Cytoplasmic male sterility (CMS) and disease susceptibility are associated with a mitochondrial gene, T-urf13, which is carried by the Texas male-sterile cytoplasm (cms-T) of maize. T-urf13 encodes a 13-kilodalton protein, URF13, which is located in the inner mitochondrial membrane. The fungal pathogens, Bipolaris maydis race T and Phyllosticta maydis, produce pathotoxins that are responsible for the virulence toward cms-T maize. Mitochondria from cms-T are specifically sensitive to the pathotoxins; sensitivity is caused by a toxin-URF13 interaction that mediates pore formation in the inner mitochondrial membrane. T-urf13 is correlated with CMS by the molecular analysis of cms-T revertants and the effects of fertility restoration. Nuclear and mitochondrial transformation experiments are proposed to test the relationship between T-urf13 and CMS. Standard and mutated URF13s are used to study their effects on CMS and to determine the structural elements of URF13 relevant to CMS. The effects of URF13 mutation on CMS and toxin sensitivity are compared to determine if the two traits rely on a common structure and mechanism. A maize mitochondrial transformation system is proposed that is based on the toxin-sensitivity response of T-urf13 and particle bombardment. The pathotoxin-URF13 interaction will be investigated to learn how URF13 forms a membrane pore.***//
