Molecular basis of disease susceptibility in the Texas cytoplasm of maize.

Abstract

Maize plants carrying the Texas, or T, cytoplasm (CMS-T) conferring cytoplasmic male sterility are susceptible to the fungal pathogens Bipolaris maydis [Cochliobolus heterostrophus] race T and Phyllosticta maydis [Mycosphaerella zeae-maydis] in contrast to maize plants carrying normal, C or S-type cytoplasms. The molecular basis of disease susceptibility in the Texas cytoplasm is reviewed with particular reference to the mitochondrial gene T-urf13. Pathotoxins produced by the fungi inhibit CMS-T maize mitochondrial function by their capacity to permeabilize the inner mitochondrial membrane after interaction with the T-urf13 gene product URF13. This promotes the loss of metabolic integrity resulting in large scale fungal colonization and subsequent necrotic lesions. The traits CMS-T and toxin sensitivity appear to be inseparable because analysis of spontaneous revertants has shown that reversion to pollen fertility is always accompanied by simultaneous reversion to toxin insensitivity among true-breeding revertants. It is suggested that T-urf13 is responsible for both traits and that CMS-T and toxin sensitivity could have a common mechanism of action.