Evolutionary Genetics of R Loci in Arabidopsis

描述（由申请人提供）：植物对病原体的防御是由r基因诱导的，r基因是一个大的多基因信号转导蛋白家族。大约有12个r基因被证明为抗性和易感性等位基因分离，其中一些已知具有古老的多态性。r基因也可以显示出快速适应性进化的证据，这可能是与病原体共同进化相互作用的结果。这两种进化过程——平衡选择和适应性进化——发生在同一个基因上是值得注意的，需要解释。本研究的总体目的是阐明自然选择作用于r基因等位基因分离的机制，并确定其适合度差异的生理基础。我们相信，这两方面的研究对于充分了解抗病变异的进化遗传学是必要的。序列变异在三个复杂的位点包含可变数量的r基因重复也将被调查。我们假设复杂基因座的进化是对强平衡选择和特定抗性等位基因的大成本的反应。

DESCRIPTION (provided by applicant): Plant defense against pathogens is induced by R-genes, a large multigene family of signal transducing proteins. Approximately a dozen R-genes have been shown to be segregating for both resistance and susceptibility alleles, and several of these are known to harbor ancient polymorphisms. R-genes can also show evidence of rapid, adaptive evolution, presumably as a consequence of coevolutionary interactions with pathogens. That both of these evolutionary processes -balancing selection and adaptive evolution -occur in the same gene is remarkable, and requires explanation. The general aims of this proposal are to elucidate the mechanisms of natural selection acting on segregating R-gene alleles and to determine the physiological basis for their fitness differences. We believe that both these pursuits are necessary to fully understand the evolutionary genetics of disease resistance variation. Sequence variation at three complex loci containing a variable number of R-gene repeats will also be investigated. We hypothesize that complex loci evolve in response to strong balancing selection and large costs of specific resistance alleles. The data will allow us to evaluate alternative hypotheses, and potentially to unite simple and complex R-gene loci under a single model of selection. Our specific aims in this grant period will be to (1) Test the hypothesis that a large cost of resistance is characteristic of long-lived polymorphisms between resistance and null susceptibility alleles; (2) Test the prediction that this cost is lower for alleles that participate in a stable polymorphism between functional alternatives; (3) Analyze the cost of Rpml resistance by characterizing R and S lines in terms of gene expression, biochemical intermediates and biochemical end products; (4) Test the role of particular defense responses in generating the cost of Rpml resistance; (5) Characterize and contrast nucleotide polymorphism of single-copy R-gene loci in a reference set of 96 A. thaliana accessions, and of tandem arrays in a subset of these samples, to identify the spectrum of evolved responses by R-genes to disease; and (6) Develop population genetic models of the major modes of R-gene polymorphism.