Evolutionary Genetics of Cytoplasmic Incompatibility Genes cifA and cifB in Prophage WO of Wolbachia.

Evolutionary Genetics of Cytoplasmic Incompatibility Genes cifA and cifB in Prophage WO of Wolbachia.
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DOI:
10.1093/gbe/evy012
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发表时间:
2018-02-01
影响因子:
3.3
通讯作者:
Newton ILG
Newton ILG
中科院分区:
生物学2区
文献类型:
--
作者:
Lindsey ARI;Rice DW;Bordenstein SR;Brooks AW;Bordenstein SR;Newton ILG

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细菌内共生体沃尔巴克氏体操纵节肢动物繁殖,以促进其通过宿主种群的母体传播。最常见的操纵是细胞质不相容性(CI):感染沃尔巴克氏体的雄性产生改变的精子,导致胚胎死亡,除非被携带相同沃尔巴克氏体的胚胎拯救。最近在沃尔巴克氏体原噬菌体WO的真核关联模块中鉴定了CI的相关基因cifA和cifB。在这里,我们使用转录组学和基因组学的方法来解决三个重要的进化方面的cif基因。首先,我们评估cifA和cifB是否包括一个经典的毒素-抗毒素操纵子在wMel和显示,这两个基因表现出显着的,转录的差异在整个主机的发展。它们可以产生双顺反子信息,尽管在它们的基因间区域中有预测的发夹终止元件。第二,cifA和cifB在噬菌体WO的多样性中强烈地共同进化。第三,我们提供了新的结构域和功能的预测,在沃尔巴克氏体的同源物,并表明,氨基酸序列有很大的不同属。最后,我们研究了cifA和cifB的保守性,发现不再诱导CI的菌株中基因的频繁降解和丢失。两者合计,我们表明,cifA和cifB表现出复杂的转录调控wMel,提供功能注释,拓宽CI诱导的潜在机制,并报告经常性侵蚀的cifA和cifB在非CI菌株,从而扩大我们的理解最广泛的形式的生殖寄生。
The bacterial endosymbiont Wolbachia manipulates arthropod reproduction to facilitate its maternal spread through host populations. The most common manipulation is cytoplasmic incompatibility (CI): Wolbachia-infected males produce modified sperm that cause embryonic mortality, unless rescued by embryos harboring the same Wolbachia. The genes underlying CI, cifA and cifB, were recently identified in the eukaryotic association module of Wolbachia’s prophage WO. Here, we use transcriptomic and genomic approaches to address three important evolutionary facets of the cif genes. First, we assess whether or not cifA and cifB comprise a classic toxin–antitoxin operon in wMel and show that the two genes exhibit striking, transcriptional differences across host development. They can produce a bicistronic message despite a predicted hairpin termination element in their intergenic region. Second, cifA and cifB strongly coevolve across the diversity of phage WO. Third, we provide new domain and functional predictions across homologs within Wolbachia, and show that amino acid sequences vary substantially across the genus. Finally, we investigate conservation of cifA and cifB and find frequent degradation and loss of the genes in strains that no longer induce CI. Taken together, we demonstrate that cifA and cifB exhibit complex transcriptional regulation in wMel, provide functional annotations that broaden the potential mechanisms of CI induction, and report recurrent erosion of cifA and cifB in non-CI strains, thus expanding our understanding of the most widespread form of reproductive parasitism.
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