The coexistence of females and hermaphrodites in plant populations, or gynodioecy, is a puzzle recognized by Darwin. Correns identified cytoplasmic inheritance of one component of sex expression, now known as cytoplasmic male sterility (CMS). Lewis established cytonuclear inheritance of gynodioecy as an example of genetic conflict. Although biologists have since developed an understanding of the mechanisms allowing the joint maintenance of CMS and nuclear male fertility restorer genes, puzzles remain concerning the inheritance of sex expression and mechanisms governing the origination of CMS. Much of the theory of gynodioecy rests on the assumption of maternal inheritance of the mitochondrial genome. Here we review recent studies of the genetics of plant mitochondria, and their implications for the evolution and transmission of CMS. New studies of intragenomic recombination provide a plausible origin for the chimeric ORFs that characterize CMS. Moreover, evidence suggests that nonmaternal inheritance of mitochondria may be more common than once believed. These findings may have consequences for the maintenance of cytonuclear polymorphism, mitochondrial recombination, generation of gynomonoecious phenotypes, and interpretation of experimental crosses. Finally we point out that CMS can alter the nature of the cytonuclear conflict that may have originally selected for uniparental inheritance.