Is rf2 a restorer gene of CMS-T in maize?

Abstract

Recently Patrick Schnable's team reported that they had cloned rf2 and determined its function [1.xMitochondrial aldehyde dehydrogenase activity is required for male fertility in maize. Liu, F. et al. Plant Cell. 2001; 13: 1063–1078PubMedSee all References, 2.xA more general mechanism of cytoplasmic male fertility?. Moller, I.M. Trends Plant Sci. 2001; 6: 560Abstract | Full Text | Full Text PDF | PubMedSee all References]. For two decades [3xCytoplasmic male sterility in maize. Laughan, J.R. and Gabay-Laughan, S. Annu. Rev. Genet. 1983; 17: 27–48Crossref | PubMedSee all References[3], male fertility restoration of CMS-T (cytoplasmic male sterility-Texas) has been described as being under the control of two restorer loci, rf1 and rf2. Rf1 and Rf2 (the restorer alleles) are dominant and are both required for male fertility restoration of CMS-T. But is rf2 a restorer gene?Cytoplasmic male sterility is a maternally inherited trait that results in the inability of plants to produce viable pollen grains. This phenomenon is often observed in nature in many plant species, and has been used extensively in hybrid production. Every time the cause of CMS has been identified, it has been mitochondrial [4xThe molecular basis of cytoplasmic male sterility and fertility restoration. Schnable, P.S. and Wise, R.P. Trends Plant Sci. 1998; 3: 175–180Abstract | Full Text | Full Text PDF | Scopus (445)See all References[4].Intra-genomic conflict [5xCytoplasmic inheritance and intragenomic conflict. Cosmides, L.M. and Tooby, J. J. Theoret. Biol. 1981; 89: 83–129Crossref | PubMed | Scopus (225)See all References[5] arises when genomes do not share the same pattern of inheritance, each genome maximizing its own transmission at the expense of the other. This is the case of cytoplasmic genes that are maternally transmitted, whereas nuclear genes are biparentally transmitted. Thus, mitochondrial genes that improve their transmission by blocking male gametogenesis will appear and spread (and are therefore mitochondrial male sterile genes) and generate a subsequent selective pressure that favors the emergence of nuclear loci restoring male fertility. These ‘restorer’ loci are believed to act specifically against the expression or the effect of sterilizing factors encoded by the mitochondrial genome. This nucleo–mitochondrial interaction can therefore be seen as the fruit of a host–parasite-like co-evolution [6xPolymorphism of attack and defense. Frank, S.A. Trends Ecol. Evol. 2000; 15: 167–171Abstract | Full Text | Full Text PDF | PubMed | Scopus (41)See all References[6]. In summary: (1) CMS requires the cytoplasmic inheritance of the genes that encode for sterilizing factors and not just the localization of these factors; (2) nuclear restoration is supposed to be specific and more-or-less exclusive (at least at the allelic level) to a given CMS.Puzzlingly, Patrick Schnable's team have shown that the RF2 protein, which exhibits an aldehyde dehydrogenase (ALDH) activity, is necessary for pollen production, not only in plants bearing T-cytoplasm but also in plants bearing a ‘normal’ non-sterilizing cytoplasm (N). There is no difference in the accumulation of the RF2 protein, or in its ALDH activity, between the T- and N-cytoplasm plants.Therefore, rf2 does not appear to work as a restorer gene acting specifically against the expression of T-cytoplasm because it is expressed and necessary for male gametogenesis of N-cytoplasm plants as well. Hypothetically, rf2 could appear as a restorer gene for any other CMS in maize.I therefore suggest that rf2 is not a restorer gene of T-CMS but rather a nuclear male fertility gene that is necessary for normal pollen development, regardless of cytoplasm. Consequently, it is not surprising to find Rf2 (the functional allele) in most maize inbreds, even though they have never been exposed to T-cytoplasm. By contrast, and as expected, Rf1, the ‘other’ restorer gene is rare.Even though rf2 does not provide clues to the restoration mechanism in CMS-T (as rf1 would if it were cloned), it does open up exciting avenues towards understanding the link between mitochondrial metabolism and male gametogenesis.