Molecular basis of genome interaction of the honeybee Apis mellifera with Nosema

我们使用蜜蜂，意大利蜜蜂，和它的微孢子虫寄生虫，微孢子虫作为一个模型系统来研究宿主-寄生虫的社会昆虫物种的共同进化。在之前的资助期间，我们可以将单个QTL定位到染色体14上，该QTL减少了丹麦蜜蜂品系中宿主肠道中的寄生虫孢子负荷，该品系已被选择用于抗微孢子虫。通过在相同染色体区域中的选择性扫描独立地确认QTL，所述区域仅包括四个开放阅读框。这些基因中的两个是抵抗微孢子虫感染的抗性机制的主要候选者。一个基因是RNAi机制的一部分，另一个基因与昆虫的先天免疫系统有关。在接下来的一段时间里，我们将研究寄生虫基因组如何与宿主防御基因进行协商。我们将使用人工进化实验，以动物宿主和模式昆虫细胞培养系统作为宿主，在两种不同的微孢子虫物种中筛选病原体基因组中的选择模式。微孢子虫将在抗性和敏感蜜蜂品系以及细胞培养系统中选择高毒力和低毒力。RNAi将用于敲低细胞培养系统的基因表达，以模拟易感宿主中的选择。使用雄蜂所产生的混合女王，是杂合子的易感性和抗性等位基因，我们将筛选在主机/病原体转录组水平的相互作用，也评估表型可塑性的重要性，在病原体毒力的主机-寄生虫的共同进化后，人工选择高，低毒力。结果将突出寄生虫的遗传适应性程度可以表现出选择的毒力，而不是毒力的表型可塑性。他们还将揭示介导微粒子毒力的常见遗传因子，并显示宿主-病原体系统可以多快地共同进化。最后，结果还将告知我们的基因级联和生理途径，已被选择的主机电阻摆在首位，这可能指向保守的细胞防御机制的影响。

We use the honeybee, Apis mellifera, and its Microsporidian parasite, Nosema as a model system to study host-parasite co-evolution in a social insect species. In the previous funding period, we could map a single QTL to chromosome 14 which reduced the parasite spore load in the host gut in a strain of Danish honeybees, which had been selected for Nosema resistance. The QTL was independently confirmed by a selective sweep in the identical chromosome region, comprising only four open reading frames. Two of these genes are prime candidates for resistance mechanisms against Nosema infections. One gene is part of the RNAi machinery and the other engages with the innate insect immune system. In the forthcoming period we want to study how the parasite genome negotiates with host defence genes.We will screen for patterns of selection in the pathogen genome in two different Nosema species using artificial evolution experiments, using both the animal host and a model insect cell culture system as host. Nosema will be selected for high and low virulence in the resistant and the susceptible honeybee strain and in the cell culture system. RNAi will be used to knock down gene expression of the cell culture system to mimic selection in a susceptible host. Using drones produced by a hybrid queen that is heterozygote for the susceptibility and the resistance allele, we will screen for interactions at the host/pathogen transcriptome level and also assess the importance of phenotypic plasticity in pathogen virulence for host-parasite co-evolution after artificial selection for high and low virulence. Results will highlight the degree of genetic adaptability the parasite can exhibit under selection for virulence, as opposed to phenotypic plasticity for virulence. They will also reveal common genetic factors that mediate Nosema virulence, and show how quickly host-pathogen systems can co-evolve. Finally, results will also inform us of the gene cascades and physiological pathways that have been affected by selection of host resistance in the first place, which could point to conserved cellular defence mechanisms.