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-基因是信号转导蛋白的一个大的多基因家族。大约有十几个R基因已被证明是分离的抗性和易感性等位基因，其中几个是已知的港口古老的多态性。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。这两个进化过程--平衡选择和适应性进化--发生在同一个基因中，这是值得注意的，需要解释。这个建议的总体目标是阐明自然选择作用于分离R-基因等位基因的机制，并确定其适合度差异的生理基础。我们相信，这两个追求是必要的，以充分了解抗病性变异的进化遗传学。还将研究含有可变数量的R基因重复的三个复杂基因座的序列变异。我们假设，复杂的基因座进化响应于强平衡选择和特定抗性等位基因的大成本。 这些数据将使我们能够评估替代假设，并有可能将简单和复杂的R基因位点统一在单一的选择模型下。我们在这一资助期内的具体目标是：（1）检验这样一个假设，即抗性和无效易感等位基因之间的长寿命多态性是抗性的巨大代价的特征;（2）检验这样一个预测，即参与功能替代品之间稳定多态性的等位基因的这种代价较低;（3）通过在基因表达、生化中间体和生化终产物方面表征R和S系来分析Rpml抗性的代价;（4）测试特定防御反应在产生Rpml抗性代价中的作用;（5）对96个A.拟南芥种质，并在这些样品的一个子集的串联阵列，以确定光谱的R-基因的进化反应的疾病;和（6）发展的R-基因多态性的主要模式的群体遗传模型。

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.