IraL is an RssB anti-adaptor that stabilizes RpoS during logarithmic phase growth in Escherichia coli and Shigella.

IraL is an RssB anti-adaptor that stabilizes RpoS during logarithmic phase growth in Escherichia coli and Shigella.
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DOI:
10.1128/mbio.01043-14
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发表时间:
2014-05-27
期刊:
影响因子:
6.4
通讯作者:
Welch RA
Welch RA
中科院分区:
生物学1区
文献类型:
--
作者:
Hryckowian AJ;Battesti A;Lemke JJ;Meyer ZC;Welch RA

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RpoS(σS),一般的应激反应σ因子,指导基因在各种应激条件下的表达。细胞σS浓度的控制对于适当缩放的σ S依赖性基因表达至关重要。保持σS适当水平的一种方法是调节其稳定性。实际上,σS降解由ClpXP蛋白酶催化,并且ClpXP对σS的识别取决于衔接蛋白RssB。在大肠杆菌K-12中存在三种抗衔接子(anti-adaptor),分别是β D、β M和β P,每种都与RssB相互作用,并在不同的胁迫条件下抑制RssB的活性,从而稳定σS。与K-12不同,一些大肠杆菌分离株(包括尿路致病性大肠杆菌菌株CFT 073)在对数生长期和稳定生长期显示出相当的σS细胞水平,表明大肠杆菌菌株之间的σS水平调节存在差异。在这里,我们描述了一种RssB抗衔接子,它在CFT 073和其他大肠杆菌和志贺氏菌菌株的对数生长期稳定σS。通过免疫印迹分析,我们表明,在对数生长期,CNOL影响σS的水平和稳定性。通过计算和基于PCR的分析,我们揭示了iraL在许多大肠杆菌致病型中发现,但在实验室适应菌株中没有发现。最后,通过细菌双杂交和copurification分析,我们证明了RssB与RssL的相互作用机制不同于其他特征性的抗衔接子。我们引入了在大肠杆菌物种中发现的第四种RssB抗适配器,并表明σS水平调节的差异可能有助于致病性和非致病性大肠杆菌菌株的宿主和生态位特异性。细菌必须科普各种环境条件才能生存。RpoS(σS)是一种通用的应激反应因子,在致病性和非致病性大肠杆菌菌株中,它指导许多基因在应激条件下的表达。σS水平和活性的调节允许适当缩放的σ S依赖性基因表达。在这里,我们描述了一种RssB抗衔接子,与先前描述的抗衔接子不同,它在没有额外应力的情况下在对数生长期稳定σS。我们还证明了iraL存在于大量的大肠杆菌和志贺氏菌分离株中。这些数据表明,含有iraL的菌株能够在不含iraL的菌株不能启动σ S依赖性基因表达的条件下启动σ S依赖性基因表达。因此,在大肠杆菌中,EFL介导的σS稳定化可能有助于宿主和生态位特异性。
RpoS (σS), the general stress response sigma factor, directs the expression of genes under a variety of stressful conditions. Control of the cellular σS concentration is critical for appropriately scaled σS-dependent gene expression. One way to maintain appropriate levels of σS is to regulate its stability. Indeed, σS degradation is catalyzed by the ClpXP protease and the recognition of σS by ClpXP depends on the adaptor protein RssB. Three anti-adaptors (IraD, IraM, and IraP) exist in Escherichia coli K-12; each interacts with RssB and inhibits RssB activity under different stress conditions, thereby stabilizing σS. Unlike K-12, some E. coli isolates, including uropathogenic E. coli strain CFT073, show comparable cellular levels of σS during the logarithmic and stationary growth phases, suggesting that there are differences in the regulation of σS levels among E. coli strains. Here, we describe IraL, an RssB anti-adaptor that stabilizes σS during logarithmic phase growth in CFT073 and other E. coli and Shigella strains. By immunoblot analyses, we show that IraL affects the levels and stability of σS during logarithmic phase growth. By computational and PCR-based analyses, we reveal that iraL is found in many E. coli pathotypes but not in laboratory-adapted strains. Finally, by bacterial two-hybrid and copurification analyses, we demonstrate that IraL interacts with RssB by a mechanism distinct from that used by other characterized anti-adaptors. We introduce a fourth RssB anti-adaptor found in E. coli species and suggest that differences in the regulation of σS levels may contribute to host and niche specificity in pathogenic and nonpathogenic E. coli strains. Bacteria must cope with a variety of environmental conditions in order to survive. RpoS (σS), the general stress response sigma factor, directs the expression of many genes under stressful conditions in both pathogenic and nonpathogenic Escherichia coli strains. The regulation of σS levels and activity allows appropriately scaled σS-dependent gene expression. Here, we describe IraL, an RssB anti-adaptor that, unlike previously described anti-adaptors, stabilizes σS during the logarithmic growth phase in the absence of additional stress. We also demonstrate that iraL is found in a large number of E. coli and Shigella isolates. These data suggest that strains containing iraL are able to initiate σS-dependent gene expression under conditions under which strains without iraL cannot. Therefore, IraL-mediated σS stabilization may contribute to host and niche specificity in E. coli.