Submitted to: Proceedings of the National Academy of Sciences (PNAS)
Publication Type: Review Article
Publication Acceptance Date: 7/1/2002
Publication Date: 8/6/2002
Citation: Wise, R.P., Pring, D.R. 2002. Nuclear-mediated mitochondrial gene regulation and male fertility in higher plants: light at the end of the tunnel? Proceedings of the National Academy of Sciences. 99:10240-10242.
Technical Abstract: The exploitation of hybrid vigor in plants usually capitalizes on cytoplasmic male sterility (CMS), a maternally inherited trait characterized by the absence of functional pollen. Hybrids of many plants are produced using CMS, wherein a male-sterile line is grown adjacent to a selected male-fertile line as pollinator, and seed formed on the male-sterile line is then grown as a hybrid. CMS systems are usually attributed to chimeric open reading frames (ORFs) in the mitochondrial genome. These ORFs encode novel proteins, which often interfere with mitochondrial function and pollen development. Evolution has provided the answer to these aberrant mitochondrial proteins through nuclear-encoded, restoration of fertility, or Rf, genes, which suppress mitochondrial abnormalities associated with male sterility. This suppression allows normal metabolic processes that lead to successful microsporogenesis. In many instances, this suppression is directly associated with Rf-gene-dependent, mitochondrial RNA modification and concurrent reduction of the CMS-associated protein. Although many mitochondrial genes associated with CMS have been characterized, the identification of Rf genes has proven elusive. Only maize Rf2a, a mitochondrial aldehyde dehydrogenase, has been identified to date. It is in this context that the observations of Bentolila et al. (Proc. Natl. Acad. Sci. 2002, in press) represent a critical advance in the fundamental understanding of post-transcriptional, mitochondrial gene regulation and the restoration of male fertility in higher plants. Bentolila et al. report the molecular identification of Petunia Rf, the first isolation of a gene that controls the expression of an organellar gene encoding cytoplasmic male sterility.