DISSERTATION RESEARCH: Quantitative Genetics of Innate Immunity in Drosophila Melanogaster
DISSERTATION RESEARCH: Quantitative Genetics of Innate Immunity in Drosophila Melanogaster
批准号:
0608196
负责人:
Andrew Clark
金额:
$1.2万
依托单位:
依托单位国家:
美国
项目类别:
Standard Grant
财政年份:
2006
资助国家:
美国
项目状态:
已结题
起止时间:
2006-06-01 至 2008-05-31
中文摘要
对各种生物的大量研究已经证实,不同个体之间的免疫功能存在着广泛的差异。果蝇,黑腹果蝇,为研究这种变异的潜在遗传基础提供了一个有用的模型系统。理解免疫功能等复杂性状的遗传变异的一个关键组成部分是破译这种变异在多大程度上代表加性变异,这决定了一个性状的进化速度。通过使用标准的杂交设计,本工作将测量免疫系统功能的加性遗传变异,以及免疫途径中关键候选基因表达的加性遗传变异。除了预测未来变异对选择的反应外,加性遗传变异的模式还可以用来推断可能对我们观察到的遗传变异产生作用的进化力量。因此,了解果蝇免疫系统中加性遗传变异的程度将有助于确定免疫系统中的功能变异是否源于多效性效应,其中对免疫功能的某些方面有利的变异对其他特征具有负面影响,或者免疫系统中的功能变异是否是由于有害突变在种群中以较低的频率分离所致。这些结果将对理解免疫系统是如何进化的,以及进化力量如何影响关键健康特征的变异具有重要意义。
英文摘要
Considerable research in a wide variety of organisms has established that there is extensive variation for immune function among different individuals. The fruit fly, Drosophila melanogaster, provides a useful model system for studying the underlying genetic basis for that variation. A key component of understanding genetic variation for complex traits such as immune function is deciphering how much of that variation represents additive variation, which determines how rapidly a trait can evolve. By using standard crossing designs, this work will measure the additive genetic variation for immune system function in D. melanogaster, as well as additive genetic variation for expression of key candidate genes in the immune pathway. In addition to predicting how variation will respond to selection in the future, patterns of additive genetic variation can be used to infer the evolutionary forces that have likely acted on the genetic variation we observe. Therefore, understanding the extent of additive genetic variation in the Drosophila immune system will help determine whether functional variation in the immune system is due to pleiotropic effects, where variants that are beneficial for some aspect of immune function have negative consequences for other traits, or whether functional variation in the immune system is due to deleterious mutations segregating at low frequency in the population. These results will have implications for understanding how immune systems evolve, and how evolutionary forces shape variation in crucial fitness traits.
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