Choi Eunsil, Jeon Hyerin, Oh Changmin, Hwang Jihwan
Microbiological Resource Research Institute, Pusan National University, Busan, South Korea.
Department of Microbiology, Pusan National University, Busan, South Korea.
Front Microbiol. 2020 Nov 9;11:597515. doi: 10.3389/fmicb.2020.597515. eCollection 2020.
The BipA (BPI-inducible protein A) protein is ubiquitously conserved in various bacterial species and belongs to the translational GTPase family. Interestingly, the function of BipA is not essential for cell growth under normal growth conditions. However, cultivation of -deleted cells at 20°C leads to cold-sensitive growth defect and several phenotypic changes in ribosome assembly, capsule production, and motility, suggesting its global regulatory roles. Previously, our genomic library screening revealed that the overexpressed ribosomal protein (r-protein) L20 partially suppressed cold-sensitive growth defect by resolving the ribosomal abnormality in -deleted cells at low temperature. Here, we explored another genomic library clone containing , which encodes a predicted transcriptional factor that is not directly associated with ribosome biogenesis. Interestingly, overexpression of in -deleted cells diminished capsule synthesis and partially restored lipopolysaccharide (LPS) core maturation at a low temperature without resolving defects in ribosome assembly or motility, indicating that YebC may be specifically involved in the regulation of exopolysaccharide and LPS core synthesis. In this study, we collectively investigated the impacts of -deletion on capsule, LPS, biofilm formation, and motility and revealed novel roles of YebC in extracellular polysaccharide production and LPS core synthesis at low temperature using this mutant strain. Furthermore, our findings suggest that ribosomal defects as well as increased capsule synthesis, and changes in LPS composition may contribute independently to the cold-sensitivity of -deleted cells, implying multiple regulatory roles of BipA.
BipA（BPI诱导蛋白A）在各种细菌物种中普遍保守，属于翻译GTP酶家族。有趣的是，在正常生长条件下，BipA的功能对细胞生长并非必不可少。然而，在20°C下培养缺失BipA的细胞会导致冷敏感生长缺陷以及核糖体组装、荚膜产生和运动性方面的几种表型变化，表明其具有全局调节作用。此前，我们的基因组文库筛选显示，过表达的核糖体蛋白（r蛋白）L20通过解决低温下缺失BipA细胞中的核糖体异常，部分抑制了冷敏感生长缺陷。在这里，我们探索了另一个包含YebC的基因组文库克隆，YebC编码一种预测的转录因子，它与核糖体生物发生没有直接关联。有趣的是，在缺失BipA的细胞中过表达YebC会减少荚膜合成，并在低温下部分恢复脂多糖（LPS）核心成熟，而不会解决核糖体组装或运动性方面的缺陷，这表明YebC可能特别参与胞外多糖和LPS核心合成的调节。在本研究中，我们共同研究了缺失BipA对荚膜、LPS、生物膜形成和运动性的影响，并利用该突变菌株揭示了YebC在低温下胞外多糖产生和LPS核心合成中的新作用。此外，我们的研究结果表明，核糖体缺陷以及荚膜合成增加和LPS组成变化可能独立导致缺失BipA细胞的冷敏感性，这意味着BipA具有多种调节作用。
