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Sortase A-mediated modification of the Streptococcus mutans transcriptome and virulence traits.
Molecular Oral Microbiology ( IF 3.7 ) Pub Date : 2019-08-09 , DOI: 10.1111/omi.12266
Xuan Chen 1 , Chengcheng Liu 1, 2 , Xian Peng 1 , Yuanli He 1 , Haixia Liu 3 , Ying Song 3 , Kaixin Xiong 1 , Ling Zou 1, 4
Affiliation  

Sortase A contributes to adhesion and biofilm formation of Streptococcus mutans by anchoring surface proteins like P1 onto the cell wall, and few other functional characterization has been annotated to this protein and its coding gene srtA. In this study we investigated that whether srtA deletion would affect S. mutans virulence determinants in addition to adhesion and further explored whether these effects were caused due to changes in S. mutans genomic transcription. We used acid‐killing assays, glycolytic rate assessments, and exopolysaccharide (EPS) formation tests to detect whether srtA deletion influenced S. mutans acid tolerance/production and glucan formation. Comparisons between RNA‐sequencing data from both the exponential and stationary phases of UA159 and the srtA‐deleted strain were made to determine the impact of srtA knockout on S. mutans genomic transcription. Results of our assays indicated that S. mutans aciduricity was enhanced in the srtA deleted strain when bacterial cells were directly subjected to pH 2.8, but the enhancement was repressed when the acid tolerance response was induced in advance. The srtA mutation strain exhibited reduced EPS formation in mature biofilms. SrtA deletion led to pleiotropic changes in the S. mutans transcriptome with a growth phase‐dependent pattern. The affected genes mainly included those involved in aciduricity, carbohydrate transport, and EPS formation. It was concluded that S. mutans srtA exhibited multiple effects on the virulence traits of this pathogen, including acid tolerance and glucan formation, and that these alterations could be partially due to transcriptional changes upon loss of srtA.

中文翻译:

分选酶A介导的变形链球菌转录组和毒力性状的修饰。

分选酶A通过将表面蛋白(如P1)锚定在细胞壁上来促进变形链球菌的粘附和生物膜形成,并且对该蛋白及其编码基因srtA进行了注释。在这项研究中,我们调查了srtA缺失是否会影响粘附力以及变形链球菌的毒力决定因素,并进一步探讨了这些影响是否是由于变形链球菌基因组转录的变化引起的。我们使用了除酸测定,糖酵解速率评估和胞外多糖(EPS)形成测试来检测srtA缺失是否影响变形链球菌。耐酸/生产和葡聚糖形成。比较了UA159和srtA缺失菌株的指数期和固定期的RNA测序数据,以确定srtA基因敲除对变形链球菌基因组转录的影响。我们的测定结果表明,当细菌细胞直接置于pH 2.8时,在srtA缺失菌株中变形链球菌酸度得到增强,但是当提前诱导耐酸反应时,突变体的酸性得以增强。所述SRTA突变菌株表现出成熟生物膜减少EPS形成。SrtA删除导致变形链球菌多效性变化具有生长阶段依赖性模式的转录组。受影响的基因主要包括与酸度,碳水化合物转运和EPS形成有关的基因。结论是,变形链球菌srtA对这种病原体的毒力特性表现出多种影响,包括耐酸性和葡聚糖形成,并且这些改变可能部分归因于srtA丧失时的转录变化。
更新日期:2019-08-09
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