鼠疫耶尔森氏菌从肠道病原体进化而来,其生命周期发生了很大变化,以适应跳蚤传播。假结核耶尔森氏菌。小插入和删除(indel),尤其是移码突变,可以对表型产生重大影响,并通过基因破坏和失活促进毒力和宿主适应。这里,我们分析了365个鼠疫菌基因组,并在核心基因组上鉴定了2,092个全基因组indel。正如最近在结核分枝杆菌中报道的那样,我们还在鼠疫菌中发现了“indelpockets”,随着平均复杂性分数在indel位置附近下降,我们推测这也可能存在于其他原核生物中。系统发育分析表明,基于indel的系统发育树可以基本反映鼠疫耶尔森氏菌主要系统发育关系,除了一些围绕大爆炸的不一致。我们观察到在系统发育的树干中出现了83个indel,在与关键代谢和推定致病性相关的假基因积累中起作用。我们还发现了32个系统组水平的同质体和7个移码疤痕(即,中断的阅读框架被第二次移码救出)。此外,我们的分析显示了基因水平上平行进化的证据,使用SSPA,rpos,rnd,和YPO0624,在巴西分离株中具有丰富的突变,这可能有利于鼠疫菌应对波动的环境。此处观察到的多样化选择信号表明,indel是鼠疫耶尔森氏菌适应性进化的重要贡献者。同时,我们提供了进一步探索的潜在目标,因为我们关注的一些基因/假基因与indel仍然没有特征。重要性鼠疫耶尔森氏菌,鼠疫的病原体,是假结核耶尔森氏菌的高致病性克隆。先前的全基因组SNP分析在其进化过程中提供了很少的适应性特征。这里通过调查鼠疫耶尔森氏菌的365个公共基因组,我们全面概述了核心基因组上的全基因组indel的一般特征及其在鼠疫耶尔森氏菌进化中的作用。检测\“indel口袋,“随着平均复杂性分数在indel位置附近下降,在结核分枝杆菌和鼠疫耶尔森氏菌中,给了我们一个线索,这种现象可能出现在其他细菌基因组中。重要的是,在indel中识别四种不同形式的选择信号将提高我们对鼠疫菌适应性进化的理解,为进一步研究该病原菌的生理机制提供了靶点。由于基于全基因组indel的进化研究在细菌中仍然很少见,我们的研究将有助于破译indels在其他物种中的作用。
The life cycle of Yersinia pestis has changed a lot to adapt to flea-borne transmission since it evolved from an enteric pathogen, Yersinia pseudotuberculosis. Small insertions and deletions (indels), especially frameshift mutations, can have major effects on phenotypes and contribute to virulence and host adaptation through gene disruption and inactivation. Here, we analyzed 365 Y. pestis genomes and identified 2,092 genome-wide indels on the core genome. As recently reported in Mycobacterium tuberculosis, we also detected \"indel pockets\" in Y. pestis, with average complexity scores declining around indel positions, which we speculate might also exist in other prokaryotes. Phylogenic analysis showed that indel-based phylogenic tree could basically reflect the phylogenetic relationships of major phylogroups in Y. pestis, except some inconsistency around the Big Bang polytomy. We observed 83 indels arising in the trunk of the phylogeny, which played a role in accumulation of pseudogenes related to key metabolism and putatively pathogenicity. We also discovered 32 homoplasies at the level of phylogroups and 7 frameshift scars (i.e., disrupted reading frame being rescued by a second frameshift). Additionally, our analysis showed evidence of parallel evolution at the level of genes, with sspA, rpoS, rnd, and YPO0624, having enriched mutations in Brazilian isolates, which might be advantageous for Y. pestis to cope with fluctuating environments. The diversified selection signals observed here demonstrates that indels are important contributors to the adaptive evolution of Y. pestis. Meanwhile, we provide potential targets for further exploration, as some genes/pseudogenes with indels we focus on remain uncharacterized. IMPORTANCE Yersinia pestis, the causative agent of plague, is a highly pathogenic clone of Yersinia pseudotuberculosis. Previous genome-wide SNP analysis provided few adaptive signatures during its evolution. Here by investigating 365 public genomes of Y. pestis, we give a comprehensive overview of general features of genome-wide indels on the core genome and their roles in Y. pestis evolution. Detection of \"indel pockets,\" with average complexity scores declining around indel positions, in both Mycobacterium tuberculosis and Y. pestis, gives us a clue that this phenomenon might appear in other bacterial genomes. Importantly, the identification of four different forms of selection signals in indels would improve our understanding on adaptive evolution of Y. pestis, and provide targets for further physiological mechanism researches of this pathogen. As evolutionary research based on genome-wide indels is still rare in bacteria, our study would be a helpful reference in deciphering the role of indels in other species.