The Response Regulator SprE (RssB) Modulates Polyadenylation and mRNA Stability in Escherichia coli

The Response Regulator SprE (RssB) Modulates Polyadenylation and mRNA Stability in Escherichia coli
复制标题

DOI:
10.1128/jb.00870-09
复制
发表时间:
2009-11-15
影响因子:
3.2
通讯作者:
Silhavy, Thomas J.
Silhavy, Thomas J.
中科院分区:
生物学3区
文献类型:
--
作者:
Carabetta, Valerie J.;Mohanty, Bijoy K.;Silhavy, Thomas J.

文献摘要

被引文献

相似文献

在大肠杆菌中,衔接蛋白SprE(RssB)控制着替代西格玛因子RpoS(西格玛(38)和西格玛(S))的稳定性。当营养物质丰富时,SprE结合RpoS并将其递送至ClpXP进行降解,但当碳源耗尽时,这一过程受到抑制。还需注意的是,SprE的过量产生是有毒性的。在此我们表明,编码多聚(A)聚合酶I(PAP I)的pcnB基因和编码RNA伴侣蛋白Hfq的hfq基因的无效突变可抑制这种毒性。由于PAP I与Hfq共同负责通过在RNA(包括mRNA)的3'端添加多聚(A)尾来靶向它们进行降解,这些数据表明SprE有助于调节大肠杆菌中的多聚腺苷酸化途径。实际上,在指数生长的细胞中,sprE缺失突变体表现出多聚腺苷酸化水平显著降低以及特定mRNA稳定性增加,这与在PAP I缺陷型菌株中观察到的情况相似。在稳定期,我们表明SprE改变了PAP I的细胞内定位。综上所述,我们提出SprE在控制转录组方面发挥着多种功能,通过其对RpoS的影响来调控所合成的物质,并通过其对特定mRNA的多聚腺苷酸化和周转的影响来调节所降解的物质。
In Escherichia coli, the adaptor protein SprE (RssB) controls the stability of the alternate sigma factor RpoS (sigma(38) and sigma(S)). When nutrients are abundant, SprE binds RpoS and delivers it to ClpXP for degradation, but when carbon sources are depleted, this process is inhibited. It also has been noted that overproduction of SprE is toxic. Here we show that null mutations in pcnB, encoding poly(A) polymerase I (PAP I), and in hfq, encoding the RNA chaperone Hfq, suppress this toxicity. Since PAP I, in conjunction with Hfq, is responsible for targeting RNAs, including mRNAs, for degradation by adding poly(A) tails onto their 3' ends, these data indicate that SprE helps modulate the polyadenylation pathway in E. coli. Indeed, in exponentially growing cells, sprE deletion mutants exhibit significantly reduced levels of polyadenylation and increased stability of specific mRNAs, similar to what is observed in a PAP I-deficient strain. In stationary phase, we show that SprE changes the intracellular localization of PAP I. Taken together, we propose that SprE plays a multifunctional role in controlling the transcriptome, regulating what is made via its effects on RpoS, and modulating what is degraded via its effects on polyadenylation and turnover of specific mRNAs.