Wybouw Nicky, Mortier Frederik, Bonte Dries
Terrestrial Ecology Unit, Department of Biology Faculty of Sciences, Ghent University Ghent Belgium.
Evol Lett. 2022 May 11;6(3):255-265. doi: 10.1002/evl3.282. eCollection 2022 Jun.
Reproductive parasites such as spread within host populations by inducing cytoplasmic incompatibility (CI). CI occurs when parasite-modified sperm fertilizes uninfected eggs and is typified by great variation in strength across biological systems. In haplodiploid hosts, CI has different phenotypic outcomes depending on whether the fertilized eggs die or develop into males. Genetic conflict theories predict the evolution of host modulation of CI, which in turn influences the stability of reproductive parasitism. However, despite the ubiquity of CI-inducing parasites in nature, there is scarce evidence for intraspecific host modulation of CI strength and phenotype. Here, we tested for intraspecific host modulation of -induced CI in haplodiploid mites. Using a single CI-inducing variant and mitochondrion, a nuclear panel was created that consisted of infected and cured near-isogenic lines. We performed a highly replicated age-synchronized full diallel cross composed of incompatible and compatible control crosses. We uncovered host modifier systems that cause striking variation in CI strength when carried by infected males. We observed a continuum of CI phenotypes in our crosses and identified strong intraspecific female modulation of the CI phenotype. Crosses established a recessive genetic basis for the maternal effect and were consistent with polygenic Mendelian inheritance. Both male and female modulation interacted with the genotype of the mating partner. Our findings identify spermatogenesis as an important target of selection for host modulation of CI strength and underscore the importance of maternal genetic effects for the CI phenotype. Our findings reveal that intraspecific host modulation of CI is underpinned by complex genetic architectures and confirm that the evolution of reproductive parasitism is contingent on host genetics.
诸如通过诱导细胞质不亲和性（CI）在宿主种群中传播的生殖寄生虫。当寄生虫修饰的精子使未感染的卵子受精时就会发生CI，其特点是在不同生物系统中强度差异很大。在单倍体二倍体宿主中，CI根据受精卵是死亡还是发育成雄性而有不同的表型结果。遗传冲突理论预测宿主对CI的调节进化，这反过来又影响生殖寄生的稳定性。然而，尽管自然界中诱导CI的寄生虫无处不在，但关于种内宿主对CI强度和表型的调节的证据却很少。在这里，我们测试了单倍体二倍体螨类中种内宿主对诱导的CI的调节。使用单一的诱导CI的变体和线粒体，创建了一个由感染和治愈的近等基因系组成的核基因组。我们进行了一个高度重复的年龄同步全双列杂交，包括不亲和和亲和的对照杂交。我们发现了宿主修饰系统，当由感染的雄性携带时，这些系统会导致CI强度的显著变化。我们在杂交中观察到了CI表型的连续变化，并确定了种内雌性对CI表型的强烈调节。杂交为母体效应建立了隐性遗传基础，并且与多基因孟德尔遗传一致。雄性和雌性调节都与交配伙伴的基因型相互作用。我们的研究结果确定精子发生是宿主调节CI强度选择的一个重要目标，并强调母体遗传效应对于CI表型的重要性。我们的研究结果表明，种内宿主对CI的调节由复杂的遗传结构支撑，并证实生殖寄生的进化取决于宿主遗传学。
