A new recessive pale yellow/sugary endosperm, embryo lethal mutant was found segregating on the selfed ear of a plant (83-3038-42) from an active Mutator population. Upon subsequent propagation, the mutant phenotype was found to vary from pale yellow to white endosperm, from sugary endosperm to empty pericarp defective, and from viviparous to embryo lethal. Outcrosses to standard of heterozygous mutant plants were crossed by a series of B-A translocations involving 19 of the 20 chromosome arms of maize. Only crosses involving TB-7Lb uncovered the mutant endosperm phenotype. Seedling tests of mutant endosperm kernels from the TB-7Lb cross produced both yellow-green and wildtype seedlings. Since our TB-7Lb source also carries the opaque5 reference allele, which has a yellow-green seedling phenotype, we suspected that the wildtype seedlings arising from mutant endosperm kernels of the TB-7Lb cross were the expected hyperploids, and the yellow-green seedlings were indicative of allelism of our mutant with o5. Subsequent allele tests conducted in our 1991-92 winter nursery proved this to be the case. We now designate our mutant as o5-3038.

We have not yet been able to rescue the viviparous embryos of homozygous o5-3038 kernels in order to determine a seedling phenotype for our mutant. However, when heterozygous with the o5 reference allele, mutant seedlings are yellow-green. A small minority of mutant seedlings are mutable, with the fine green revertant sectors indicative of late reversion events and commonly found in Mu-induced seedling mutants. While it is likely that the reversion events are occurring in the o5-3038 allele, we have not yet ruled out the possibility that the reversion is occurring in the (normally stable) o5 reference allele in the presence of an active Mutator system.

Kernels that are heterozygous for both o5-3038 and the o5 reference allele are distinctly pale yellow, and range from sugary to shrunken-opaque. This is a phenotype intermediate between that of the two homozygous alleles (homozygotes of the o5 reference allele have yellow, shrunken-opaque endosperms in our genetic backgrounds). Furthermore, the intermediate pale yellow endosperm phenotype of the mutant heterozygotes indicates that the white endosperm aspect of the o5-3038 phenotype is due to mutation at the opaque5 locus, and is not due to a coincident mutation or deletion at some other closely linked (and currently unknown) white endosperm locus.

The white endosperm, viviparous embryo phenotype of o5-3038 suggests that the gene product of the O5 gene may be involved in the carotenoid biosynthetic pathway. Why the other known o5 mutants do not have white or pale endosperms as well remains a mystery. Perhaps the other o5 mutant alleles are leaky and produce enough wildtype gene product to give normal appearing endosperm carotenoid levels, or perhaps opaque5 is a complex locus with separate components affecting endosperm carotenoids, seedling carotenoids (some o5 mutants produce albino seedlings, some produce yellow-green or luteus seedlings), and/or plastid structure and development. (See Stinard, MNL65:18-19, for a discussion on how nuclear genes affecting both endosperm and seedling phenotypes could be affecting plastid structure and development. It is conceivable that a mutation that disrupts plastid structure or development could create deleterious lesions in the membranes of the plastids in which carotenoid biosynthesis occurs, resulting in a reduced carotenoid content in both endosperm and seedling. Lesions in the endosperm amyoplasts could also affect starch and protein biosynthesis, leading to the sugary/opaque endosperm phenotype of mutant o5 kernels.) 

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