of tapering length.8

Sturtevant counters that chromosomes are regionally differentiated, physiologically and visibly. Particular and identifiable regions are necessary for particular reactions in the organisms, and these particular regions behave as units in heredity, that is in crossing-over. These three propositions prove the existence of the gene. When Goldschmidt says that phenotypic effects of sectional deficiencies are best considered as due to position effects rather than to a loss of genes, he has failed to recognize the simple fact that in many cases such sectional deficiencies have been produced by crossing-over between inversions, neither of which has such: a position effect. All the sequences of loci present in the deficient chromosome can be shown to have no such effect, and the missing sections can be shown on independent grounds to have exactly the properties missing in the deficient chromosome.9 Goldschmidt and Sturtevant are evidently in disagreement.

What happens when a gene mutates? Any answer to this question must consider that mutants can change back to the wild type. Mutants are allelic to the wild type at the same locus, by definition. Catcheside says, "In the pantothenicless (5531) and lysineless (4545) mutants, which have never yet been known to revert, it is suspected that the genes may have been lost either in part or totally. Mutants capable of backinutation though hetercatalytically inactive are able to reproduce themselves accurately, through not having lost the essential autocatalytic activity."10 What actually happens when a gene mutates is not known, but the change cannot be very drastic, for it can backmutate to the normal form, unless it is lost. Mutations leading to the reassumption of the wild pheontype have been noted frequently in bacteriological studies.11

It is impossible to be certain that any given mutation is due to a change in the composition of one or more genes rather than in the arrangement of unchanged genes with! respect to each other.9 That is in a position effect. A mutant allele is recognized by a distinctly different action in the organism. This difference might~ spring either from the mutant allele producing an enzyme with an altered specificity (an enzyme catalyzing a different chemical reaction) or an enzyme with the same specificity but with an altered degree of activity. Most experiments support the latter view, and in general almost all mutant alleles appear to possess the same specific activity as the wild type but to a lesser degree. No case of mutation of a gene to an allele which mediates the production of an enzyme of altered, specificity has so far been encountered.10 It would be difficult to detect it if it were suspected. Then too, it would be impossible to know whether or not a closely related gene is involved in an apparent change of specificity, as crossover may not occur between them. This means that we have no way of being sure that -a chemical change has resulted when a gene mutates, but even if it has, it has never been known to change the gene's characteris:tic behaviour.

Recently a type of mutant has been discovered that some geneticists feel is an exception to this rule. It was discovered in Neurospora by Houlahan and Mitchell. It enabled a Pyrimidineless mutant (37301) to grow in a culture media without added Pyrimidine, and so was called a suppressor mutant because it suppressed the effect of the Pyrimidineless mtitant.3 During the uncertainty that precedes a better understanding of the suppressor mutant, many evolutionists will claim it as the basis of evolutionary change.12 In other words, the search for evolutionary significant mutants has been narrowed to a single recently discovered phenomena known as a suppressor mutant; but I am sure that when these mutants are more thoroughly studied they also will be found in multiple, graded alleles and will show back-mutation, hence any progressive change is improbable. It is noteworthy that they are found in a compensatory capacity. These may represent the normal way by which defects biochemically and embryologically are regulated.

It is not known whether the suppressor takes over the lost enzyme function or merely alters the cellular environment so that the mutant enzymes, unstable in the normal environment, become stabilized. In Drosophila, suppressors are known that suppress two or more mutations known from genetic evidence to be concerned in different physiological reactions. In these cases it is highly improbable that the suppressors have taken over simultaneously the functions of the normal alleles of two or more diverse genes.10

In conclusion, it is evident how sparse our knowledge is of the nature of the gene or how it controls morphogenesis and physiology. It appears however, that genes are closely associated with steps in metabolic pathways,. possibly through single enzyme systems and that mutations affect the rate, onset, or termination of these enzyme systems but not their specificity. We have no evidence that a gene has ever mutated into a new and different one with a specificity controlling a new biochemical process. Yet evolution requires this sort of change. In view of this, is it not time to reconsider the natural selection of gene mutations as the mechanism by which Phylogeny has occured?


1.Marsland, D., Piinciples of Modern Biology, P. 703 (1945).
2. Lawrence, W. J. C., Biochem. Soc. Spnp. 4, 7 (1950).
3. Houlahan, M. B. and Mitchell, H. K., Proc. Nat. Acad. Sci., Wash., 33, 223 (1947).
4. Haldane, J. B. S., Biochem. Soc. Synip. 4, 1 (1950).
5. Carr, H. G., Biochem. Soc. Symp. 4, 25 (1950).
6. Beadle, G. W. Genetics in the 20th Century, p. 227 (1951).
7. Goldschmidt, R. B., Physiol, Genetics, p. 78 (1938).
8. Goldschmidt, R. B., Experientia 2-6, 197 & 2-7, 250 (1946).
9. Sturtevant, A. H., Gen. in the 20ih Century, p. 108 (1951).
10- Catcheside, D. G., Biochem Soc. Symp. 4, 32 (1950).
11. Lederberg, J., Gen. 20th Cent. p. 275 (1951).
12. Horowitz, N. H., Advances in Genetics 3, 40 (1950).