Mutational analysis of glucose transport regulation and glucose-mediated virulence gene repression in Listeria monocytogenes
Mutational analysis of glucose transport regulation and glucose-mediated virulence gene repression in Listeria monocytogenes
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DOI：
10.1111/j.1365-2958.2011.07692.x
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发表时间：
2011-07-01
影响因子：
3.6
通讯作者：
Milohanic, Eliane
中科院分区：
文献类型：
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作者：
Ake, Francine M. D.;Joyet, Philippe;Milohanic, Eliane
单核细胞增生李斯特菌通过非PTS渗透酶和磷酸烯醇丙酮酸：碳水化合物磷酸转移酶系统（PTS）转运葡萄糖/甘露糖。两个甘露糖类PTS由组成型表达的mpoABCD和诱导型manLMN操纵子编码。man操纵子编码主要的葡萄糖转运蛋白，因为manL或manM缺失显著减慢葡萄糖利用，而mpoA缺失没有影响。PTS（Mpo）主要作为组成型合成的葡萄糖传感器，通过磷酸化和与LevR样转录激活因子ManR相互作用来控制man操纵子的表达。EIIB（Mpo）在ManR调节中起双重作用：P类似于EIIB（Mpo），在没有葡萄糖磷酸化的情况下占主导地位，从而抑制ManR活性，而在葡萄糖摄取期间占主导地位的未磷酸化的EIIB（Mpo）需要使ManR活性。与mpoA相反，mpoB的缺失因此强烈抑制man操纵子表达和葡萄糖消耗。Delta ptsI（EI）突变体可能通过GlcU样非PTS转运蛋白以更慢的速率消耗葡萄糖。有趣的是，ptsI，manL，manM或mpoB的缺失导致PrfA介导的毒力基因表达升高。PTS（Man）是葡萄糖介导的PrfA抑制的主要参与者，因为Delta mpoA突变体显示出正常的PrfA活性。显示PrfA去阻遏的四种突变体不含或仅含很少的未磷酸化EIAB（Man）（ManL），其可能在葡萄糖介导的PrfA调节中起核心作用。
Listeria monocytogenes transports glucose/mannose via non-PTS permeases and phosphoenolpyruvate: carbohydrate phosphotransferase systems (PTS). Two mannose class PTS are encoded by the constitutively expressed mpoABCD and the inducible manLMN operons. The man operon encodes the main glucose transporter because manL or manM deletion significantly slows glucose utilization, whereas mpoA deletion has no effect. The PTS(Mpo) mainly functions as a constitutively synthesized glucose sensor controlling man operon expression by phosphorylating and interacting with ManR, a LevR-like transcription activator. EIIB(Mpo) plays a dual role in ManR regulation: P similar to EIIB(Mpo) prevailing in the absence of glucose phosphorylates and thereby inhibits ManR activity, whereas unphosphorylated EIIB(Mpo) prevailing during glucose uptake is needed to render ManR active. In contrast to mpoA, deletion of mpoB therefore strongly inhibits man operon expression and glucose consumption. A Delta ptsI (EI) mutant consumes glucose at an even slower rate probably via GlcU-like non-PTS transporters. Interestingly, deletion of ptsI, manL, manM or mpoB causes elevated PrfA-mediated virulence gene expression. The PTS(Man) is the major player in glucose-mediated PrfA inhibition because the Delta mpoA mutant showed normal PrfA activity. The four mutants showing PrfA derepression contain no or only little unphosphorylated EIIAB(Man) (ManL), which probably plays a central role in glucose-mediated PrfA regulation.