Abstract

BackgroundThe plant trait of cytoplasmically-inherited male sterility (CMS) and its suppression by nuclear restorer-of-fertility (Rf) genes can be viewed as a genetic arms race between the mitochondrial and nuclear genomes. Most nuclear Rf genes have been shown to encode P-type pentatricopeptide repeat proteins (PPRs). Phylogenetic analysis of P-class PPRs from sequenced plants genomes has shown that Rf-proteins cluster in a distinct clade of P-class PPRs, RFL-PPRs, that display hallmarks of positive evolutionary selection. Genes encoding RFL-PPRs (RFLs) within a given plant genome tend to be closely related both in sequence and position, but a detailed understanding of how such species-specific expansion occurs is lacking. In the canola, (oilseed rape) species Brassica napus, previous work has indicated the nuclear restorer genes for the two native forms of CMS, Rfn (for nap CMS) and Rfp (pol CMS), represent alternate haplotypes, or alleles, of a single nuclear locus.ResultsFine genetic mapping indicates that Rfn does indeed localize to the same genomic region as Rfp. We find this region is enriched in RFL genes, three of which, based on their position and expression, represent potential candidates for Rfn; one of these genes, designated PPR4, is a preferred candidate in that it is not expressed in the nap CMS line. Comparison of the corresponding regions of the genomes of B. rapa, B. oleracea, Arabidopsis thaliana and A. lyrata provides insight into the expansion of this group of RFL genes in different lines of evolutionary descent.ConclusionsUnlike other nuclear restorer loci containing multiple RFL genes, the RFL genes in the Rf region of B. napus are not present in tandem arrays but rather are dispersed in genomic location. The genes do not share similar flanking non-coding regions and do not contain introns, indicating that they have duplicated primarily through a retrotransposition-mediated process. In contrast, segmental duplication has been responsible for the distribution of the 10 sequences we annotated as RFL genes in the corresponding region of the A. lyrata genome. Our observations define the Brassica Rf locus and indicate that different mechanisms may be responsible for the proliferation of RFL genes even among closely related genomes.Electronic supplementary materialThe online version of this article (doi:10.1186/s12864-016-3117-0) contains supplementary material, which is available to authorized users.

Highlights

  • The plant trait of cytoplasmically-inherited male sterility (CMS) and its suppression by nuclear restorerof-fertility (Rf) genes can be viewed as a genetic arms race between the mitochondrial and nuclear genomes

  • Identification of a BAC clone corresponding to the Rfp/Rfn region A B. rapa cosmid clone containing a polymorphism tightly linked to Rfp, a SNP in the gene corresponding to A. thaliana At1g12910 at chromosome 1 coordinate 4.395 [35], was recovered, sequenced and used as a source of probes to screen a B. napus bacterial artificial chromosome (BAC) library derived from a line with the Rfn genotype at the restorer locus

  • At the outset of this study, our goals were to map the Rfn region with sufficient resolution that we could further clarify the relationship of this gene with Rfp, the restorer for the other native CMS system in B. napus, and to identify a limited number of candidate genes that could be tested for their capacity to rescue the nap CMS trait through transgenic complementation

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Summary

Introduction

The plant trait of cytoplasmically-inherited male sterility (CMS) and its suppression by nuclear restorerof-fertility (Rf) genes can be viewed as a genetic arms race between the mitochondrial and nuclear genomes. Most nuclear Rf genes have been shown to encode P-type pentatricopeptide repeat proteins (PPRs). Cytoplasmic male sterility (CMS) is a widespread, maternally inherited trait of flowering plants that results from the expression of novel genes in the mitochondrial genome. The CMS phenotype is often masked by the presence of nuclear restorer genes. These genes are specific to each form of CMS and in general act to down-regulate, at the post-transcriptional level, the expression of the cognate novel CMS-causing mitochondrial genes. CMS is revealed in nature via gynodioecy, populations consisting

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