In MNL 61:11-13, we reported on the occurrence of 1:1 (mutable: nonmutable kernels) ears in crosses of Mutator-induced mutable a1 mutants (a1-Mum). These ratios were found in about half the crosses of plants from stable a1-Mum kernels to plants from non-a1-Mum kernels segregating on the same 1:1 outcross ear, from which the stable kernels came. It was proposed that the 1:1 ratios were due to the presence, in the heterozygous condition, of a regulator of somatic mutability in half of the plants from non-a1-Mum kernels. Further evidence that a regulator was involved was obtained when plants from mutable kernels found on 1:1 ears were outcrossed to a standard a1 sh2 stock. These crosses in turn produced 1:1 ears.

A possible alternative explanation for these ratios would be the segregation of a second aleurone gene, such as r or c. For example, if the original 1:1 ear resulted from the cross of a plant that had the genotype R/r; a1-Mum/a1 sh2 x r/r; a1 sh2/a1 sh2, the crosses as outlined above would have given the observed results. In such a situation, the stable seeds from 1: 1 ears will be r/r; a1-Mum/a1 sh2, and one half of the non-a1-Mum kernels would be r/r; a1 sh2/a1 sh2 and one half would be r/r; a1 sh2/a1 sh2. Plants from the r/r; a1 sh2/a1 sh2 kernels crossed with plants from the stable (r/r; a1-Mum a1-Mum) kernels will give ears with 1:1 ratios due to the segregation of the r alleles. Also, a plant from a mutable kernel (R/r; a1-Mum/a1 sh2) from a 1:1 ear when crossed to a r/r, a1 sh2/a1 sh2 tester would give a 1:1 ratio.

Unfortunately, such an explanation for these ratios is a possibility in some of our stocks and must be ruled out before we can say conclusively that we are dealing with a regulator of somatic mutability (an autonomous element). Our a1 sh2 tester stocks were all descended from a1 sh2 kernels isolated from self pollinated purple aleurone/a1 sh2 F1 plants, which segregated in 3:1 ratios for purple:a1 sh2 kernels. However, later tests indicated that some, but not all, of our a1 sh2 stocks used before 1985 were segregating for a second aleurone gene. How this second gene gained entry into our stock is unknown. Mutation is a possible, but unlikely, source. A more likely source would be contamination from a generous border of Illini Extra Sweet sweetcorn that surrounds our experimental plots each year to protect them from the ravages of a large raccoon population, which invades our field from an adjacent wildlife preserve.

We have evidence, however, which indicates that some 1:1 ratios are real. The 1:1 ratios reported in Table 1 of last year's article could not be the result of the presence of a second recessive aleurone gene. Plants from stable kernels of the 85-86 crosses were crossed to homozygous purple aleurone stocks, and the plants from the resulting kernels (50 from each cross planted) were self pollinated. In all cases, there was no evidence of a second gene segregating. The outcrosses of plants from mutable kernels (i.e., the 1986 crosses, mistakenly indicated as 1985 in the heading of Table 1, MNL 61:11-13, 1987) to plants from standard a1 sh2 were made to a newly isolated a1 sh2 stock, eliminating the possibility of a second recessive aleurone gene being present. Thus these 1: 1 ratios are real. Further tests have also been made with some of the crosses reported in Table 2 from last year's article. A plant from a stable kernel, which was found on the ear from which the kernels for families 2274 and 2295 came, was outcrossed to a homozygous purple aleurone stock. One half of the plants from approximately 100 kernels of these outcrossed ears, when self pollinated, segregated for a1 and r, while the remaining plants only segregated for a1. Similar outcrosses of plants from two stable kernels from the ear providing kernels for families 2275 and 2300 were made. All plants of one of these outcrosses segregated for only a1 when self pollinated, while for the second outcross half of the plants segregated for a1 and r and half segregated only for a1. Thus none of the 3 plants, which were derived from stable kernels, tested to be r r as required for stable kernels if the segregation of r is responsible for the 1:1 ratio. In addition, mutable kernels from 1:1 ears of families 2274 (2295), and 2275 (2300), when crossed to a1 sh2 tester, frequently produced 1:1 ratios. The a1 sh2 stocks used in these crosses were newly isolated from purple aleurone crosses and thus would not be carrying another recessive aleurone gene.

The above results suggest that at least some, and perhaps all, of the 1:1 ratios reported last year were real and not due to the segregation of a second aleurone color gene. However, to confirm this conclusion, stable kernels from the 1:1 ears of families 86-2274, 86-2275, 86-2280, 86-2281 and 86-2282, listed in Table 2 of the 1987 report, have been planted in the winter nursery and will be crossed with a2, c1, c2 and r testers to establish, with certainty, the aleurone genotype of each of these lines.

We are also testing the Illini Extra Sweet line with the aleurone testers to establish its aleurone genotype to determine if it was the possible source of the second recessive aleurone gene found in some of our older a1 sh2 stocks.

Donald S. Robertson

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