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噬菌体样化脓性链球菌染色体岛(SpyCI)与突变表型:受生长状态调控及由SpyCI编码的启动子挽救

Phage-Like Streptococcus pyogenes Chromosomal Islands (SpyCI) and Mutator Phenotypes: Control by Growth State and Rescue by a SpyCI-Encoded Promoter.

作者信息

Scott Julie, Nguyen Scott V, King Catherine J, Hendrickson Christina, McShan W Michael

机构信息

Department of Pharmaceutical Sciences, The University of Oklahoma Health Sciences Center Oklahoma City, OK, USA.

出版信息

Front Microbiol. 2012 Aug 30;3:317. doi: 10.3389/fmicb.2012.00317. eCollection 2012.

DOI:10.3389/fmicb.2012.00317
PMID:22969756
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3430984/
Abstract

We recently showed that a prophage-like Streptococcus pyogenes chromosomal island (SpyCI) controls DNA mismatch repair and other repair functions in M1 genome strain SF370 by dynamic excision and reintegration into the 5' end of mutL in response to growth, causing the cell to alternate between a wild type and mutator phenotype. Nine of the 16 completed S. pyogenes genomes contain related SpyCI integrated into the identical attachment site in mutL, and in this study we examined a number of these strains to determine whether they also had a mutator phenotype as in SF370. With the exception of M5 genome strain Manfredo, all demonstrated a mutator phenotype as compared to SpyCI-free strain NZ131. The integrase gene (int) in the SpyCIM5 contains a deletion that rendered it inactive, and this deletion predicts that Manfredo would have a pronounced mutator phenotype. Remarkably, this was found not to be the case, but rather a cryptic promoter within the int ORF was identified that ensured constitutive expression of mutL and the downstream genes encoded on the same mRNA, providing a striking example of rescue of gene function following decay of a mobile genetic element. The frequent occurrence of SpyCI in the group A streptococci may facilitate bacterial survival by conferring an inducible mutator phenotype that promotes adaptation in the face of environmental challenges or host immunity.

摘要

我们最近发现,一种类原噬菌体的化脓性链球菌染色体岛(SpyCI)通过动态切除并重新整合到mutL的5'端来响应生长,从而控制M1基因组菌株SF370中的DNA错配修复和其他修复功能,导致细胞在野生型和突变体表型之间交替。16个已完成测序的化脓性链球菌基因组中有9个含有整合到mutL中相同附着位点的相关SpyCI,在本研究中,我们检测了其中一些菌株,以确定它们是否也像SF370一样具有突变体表型。除了M5基因组菌株曼弗雷多外,与不含SpyCI的菌株NZ131相比,所有菌株均表现出突变体表型。SpyCIM5中的整合酶基因(int)存在一个缺失,使其失去活性,而这种缺失预示着曼弗雷多会有明显的突变体表型。值得注意的是,事实并非如此,而是在int开放阅读框内发现了一个隐蔽启动子,该启动子确保了mutL以及同一mRNA上编码的下游基因的组成型表达,这为移动遗传元件衰变后基因功能的挽救提供了一个显著例子。A群链球菌中SpyCI的频繁出现可能通过赋予一种可诱导的突变体表型来促进细菌存活,这种表型有助于在面对环境挑战或宿主免疫时促进适应性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8c94/3430984/c2c6ea24f561/fmicb-03-00317-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8c94/3430984/650bbe183f2f/fmicb-03-00317-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8c94/3430984/7b801b115037/fmicb-03-00317-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8c94/3430984/eb601d7a096a/fmicb-03-00317-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8c94/3430984/02ea518b08bb/fmicb-03-00317-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8c94/3430984/c36dcf2d9708/fmicb-03-00317-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8c94/3430984/132fa9a1815f/fmicb-03-00317-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8c94/3430984/aee3d221d670/fmicb-03-00317-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8c94/3430984/c2c6ea24f561/fmicb-03-00317-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8c94/3430984/650bbe183f2f/fmicb-03-00317-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8c94/3430984/7b801b115037/fmicb-03-00317-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8c94/3430984/eb601d7a096a/fmicb-03-00317-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8c94/3430984/02ea518b08bb/fmicb-03-00317-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8c94/3430984/c36dcf2d9708/fmicb-03-00317-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8c94/3430984/132fa9a1815f/fmicb-03-00317-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8c94/3430984/aee3d221d670/fmicb-03-00317-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8c94/3430984/c2c6ea24f561/fmicb-03-00317-g008.jpg

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