Department of Microbiology, Harvard Medical School, Boston, United States.
Howard Hughes Medical Institute, Chevy Chase, United States.
Elife. 2020 Mar 13;9:e54761. doi: 10.7554/eLife.54761.
Members of the suborder of Actinobacteria have a unique cell surface architecture and, unlike most well-studied bacteria, grow by tip-extension. To investigate the distinct morphogenic mechanisms shared by these organisms, we performed a genome-wide phenotypic profiling analysis using as a model. A high-density transposon mutagenized library was challenged with a panel of antibiotics and other stresses. The fitness of mutants in each gene under each condition was then assessed by transposon-sequencing. Clustering of the resulting phenotypic fingerprints revealed a role for several genes of previously unknown function in surface biogenesis. Further analysis identified CofA (Cgp_0016) as an interaction partner of the peptidoglycan synthase PBP1a that promotes its stable accumulation at sites of polar growth. The related proteins were also found to interact, highlighting the utility of our dataset for uncovering conserved principles of morphogenesis for this clinically relevant bacterial suborder.
放线菌亚目的成员具有独特的细胞表面结构，与大多数研究充分的细菌不同，它们通过尖端延伸生长。为了研究这些生物体共有的独特形态发生机制，我们使用 作为模型进行了全基因组表型分析。使用高密度转座子诱变文库对一组抗生素和其他应激原进行了挑战。然后，通过转座子测序评估了每个基因在每种条件下的突变体适应性。对产生的表型指纹进行聚类，发现了几个先前未知功能的基因在表面生物发生中的作用。进一步的分析确定了 CofA（Cgp_0016）作为肽聚糖合酶 PBP1a 的相互作用伙伴，促进其在极性生长部位的稳定积累。还发现相关的 蛋白相互作用，突出了我们的数据集在揭示这个与临床相关的细菌亚目的形态发生保守原则方面的效用。
