5. Effect of X-rays upon Dominant Mutation of a. No dominant mutations have been found in X-ray progenies of maize in experiments in which hundreds of recessive mutations have been observed. The evidence against the occurrence of dominant mutation induced by X-ray is however inconclusive, for the following reasons:

(1) The number of genes capable of showing dominant mutation may be much smaller than the number capable of showing recessive mutation, since many genes may be already fixed by natural selection at a level maximal for gene action. The possibility of inducing dominant mutation can, therefore, be tested critically only with known recessives.

(2) Among known recessives many may be themselves deficiencies and, therefore, incapable of dominant mutation. Critical evidence of failure to mutate to a dominant allele therefore may be obtained only from recessive genes which have previously been known to mutate to a dominant allele.

(3) The only recessive alleles which meet this requirement are the variegation genes, which may be regarded as unstable recessive mutating frequently to a dominant allele. In these the spontaneous frequency of dominant mutation is so high that an effect of X-rays in inducing additional dominant mutation probably would not be appreciable.

It is possible to avoid these difficulties in the case of one gene. The recessive a₁ has several known dominant alleles. The effect of Dt proved that it is capable of dominant mutation. In the absence of Dt it is not mutable, and would therefore permit recognition of even a slight effect of X-rays in inducing mutation. Since the effect of mutation is recognizable in minute sectors the treatment may be applied in a fairly advanced stage endosperm development, so that many hundreds of cells are tested for mutation by the examination of a single endosperm. It is therefore possible to test for the occurrence of this mutation in practically unlimited populations.

The seed to be irradiated was produced by the cross a a × A a, both parents being homozygous for dt dt and for the complementary factors required for aleurone color. The endosperms of half of the seeds produced are A a a. These serve to indicate the size of sectors resulting from genetic alterations induced by irradiation at the stage chosen, since induced deficiencies of A result in sectors of colorless aleurone. In the colorless seeds, induced dominant mutation of any one of the 3 a genes would result in a corresponding sector of colored aleurone. The colored seeds thus provide a basis for calculation of the number of opportunities for detectable mutation in the colorless seeds, and a basis for comparison of the relative frequency of induced dominant mutation and deficiency. Treatment was applied 73-81 hours after pollination.

The mutability of the a gene in both parental stocks was tested by crossing with a^dl Dt, a^dl being an a allele with negligibly low dominant mutation rate in the presence of Dt. From the results of these crosses the number of dominant mutations which would be expected in the a a a seeds under the influence of various doses of Dt may be calculated.

The results show failure of X-rays to induce dominant mutation in a population estimated at 5,700,000 cells, each containing three a's capable of mutation. The cell population of equal size in sib seeds yielded approximately 100,000 losses of A (deficiencies or recessive mutations) from cells containing only one A gene each. The number of mutations to A which would have occurred in the same populations under the influence of Dt, calculated from the test crosses mentioned, was over 16,000 for a single dose of Dt, or about 1.6 times this number for homozygous Dt Dt Dt seeds.

L. J. Stadler