The evolutionary genetics and genomics of Wolbachia effects on host physiology

项目总结 在生命之树的另一边，物种相互作用。这包括动物和微生物之间的相互作用 殖民他们。许多动物在它们的细胞内藏有微生物，并形成内共生联系。 内共生菌可以对宿主生物学和适应性产生深远的影响，但这些影响的后果 取决于宿主群体中内共生菌的流行情况。而一些内生共生菌进化为专性 在人际关系方面，许多联系是自发的，既有感染的宿主，也有未感染的宿主。沃尔巴克氏菌 细菌扮演着这两个角色，但它们通常与节肢动物形成兼职关系。的确，是兼职的 沃尔巴克氏变种感染大多数昆虫，使它们成为自然界中最常见的内共生体。尽管如此 在分类流行方面，沃尔巴克氏菌在寄主系统内和寄主系统之间的频率差异很大。其作用机制 这种变异背后的原因尚不清楚。填补这一知识空白对于理解丰富的 并提高沃尔巴克氏菌的生物防治效果，其中媒介控制组是 试图在蚊子种群中建立阻止病原体的沃尔巴克氏菌变异株以减少人类 疾病传播(特别是登革热)。以实现对机制的全面了解 控制着沃尔巴克氏菌的传播，我们实验室的研究将朝着三个方向发展。首先，许多沃尔巴克氏菌 导致细胞质不相容(CI)，当感染的雄性与未感染的雌性交配时，会杀死胚胎。 这促进了沃尔巴克氏菌在自然和媒介系统中的传播。然而，导致CI的雄性很少杀死所有人 当后代与未感染的雌性交配时，CI强度从非常弱(大多数卵孵化)不等 完成(没有蛋孵化)。我们将确定导致这种变异的分子机制。 其次，虽然沃尔巴克氏菌是通过母体传播的，但传播率差异很大。我们最近 发现寒冷的温度会干扰母体沃尔巴克氏菌的传播。我们将利用这一发现来 剖析传播率变异的细胞遗传学基础。第三，我们的研究表明， 沃尔巴克氏菌与几千年前分叉的沃尔巴克氏菌交换，感染分叉的宿主 几百万年前。这意味着沃尔巴克氏菌在小说中经常以最初罕见的频率出现 寄主物种，必须增加寄主适合度，才能传播并最终建立。我们将比较以下几种方法的效果 “老的”和“年轻的”感染对宿主健康的影响--在自然和不同的宿主背景下--以量化如何 许多沃尔巴克氏菌可能会分化，并在新宿主中成功传播。这些项目加在一起将 利用分布在果蝇属中的近5000万年的沃尔巴克氏菌分歧来 了解控制沃尔巴克氏菌传播的机制。更广泛地说，这项研究将促进更深层次的 了解自然界内共生菌流行的原因和后果。

PROJECT SUMMARY Across the tree of life species interact. This includes interactions between animals and microorganisms that colonize them. Many animals harbor microbes inside their cells and form endosymbiotic associations. Endosymbionts can have profound effects on host biology and fitness, but the consequences of these effects depend on endosymbiont prevalence in host populations. While some endosymbionts evolve obligate relationships, many associations are facultative, with both infected and uninfected host individuals. Wolbachia bacteria play both roles, but they usually form facultative relationships with arthropods. Indeed, facultative Wolbachia variants infect most insects making them the most common endosymbionts in nature. Despite this taxonomic prevalence, Wolbachia frequencies vary widely within and among host systems. The mechanisms underlying this variation remain unknown. Filling this gap in knowledge is crucial to understand the abundance of Wolbachia in nature and to improve the efficacy of Wolbachia biocontrol, where vector-control groups are attempting to establish pathogen-blocking Wolbachia variants in mosquito populations to reduce human disease transmission (particularly dengue). To achieve a comprehensive understanding of the mechanisms that govern Wolbachia spread, research in our lab will advance in three directions. First, many Wolbachia cause cytoplasmic incompatibility (CI) that kills embryos when infected males mate with uninfected females. This promotes Wolbachia spread in natural and in vector systems. However, CI-inducing males rarely kill all offspring when mated with uninfected females such that CI strength varies from very weak (most eggs hatch) to complete (no eggs hatch). We will determine the molecular mechanisms responsible for this variation. Second, while Wolbachia are maternally transmitted, transmission rates vary significantly. We recently discovered that cold temperatures disrupt maternal Wolbachia transmission. We will leverage this discovery to dissect the cellular-genetic basis of transmission rate variation. Third, our research has demonstrated rapid Wolbachia host switching with Wolbachia that diverged thousands of years ago infecting hosts that diverged many millions of years ago. This implies that Wolbachia regularly occur at initially rare frequencies in novel host species and must increase host fitness to spread and ultimately establish. We will compare effects of “old” and “young” infections on host fitness—in both natural and divergent host backgrounds—to quantify how much Wolbachia may diverge and still successfully spread in novel hosts. Together, these projects will leverage nearly 50 million years of Wolbachia divergence distributed across the Drosophila genus to understand the mechanisms that govern Wolbachia spread. More broadly, this research will promote a deeper understanding of the causes and consequences of endosymbiont prevalence in nature.