PDF(Pubmed)
Abstract：
Cytoplasmic incompatibility (CI), a non-Mendelian genetic phenomenon, involves the manipulation of host reproduction by Wolbachia, a maternally transmitted alphaproteobacterium. The underlying mechanism is centered around the CI Factor (CIF) system governed by two genes, cifA and cifB, where cifB induces embryonic lethality, and cifA counteracts it. Recent investigations have unveiled intriguing facets of this system, including diverse cifB variants, prophage association in specific strains, copy number variation, and rapid component divergence, hinting at a complex evolutionary history. We utilized comparative genomics to systematically classify CIF systems, analyze their locus structure and domain architectures, and reconstruct their diversification and evolutionary trajectories. Our new classification identifies ten distinct CIF types, featuring not just versions present in Wolbachia, but also other intracellular bacteria, and eukaryotic hosts. Significantly, our analysis of CIF loci reveals remarkable variability in gene composition and organization, encompassing an array of diverse endonucleases, variable toxin domains, deubiquitinating peptidases (DUBs), prophages, and transposons. We present compelling evidence that the components within the loci have been diversifying their sequences and domain architectures through extensive, independent lateral transfers and interlocus recombination involving gene conversion. The association with diverse transposons and prophages, coupled with selective pressures from host immunity, likely underpins the emergence of CIF loci as recombination hotspots. Our investigation also posits the origin of CifB-REase domains from mobile elements akin to CR (Crinkler-RHS-type) effectors and Tribolium Medea1 factor, which is linked to another non-Mendelian genetic phenomenon. This comprehensive genomic analysis offers novel insights into the molecular evolution and genomic foundations of Wolbachia-mediated host reproductive control.
摘要：
细胞质不相容性（CI），一种非孟德尔遗传现象,涉及Wolbachia操纵宿主繁殖，一种通过母体传播的α变形杆菌。潜在的机制围绕着由两个基因控制的CIF系统，CIFA和CIFB,CIFB诱导胚胎致死，CIFA抵消了它。最近的调查揭示了这个系统的有趣方面，包括不同的CIFB变体，在特定菌株中的propage关联，拷贝数变化，和快速的成分发散，暗示着复杂的进化史.我们利用比较基因组学对CIF系统进行了系统分类，分析它们的基因座结构和结构域结构，并重建它们的多样化和进化轨迹。我们的新分类确定了10种不同的CIF类型，不仅仅是Wolbachia的版本，还有其他细胞内细菌，和真核宿主。重要的是,我们对CIF基因座的分析揭示了基因组成和组织的显着变异性，包括一系列不同的核酸内切酶，可变毒素结构域，去泛素化肽酶（DUB），预言,和转座子。我们提供了令人信服的证据，表明基因座内的组件已经通过广泛的，涉及基因转换的独立侧向转移和基因座间重组。与不同的转座子和先知的联系，再加上宿主免疫的选择性压力，CIF位点的出现可能是重组热点的基础。我们的调查还认为CifB-REase结构域起源于类似于CR效应子和TriboliumMedea1因子的移动元素，这与另一种非孟德尔遗传现象有关。这种全面的基因组分析为Wolbachia介导的宿主生殖控制的分子进化和基因组基础提供了新的见解。
