In view of accumulating evidence that cytoplasmic male sterility (CMS) in some species results from an inability to generate the high ATP/ADP ratios required for specific stages of differentiation in the reproductive cycle, a number of aspects of ATP metabolism are being examined in CMS and male fertile plants.In experiments designed to test mitochondrial efficiency in ATP export, organelles from CMS plants performed very poorly when compared with normal lines. It is proposed that although most of the molecules involved in mitochondrial ATP production are nuclear encoded, the lesions in mitochondrial (mt)DNA known to accompany the CMS phenotype may be expressed as small modifications within the architecture of the mitochondrial membrane. To detect whether such changes could affect the ADP-ATP translocator in the membrane, two sets of experiments were carried out to determine a 'Km' for the translocator. The two methods employed were based on different precepts, but nevertheless indicated a 'Km' for the mitochondrial translocator in CMS lines which differed dramatically from that of male fertile plants. The view that CMS in Petunia hybrida thus might result from small differences in mtDNA encoded membrane proteins is considered in the light of the cytological changes seen to accompany CMS in these plants, as well as in the context of current theories advanced to explain CMS in other species.