Dynamics of nuclear-mitochondrial interactions in the canola plant Brassica napus

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The genetic interaction between pathogens and host organisms has led to the concept of a genetic arms race: genes evolve in pathogens that allow them to evade host defenses, and in response genes evolve in hosts that allow them to resist such new pathogenic strains. Cytoplasmic male sterility (CMS) is a widespread trait among higher plants that results from the expression of novel open reading frames (ORFs) in mitochondrial DNA (mtDNA). In many cases, nuclear genes termed restorers-of-fertility (Rf) have been identified that suppress the CMS phenotype. Such restorer genes are specific for a particular form of CMS and function by down-regulating the expression of the novel, CMS-associated ORF. CMS can be viewed as a particularly interesting "intra-genomic" type of arms race: maternally inherited CMS-conferring mtDNAs spread in a population due to the selective advantage of not allocating resources into pollen production; as CMS individuals become more frequent, pollen becomes limiting, creating the selective pressure for evolution of new restorers. Studies from my laboratory over the last 15 year have revealed features of CMS / restorer gene systems of the canola plant Brassica napus that suggest these systems may provide a useful insight into this arms race. More recently, we discovered that ORF containing gene arrangements responsible for the two forms of B. napus CMS are present at substoichiometric levels in mitochondria in which they are not expected to occur, including mitochondria of one of the progenitor species of B. napus. In addition, we have now cloned and characterized one form of the Brassica nuclear restorer locus. The proposed studies build on this recent work and may allow us to obtain a comprehensive understanding of how CMS-restorer systems evolve. Specifically, we will determine if alteration mt genomic configurations can lead to amplification of the substoichiometric CMS-associated gene arrangements and male sterility; we will characterize the different forms of the restorer locus to gain insight into the molecular events by which the restorers evolved; and we will identify specific restorer genes and the molecules the proteins they encode interact with.