GENETICS AND ULTRASTRUCTURE OF A CYTOPLASMICALLY INHERITED YELLOW MUTANT IN SOYBEANS

A chimeric plant was observed in the F2 generation of a cross between a male-sterile line and a plant introduction homozygous for a chromosome interchange in soybeans [Glycine max (L.) Merr.]. F3 progeny of this plant included one chimera, 36 yellow plants and 16 green plants. The yellow plants, which progressively turn green, were viable and fertile in field, greenhouse and growth-chamber environments. Reciprocal cross-pollinations were made between these yellow plants and four known nuclear yellow mutant plants, between these yellow plants and sibling green plants and between these yellow plants and unrelated green plants. Segregation data from F1 and F2 generations indicated cytoplasmic inheritance of the newly discovered yellow phenotype. Pollinations in which reciprocal F1 hybrid plants were used as male or female parents were made with unrelated green plants. Observations in F1 and F2 generations substantiated the hypothesis of cytoplasmic inheritance. No interactions have been observed between this mutant and the various nuclear backgrounds. This is the first report of a cytoplasmically inherited mutant affecting plant color in soybeans. Exchange grafts were made between cytoplasmic yellow plants and sibling green plants and between cytoplasmic yellow plants and unrelated green plants. The phenotype was controlled by the scion, indicating that graft-transmissible agents were not involved. When grown in darkness, cytoplasmic yellow plants and normal green plants accumulated the same amount of protochlorophyllide. Cytoplasmic yellow plants grown in dim light accumulated slightly less chlorophyll than did their green siblings. Electron photomicrographs showed that the prolamellar body (a structure associated with synthesis of protochlorophyllide) and chloroplast ultrastructure were normal in the cytoplasmic yellow mutant. These observations led to the hypothesis that the synchrony involved in deposition of nuclear and cytoplasmic gene products during organelle development is impaired in this cytoplasmic mutant.