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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Streptococcal viability and diminished stress tolerance in mutants lacking the signal recognition particle pathway or YidC2
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Streptococcal viability and diminished stress tolerance in mutants lacking the signal recognition particle pathway or YidC2

机译：缺乏信号识别颗粒途径或YidC2的突变体中链球菌的生存力和胁迫耐受性降低

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摘要

The signal recognition particle (SRP)-translocation pathway is conserved in all three domains of life and delivers membrane and secretory proteins to the cytoplasmic membrane or endoplasmic reticulum. We determined the requirement in the cariogenic oral pathogen Streptocococcus mutans of the three universally conserved elements of the SRP pathway: Ffh/SRP54, scRNA, and FtsY/SR alpha. Previously, we reported that insertional interruption of S. mutans ffh was not lethal, but resulted in acid sensitivity. To test whether S. mutans could survive extensive disruption of the SIRP pathway, single and double deletions of genes encoding Ffh, scRNA, and FtsY were generated. Without environmental stressors, all mutant strains were viable, but unlike the wild-type, none could initiate growth at pH 5.0 or in 3.5% NaCl. Survival of challenge with 0.3 mM H2O2 was also diminished without ffh. Members of the YidC/Oxa1/Alb3 family are also ubiquitous, involved in the translocation and assembly of membrane proteins, and have been identified in prokaryotes/mitochondria/chloroplasts. Two genes encoding YidC homologs, YidC1 and YidC2, are present in streptococcal genomes with both expressed in S. mutans. Deletion of YidC1 demonstrated no obvious phenotype. Elimination of YidC2 resulted in a stress-sensitive phenotype similar to SRP pathway mutants. Mutants lacking both YidC2 and SIRP components were severely impaired and barely able to grow, even in the absence of environmental stress. Here, we report the dispensability of the cotranslational SRP protein translocation system in a bacterium. in S. mutans, this pathway contributes to protection against rapid environmental challenge and may overlap functionally with YidC2.
机译：信号识别颗粒（SRP）易位途径在生命的所有三个域中均得到保守，并将膜和分泌蛋白传递至细胞质膜或内质网。我们确定了SRP途径中三个普遍保守的元素（Ffh / SRP54，scRNA和FtsY / SR alpha）在致龋口腔病原体变形链球菌中的需求。以前，我们报道了变形链球菌ffh的插入中断不是致命的，但导致了酸敏感性。为了测试变形链球菌能否在SIRP途径的广泛破坏中幸存，生成了编码Ffh，scRNA和FtsY的基因的单缺失和双缺失。没有环境胁迫因素，所有突变菌株都是可行的，但与野生型不同，没有一个菌株可以在pH 5.0或3.5％NaCl中引发生长。在没有ffh的情况下，使用0.3 mM H2O2攻击的存活期也减少了。 YidC / Oxa1 / Alb3家族的成员也普遍存在，参与膜蛋白的易位和组装，并已在原核生物/线粒体/叶绿体中鉴定出。两种编码YidC同源物的基因YidC1和YidC2存在于链球菌基因组中，两者均在变形链球菌中表达。 YidC1的删除没有表现出明显的表型。消除YidC2会导致类似于SRP途径突变体的应激敏感表型。缺乏YidC2和SIRP成分的突变体严重受损，即使在没有环境压力的情况下也几乎无法生长。在这里，我们报告在细菌中共翻译SRP蛋白易位系统的可分配性。在变形链球菌中，该途径有助于防止快速的环境挑战，并可能在功能上与YidC2重叠。

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