Molecular studies of cytoplasmic male sterility in maize

Abstract
A few extra genes that are not found in the mitochondria of other organisms are encoded by plant mitochondrial genomes. Current evidence suggests that the cytoplasmic male sterility (CMS) trait of maize is due to mitochondrial gene mutations. In the sterile maize (CMS-T) a unique mitochondrial gene, designated urf /13-T, appears to cause CMS and susceptibility to the fungal pathogen Helminthosporium maydis race T, and its pathotoxin, T-toxin. The urf 13-T gene encodes a 13 kDa polypeptide that is located in the mitochondrial membrane. In CMS-T two nuclear restorer genes, Rf 1 and Rf 2, countermand the CMS trait and restore viable pollen production. The Rf 1 locus appears to contribute to pollen restoration by reducing the expression of the 13 kDa protein. The function of the Rf 2 gene is unknown. T-toxin and the insecticide methomyl inhibit respiration of mitochondria from CMS-T but not from other maize cytoplasms. When the urf 13-T gene is transformed into E. coli cells and expressed, bacterial respiration is inhibited by both T-toxin and methomyl. Respiration is not inhibited by these compounds in the absence of the 13 kDa protein or with a truncated version of the protein. These studies indicate that the 13 kDa protein is responsible for conferring sensitivity to T-toxin and methomyl. The male-sterile cytoplasm, CMS-C, contains mutations of the mitochondrial genes atp 9, atp 6 and cox II. These mutations have resulted from rearrangements involving portions of mitochondrial genes and chloroplast DNA. One of these gene mutations may be responsible for CMS; however, we currently have no evidence confirming this possibility. Nevertheless, it is clear that different factors cause male sterility in CMS-T and CMS-C because the urf 13-T gene is only found in CMS-T.