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解析革兰氏阳性菌中SLOG超家族蛋白YpsA的作用

Deciphering the Role of a SLOG Superfamily Protein YpsA in Gram-Positive Bacteria.

作者信息

Brzozowski Robert S, Huber Mirella, Burroughs A Maxwell, Graham Gianni, Walker Merryck, Alva Sameeksha S, Aravind L, Eswara Prahathees J

机构信息

Department of Cell Biology, Microbiology and Molecular Biology, University of South Florida, Tampa, FL, United States.

National Center for Biotechnology Information, National Library of Medicine, National Institutes of Health, Bethesda, MD, United States.

出版信息

Front Microbiol. 2019 Apr 5;10:623. doi: 10.3389/fmicb.2019.00623. eCollection 2019.

Abstract

Bacteria adapt to different environments by regulating cell division and several conditions that modulate cell division have been documented. Understanding how bacteria transduce environmental signals to control cell division is critical in understanding the global network of cell division regulation. In this article we describe a role for YpsA, an uncharacterized protein of the SLOG superfamily of nucleotide and ligand-binding proteins, in cell division. We observed that YpsA provides protection against oxidative stress as cells lacking show increased susceptibility to hydrogen peroxide treatment. We found that the increased expression of leads to filamentation and disruption of the assembly of FtsZ, the tubulin-like essential protein that marks the sites of cell division in . We also showed that YpsA-mediated filamentation is linked to the growth rate. Using site-directed mutagenesis, we targeted several conserved residues and generated YpsA variants that are no longer able to inhibit cell division. Finally, we show that the role of YpsA is possibly conserved in Firmicutes, as overproduction of YpsA in also impairs cell division.

摘要

细菌通过调节细胞分裂来适应不同环境,并且已经记录了几种调节细胞分裂的条件。了解细菌如何转导环境信号以控制细胞分裂对于理解细胞分裂调控的全局网络至关重要。在本文中,我们描述了YpsA(一种核苷酸和配体结合蛋白的SLOG超家族中未表征的蛋白质)在细胞分裂中的作用。我们观察到,由于缺乏YpsA的细胞对过氧化氢处理的敏感性增加,YpsA可提供针对氧化应激的保护。我们发现YpsA表达增加会导致丝状化以及FtsZ组装的破坏,FtsZ是一种微管蛋白样必需蛋白,它标记了细菌中的细胞分裂位点。我们还表明,YpsA介导的丝状化与生长速率相关。使用定点诱变,我们针对几个保守残基并生成了不再能够抑制细胞分裂的YpsA变体。最后,我们表明YpsA的作用可能在厚壁菌门中保守,因为在枯草芽孢杆菌中过量表达YpsA也会损害细胞分裂。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5872/6459960/35c623eaf513/fmicb-10-00623-g0001.jpg

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