Abstract
Cytoplasmic male sterility (CMS) is a widespread phenotype in plants, which present a defect in the production of functional pollen. The male sterilizing factors usually consist of unusual genes or open reading frames encoded by the mitochondrial genome. CMS can be suppressed by specific nuclear genes called restorers of fertility (Rfs). In the majority of cases, Rf genes produce proteins that act directly on the CMS conferring mitochondrial transcripts by binding them specifically and promoting processing events. In this review, we explore the wide array of mechanisms guiding fertility restoration. PPR proteins represent the most frequent protein class among identified Rfs and they exhibit ideal characteristics to evolve into restorer of fertility when the mechanism of restoration implies a post-transcriptional action. Here, we review the literature that highlights those characteristics and help explain why PPR proteins are ideal for the roles they play as restorers of fertility.
Highlights
Cytoplasmic male sterility (CMS) has been characterized in over 140 natural species (Laser and Lersten, 1972)
It highlights the wide array of mechanisms guiding fertility restoration, which are in most cases unique to each CMS
PPR proteins exhibit ideal characteristics to evolve into restorer of fertility when the mechanism of restoration implies a post-transcriptional action on mitochondrial gene expression
Summary
Cytoplasmic male sterility (CMS) has been characterized in over 140 natural species (Laser and Lersten, 1972). Several studies have demonstrated the existence of a recognition code between the identity of specific amino acids within the repeats and the target RNA sequence of the PPR protein studied (Barkan et al, 2012; Takenaka et al, 2013; Yagi et al, 2013); the identity of the 5th and the 35th amino acids of each motif have been shown to be important (residue numbering according to Yin et al, 2013 and discussed in Cheng et al, 2016) These two amino acids are generally positively charged (Small and Peeters, 2000; Ban et al, 2013). We encourage readers who want more details on CMS genes to refer to specialized reviews (Hanson and Bentolila, 2004; Chen and Liu, 2014)
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