The genetic architecture of susceptibility to parasites.
The genetic architecture of susceptibility to parasites.
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DOI：
10.1186/1471-2148-8-187
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发表时间：
2008-06-30
影响因子：
3.4
通讯作者：
Schmid-Hempel P
中科院分区：
文献类型：
--
作者：
Wilfert L;Schmid-Hempel P
寄主与寄生虫之间的拮抗性协同进化被认为是维持寄主有性生殖和重组等遗传变异的潜在驱动力。对这一假说的检验需要关于宿主-寄生虫相互作用的遗传基础的信息，例如涉及多少基因，这些基因的影响有多大，以及基因座之间是否存在上位性。在这里，我们研究了数量抗性的遗传结构在动物和植物宿主的串联已发表的研究，已确定的数量性状位点（QTL）在动物和植物的宿主抗性。总的来说，这些研究表明，宿主抗性受少数位点的影响。我们特别表明，额外的上位性相互作用，特别是在不同染色体上的基因座之间，解释了大多数的影响。此外，我们发现，当实验重复使用不同的主机或寄生虫的基因型在其他相同的条件下，宿主抗性的潜在遗传结构可以显着变化-也就是说，涉及不同的QTL和上位性相互作用。当寄主和寄生虫类型保持不变，但在不同环境中重复试验时，QTL和上位性位点的变化要小得多。这种模式的遗传结构的变异性预测基因型之间的强烈相互作用，并证实了不同的宿主-寄生虫组合在不同的环境条件下的流行。此外，上位性是决定寄主抗性表型变异的主要因素。由于上位性似乎主要发生在染色体之间，而不是染色体内，分离和染色体数目，而不是通过交换重组应该是影响宿主抗性适应性变化的主要因素。
The antagonistic co-evolution of hosts and their parasites is considered to be a potential driving force in maintaining host genetic variation including sexual reproduction and recombination. The examination of this hypothesis calls for information about the genetic basis of host-parasite interactions – such as how many genes are involved, how big an effect these genes have and whether there is epistasis between loci. We here examine the genetic architecture of quantitative resistance in animal and plant hosts by concatenating published studies that have identified quantitative trait loci (QTL) for host resistance in animals and plants. Collectively, these studies show that host resistance is affected by few loci. We particularly show that additional epistatic interactions, especially between loci on different chromosomes, explain a majority of the effects. Furthermore, we find that when experiments are repeated using different host or parasite genotypes under otherwise identical conditions, the underlying genetic architecture of host resistance can vary dramatically – that is, involves different QTLs and epistatic interactions. QTLs and epistatic loci vary much less when host and parasite types remain the same but experiments are repeated in different environments. This pattern of variability of the genetic architecture is predicted by strong interactions between genotypes and corroborates the prevalence of varying host-parasite combinations over varying environmental conditions. Moreover, epistasis is a major determinant of phenotypic variance for host resistance. Because epistasis seems to occur predominantly between, rather than within, chromosomes, segregation and chromosome number rather than recombination via cross-over should be the major elements affecting adaptive change in host resistance.
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