Evolutionary Genetics of R Loci in Arabidopsis

描述(申请人提供)：植物对病原体的防御是由R基因诱导的，这是一个信号转导蛋白的大的多基因家族。大约有十几个R基因被证明同时分离了抗性和易感等位基因，其中几个已知含有古老的多态。R基因还可以显示出快速、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--都发生在同一个基因上，这是值得注意的，需要解释。这一建议的总体目的是阐明自然选择作用于分离R基因等位基因的机制，并确定它们适应度差异的生理基础。我们认为，这两个方面的追求对于充分理解抗病变异的进化遗传学是必要的。还将研究包含可变数量的R基因重复的三个复杂基因座的序列变异。我们假设，复杂的基因座是对强大的平衡选择和大量的特定抗性等位基因成本的反应而演变的。 这些数据将使我们能够评估可供选择的假说，并有可能在单一选择模式下将简单和复杂的R基因座位结合起来。我们在此授权期的具体目标将是：(1)验证抗性和无效感病等位基因之间的长期多态具有大的抗性代价的假设；(2)检验参与功能替代之间稳定多态的等位基因的这种代价较低的预测；(3)通过从基因表达、生化中间体和生化最终产物的角度表征R和S品系，分析Rpm1抗性的代价；(4)测试特定的防御反应在产生Rpm1抗性代价中的作用；(5)对96份拟南星天牛种质的单拷贝R基因座和部分样本的串联阵列的核苷酸多态性进行表征和比较，以确定R基因对疾病的进化反应谱；(6)建立R基因多态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.