Impacts of a DUF2207 Family Protein on Streptococcus mutans Stress Tolerance Responses and Biofilm Formation.
Impacts of a DUF2207 Family Protein on Streptococcus mutans Stress Tolerance Responses and Biofilm Formation.
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DOI：
10.3390/microorganisms11081982
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发表时间：
2023-08-01
期刊：
影响因子：
4.5
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中科院分区：
文献类型：
--
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变异链球菌SMU.243基因座是DUF 2207家族蛋白的一个成员，在所有细菌中高度保守，但功能未知。探讨其在S. 243-缺陷突变体，并分析了SMU.243缺失对细菌生长、胁迫耐受反应和生物膜形成的影响。与野生型UA 159相比，S.当在低pH和甲基紫精存在下生长时，缺少SMU.243的变形杆菌显示出降低的生长速率和降低的过夜培养密度（p < 0.01）。相对于亲本菌株，缺陷突变体在pH 2.8的缓冲液中孵育后（p < 0.01）和在含有58 mM过氧化氢的缓冲液中孵育60分钟后（p < 0.001）也具有降低的存活率，并且具有降低的生物膜形成能力，特别是在蔗糖存在下（p < 0.01）。为了研究SMU.243和uppP之间的任何随后的功能/表型联系，使用等位基因交换诱变产生uppP缺陷突变体，uppP位于SMU.243的紧下游并编码参与载体脂质磷酸十一异戊二烯酯的再循环的十一异戊二烯焦磷酸磷酸酶。与SMU.243突变体不同，uppP的缺失影响细胞包膜生物发生，并导致对杆菌肽的敏感性大幅增加。此外，两个变异的形态突变体，一个形成粗糙的菌落和其他形成粘液，光滑的菌落，也出现后uppP的删除。结果表明，SMU.243编码的DUF 2207家族蛋白在S.变形链球菌在胁迫耐受反应和生物膜形成中起重要作用，但与下游uppP不同的是，变形链球菌似乎不参与细胞包膜的生物合成，尽管变形链球菌的确切作用是在细胞膜形成中起重要作用，但与下游uppP不同的是，变形链球菌似乎不参与细胞包膜的生物合成。变异人的生理学有待进一步研究。
Locus SMU.243 in Streptococcus mutans was annotated as a member of the DUF2207 family proteins highly conserved in all bacteria but with unknown function. To investigate its role in S. mutans physiology, a SMU.243-deficient mutant was constructed using allelic exchange mutagenesis, and the impacts of SMU.243 deletion on bacterial growth, stress tolerance response, and biofilm formation were analyzed. Compared to the wild-type UA159, S. mutans lacking SMU.243 displayed a reduced growth rate and a reduced overnight culture density (p < 0.01) when grown at low pH and in the presence of methyl viologen. Relative to the parent strain, the deficient mutant also had a reduced survival rate following incubation in a buffer of pH 2.8 (p < 0.01) and in a buffer containing hydrogen peroxide at 58 mM after 60 min (p < 0.001) and had a reduced capacity in biofilm formation especially in the presence of sucrose (p < 0.01). To study any ensuing functional/phenotypical links between SMU.243 and uppP, which is located immediately downstream of SMU.243 and encodes an undecaprenyl pyrophosphate phosphatase involved in recycling of carrier lipid undecaprenyl phosphate, a uppP deficient mutant was generated using allelic exchange mutagenesis. Unlike the SMU.243 mutant, deletion of uppP affected cell envelope biogenesis and caused major increases in susceptibility to bacitracin. In addition, two variant morphological mutants, one forming rough colonies and the other forming mucoid, smooth colonies, also emerged following the deletion of uppP. The results suggest that the SMU.243-encoded protein of the DUF2207 family in S. mutans plays an important role in stress tolerance response and biofilm formation, but unlike the downstream uppP, does not seem to be involved in cell envelope biogenesis, although the exact roles in S. mutans’ physiology awaits further investigation.
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