The evolutionary genetics and genomics of Wolbachia effects on host physiology

项目摘要 在生命之树上，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。许多动物的细胞内都有微生物，并形成内共生体。 内共生体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 取决于宿主种群中内共生体的流行。虽然有些内共生体进化成专性的 与感染和未感染的宿主个体的关系相比，许多关联是兼性的。Wolbachia 细菌扮演这两种角色，但它们通常与节肢动物形成兼性关系。事实上， 沃尔巴克氏体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 分类流行率，沃尔巴克氏体的频率在宿主系统内和宿主系统之间变化很大。的机制 这种变化的根本原因仍然未知。填补这一知识空白对于理解 和提高沃尔巴克氏体生物防治的效力，其中媒介控制组是 试图在蚊子种群中建立病原体阻断沃尔巴克氏体变体，以减少人类 疾病传播（特别是登革热）。为了全面了解这些机制， 我们实验室的研究将朝三个方向发展。首先，许多沃尔巴克氏体 当受感染的雄性与未受感染的雌性交配时，引起细胞质不相容性（CI），杀死胚胎。 这促进了沃尔巴克氏体在自然和媒介系统中的传播。然而，诱导CI的雄性很少杀死所有 当与未感染的雌性交配时，后代的CI强度从非常弱（大多数卵孵化） 完成（没有鸡蛋孵化）。我们将确定这种变化的分子机制。 其次，虽然沃尔巴克氏体是由母亲传播的，但传播率差异很大。我们最近 发现寒冷的温度会破坏母体沃尔巴克氏体的传播。我们将利用这一发现 剖析传播率变化的细胞遗传基础。第三，我们的研究表明， 沃尔巴克氏体宿主与数千年前分化的沃尔巴克氏体交换感染分化的宿主 在几百万年前。这意味着沃尔巴克氏体在小说中以最初罕见的频率规律地发生。 宿主物种，必须增加宿主适应性才能传播并最终建立。我们将比较 “老”和“年轻”感染对宿主适应性的影响-在自然和不同的宿主背景下-以量化如何 许多沃尔巴克氏体可能会分化，但仍然在新的宿主中成功传播。这些项目将共同 利用分布在果蝇属中近5000万年的沃尔巴克氏体分歧， 了解沃尔巴克氏体传播的机制更广泛地说，这项研究将促进更深入的 了解自然界内共生体普遍存在的原因和后果。

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.