Mitochondrial effects on flower and pollen development

Cytoplasmic male sterility (CMS) is a maternally inherited phenotype characterized by the inability of a plant to produce viable pollen. This trait is a valuable tool used by plant breeders in hybrid seed production and by molecular biologists to study the interaction the nuclear and mitochondrial genomes. CMS is caused by perturbed interaction of proteins encoded by mitochondrial and nuclear genes. Mitochondrial CMS genes of several crop plants originated from rearrangements of mitochondrial DNA sequences leading to aberrant gene products and/or altered levels of normal gene products. It is proposed that CMS genes primarily impair mitochondrial function that in turn results in male sterility. Nuclear restorer genes interfere with the expression of aberrant proteins or suppress by other means the effect of mitochondrial CMS genes thereby restoring fertility. Most of the identified restorer genes encode PPR proteins. As in the case of human 'mitochondrial diseases', it is not yet exactly understood how the mitochondrial defect can bring about a specific phenotype. Recently, first candidates of nuclear 'target genes' were identified, the expression of which is affected by CMS genes. They encode MADS-box transcription factors specifying organ identity in flower development or proteins involved in programmed cell death. Those target genes are thought to be responsible for the defective formation of male flower organs and pollen. © 2005 Elsevier B.V. and Mitochondria Research Society. All rights reserved.