A conditional mutant of spontaneous origin which prevents differentiation of the aleurone has been recovered. In the affected kernels, the aleurone fails to develop in some regions resulting in a mosaic pattern of aleuroneless patches on the surface of the kernel. The degree of expression is quite variable ranging from kernels on which about 75% of the surface is defective to seeds having, at most, several minute sectors without aleurone cells, or no deficient regions at all.

The patterns of expression on the kernel surface vary considerably also. In some cases, there is only a small region in the center of the crown which is aleuroneless. In others, the abgerminal side may be completely devoid of aleurone with a gradient of increasing numbers of cells over the crown towards the germinal surface. In yet other cases, the opposite occurs with the germinal side deficient and the abgerminal surface normal.

On a given ear, the phenotypic patterns tend to be similar. Although there is latitude in expression, no case has been observed in which kernels having a deficient germinal surface occur on the same ear with those defective on the abgerminal side.

Scanning EM studies of aleuroneless and normal kernels have revealed size and shape differences between the aleurone cells of the two types. The cells on defective kernels are generally larger and more irregular in shape than those on normal ones. These differences may be due to abnormal differentiation of the aleurone cells or simply to the fact that there is less compaction on the defective kernels and hence, more room to expand.

The phenotype first appeared on ears of two unrelated stocks in which the pollen came from sibling plants of a third line; hence, the mutant was carried by the male parent. When it arose is uncertain since it could have been transmitted through a number of generations without the conditions necessary for expression of the phenotype (see below). Since the phenotype was expressed in the heterozygote, either the mutant allele is dominant or dosage effect is involved.

On two of the ears from these crosses, distribution of the phenotype was not random. Kernels with the most extreme expression occurred about an inch above the base and the degree of expression diminished in both directions from that point. Kernels on the distal portion of the ear showed either slight expression or no aleurone deficiencies at all. This distribution parallels the sequence of ovule development. Those about an inch above the base are most advanced with maturation proceeding in both directions.

When aleuroneless mosaic kernels were grown and used as both males and females in crosses with unrelated lines, the phenotype was expressed in the offspring but infrequently. In the progeny of both sexes there were cases in which kernels exhibiting the phenotype were clustered in a particular region of the ear but not necessarily at the oldest point.

In some instances, the phenotype has skipped a generation. When plants derived from normal sibs of aleuroneless kernels were outcrossed to unrelated lines, the phenotype was expressed in some kernels but infrequently.

The clustering of mutant expression at a point along the length of the ear suggests that either ovule age at the time of fertilization, or some condition present when the affected ovules developed but not when others matured, was responsible for appearance of the mutant phenotype. The fact that the aleuroneless allele was introduced through the male in some of the crosses indicates that the ovule was preconditioned by some factor which allowed expression of the character in the resulting caryopsis. Tests are currently under way to identify the factor(s) responsible for phenotypic expression.

John P. Mottinger

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