Zhu Xiaoying, Lu Qunfeng, Li Yulei, Long Qinqin, Zhang Xinyu, Long Xidai, Cao Demin
Clinical Pathological Diagnosis & Research Center, The Affiliated Hospital of Youjiang Medical University for Nationalities, Baise, Guangxi, China.
Medical College, Guangxi University, Nanning, Guangxi, China.
Front Microbiol. 2023 Nov 23;14:1292897. doi: 10.3389/fmicb.2023.1292897. eCollection 2023.
bacteria, encompassing both slow growth (SGM) and rapid growth mycobacteria (RGM), along with true pathogenic (TP), opportunistic pathogenic (OP), and non-pathogenic (NP) types, exhibit diverse phenotypes. Yet, the genetic underpinnings of these variations remain elusive.
Here, We conducted a comprehensive comparative genomics study involving 53 species to unveil the genomic drivers behind growth rate and pathogenicity disparities.
Our core/pan-genome analysis highlighted 1,307 shared gene families, revealing an open pan-genome structure. A phylogenetic tree highlighted clear boundaries between SGM and RGM, as well as TP and other species. Gene family contraction emerged as the primary alteration associated with growth and pathogenicity transitions. Specifically, ABC transporters for amino acids and inorganic ions, along with quorum sensing genes, exhibited significant contractions in SGM species, potentially influencing their distinct traits. Conversely, TP strains displayed contraction in lipid and secondary metabolite biosynthesis and metabolism-related genes. Across the 53 species, we identified 26 core and 64 accessory virulence factors. Remarkably, TP and OP strains stood out for their expanded mycobactin biosynthesis and type VII secretion system gene families, pivotal for their pathogenicity.
Our findings underscore the importance of gene family contraction in nucleic acids, ions, and substance metabolism for host adaptation, while emphasizing the significance of virulence gene family expansion, including type VII secretion systems and mycobactin biosynthesis, in driving mycobacterial pathogenicity.
细菌包括生长缓慢的分枝杆菌(SGM)和生长快速的分枝杆菌(RGM),以及真正致病性(TP)、机会致病性(OP)和非致病性(NP)类型,呈现出多样的表型。然而,这些变异的遗传基础仍然难以捉摸。
在此,我们进行了一项全面的比较基因组学研究,涉及53个物种,以揭示生长速率和致病性差异背后的基因组驱动因素。
我们的核心/泛基因组分析突出了1307个共享基因家族,揭示了一个开放的泛基因组结构。系统发育树突出了SGM和RGM之间以及TP与其他物种之间的清晰界限。基因家族收缩成为与生长和致病性转变相关的主要变化。具体而言,氨基酸和无机离子的ABC转运蛋白以及群体感应基因在SGM物种中表现出显著收缩,可能影响它们的独特性状。相反,TP菌株在脂质和次生代谢物生物合成及代谢相关基因中表现出收缩。在这53个物种中,我们鉴定出26个核心毒力因子和64个辅助毒力因子。值得注意的是,TP和OP菌株因其扩展的分枝杆菌素生物合成和VII型分泌系统基因家族而突出,这些基因家族对其致病性至关重要。
我们的研究结果强调了基因家族在核酸、离子和物质代谢方面的收缩对于宿主适应性的重要性,同时强调了毒力基因家族扩展的重要性,包括VII型分泌系统和分枝杆菌素生物合成,在推动分枝杆菌致病性方面的作用。