Mitochondrion role in molecular basis of cytoplasmic male sterility

•Incompatibilities between mitochondrial and nuclear genomes lead to CMS.•Chimeric structure and transmembrane domains characterize CMS associated orfs.•CMS involves reactive oxygen production and programmed cell death.•Whole mitochondrial genome sequencing for deeper insights into mtDNA rearrangements•Nuclear pentatricopeptide repeat genes or non-PPR genes can restore male fertility.

Cytoplasmic male sterility and its fertility restoration via nuclear genes offer the possibility to understand the role of mitochondria during microsporogenesis. In most cases rearrangements in the mitochondrial DNA involving known mitochondrial genes as well as unknown sequences result in the creation of new chimeric open reading frames, which encode proteins containing transmembrane domains. So far, most of the CMS systems have been characterized via restriction fragment polymorphisms followed by transcript analysis. However, whole mitochondrial genome sequence analyses comparing male sterile and fertile cytoplasm open options for deeper insights into mitochondrial genome rearrangements. We more and more start to unravel how mitochondria are involved in triggering death of the male reproductive organs. Reduced levels of ATP accompanied by increased concentrations of reactive oxygen species, which are produced more under conditions of mitochondrial dysfunction, seem to play a major role in the fate of pollen production. Nuclear genes, so called restorer-of-fertility are able to restore the male fertility. Fertility restoration can occur via pentatricopeptide repeat (PPR) proteins or via different mechanisms involving non-PPR proteins.