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I 型毒素-抗毒素系统 SprG1/SprF1 对基因表达的影响。

Impacts of the Type I Toxin-Antitoxin System, SprG1/SprF1, on Gene Expression.

机构信息

Department of Analytical Biochemistry, Faculty of Biochemistry, Biophysics and Biotechnology, Jagiellonian University, 30-387 Krakow, Poland.

Department of Analytical Chemistry and Biochemistry, Faculty of Materials Science and Ceramics, AGH University of Science and Technology, 31-007 Krakow, Poland.

出版信息

Genes (Basel). 2021 May 18;12(5):770. doi: 10.3390/genes12050770.

DOI:10.3390/genes12050770
PMID:34070083
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8158120/
Abstract

Type I toxin-antitoxin (TA) systems are widespread genetic modules in bacterial genomes. They express toxic peptides whose overexpression leads to growth arrest or cell death, whereas antitoxins regulate the expression of toxins, acting as labile antisense RNAs. The () genome contains and expresses several functional type I TA systems, but their biological functions remain unclear. Here, we addressed and challenged experimentally, by proteomics, if the type I TA system, the SprG1/SprF1 pair, influences the overall gene expression in . Deleted and complemented strains were analyzed for their proteomes, both intracellular and extracellular, during growth. Comparison of intracellular proteomes among the strains points to the SprF1 antitoxin as moderately downregulating protein expression. In the strain naturally expressing the SprG1 toxin, cytoplasmic proteins are excreted into the medium, but this is not due to unspecific cell leakages. Such a toxin-driven release of the cytoplasmic proteins may modulate the host inflammatory response that, in turn, could amplify the infection spread.

摘要

I 型毒素-抗毒素(TA)系统是细菌基因组中广泛存在的遗传模块。它们表达毒性肽,过量表达会导致生长停滞或细胞死亡,而抗毒素则调节毒素的表达,作为不稳定的反义 RNA 发挥作用。基因组中包含并表达了几个功能齐全的 I 型 TA 系统,但它们的生物学功能仍不清楚。在这里,我们通过蛋白质组学实验解决并挑战了 I 型 TA 系统 SprG1/SprF1 对的表达是否会影响的整体基因表达。在生长过程中,对缺失和互补菌株的细胞内和细胞外蛋白质组进行了分析。菌株间细胞内蛋白质组的比较表明,SprF1 抗毒素适度地下调了蛋白质的表达。在天然表达 SprG1 毒素的菌株中,细胞质蛋白被分泌到培养基中,但这并不是由于非特异性的细胞渗漏。这种由毒素驱动的细胞质蛋白释放可能会调节宿主炎症反应,进而放大的感染传播。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c689/8158120/62f2213a7a31/genes-12-00770-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c689/8158120/c2f0166351e7/genes-12-00770-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c689/8158120/b2e466366d2f/genes-12-00770-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c689/8158120/0be59f88fce5/genes-12-00770-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c689/8158120/62f2213a7a31/genes-12-00770-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c689/8158120/c2f0166351e7/genes-12-00770-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c689/8158120/b2e466366d2f/genes-12-00770-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c689/8158120/0be59f88fce5/genes-12-00770-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c689/8158120/62f2213a7a31/genes-12-00770-g004.jpg

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