Critical Role of a Single Position in the −35 Element for Promoter Recognition by
            <i>Mycobacterium tuberculosis</i>
            SigE and SigH

Song, Taeksun; Song, Suk-Won; Raman, Sahadevan; Anaya, Mauricio; Husson, Robert N.

doi:10.1128/jb.01642-07

Cited by 43 publications

(42 citation statements)

References 16 publications

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“…4), it is unlikely that P1 is recognized by E in vivo. This hypothesis is also supported by the fact that the P1 promoter sequence is distant (even if somewhat related because of degenerate bases) from the reported E consensus promoter (32) and by the observation that the SDS-mediated induction of sigE is maintained in a sigE mutant strain (22). Since ECF sigma factors usually recognize similar promoters, it is possible that P1 is indeed recognized in vivo by an ECF sigma factor that is different from E , which could be able to recognize it under less-stringent in vitro conditions.…”

Section: Discussionmentioning

confidence: 67%

Evidence of Complex Transcriptional, Translational, and Posttranslational Regulation of the Extracytoplasmic Function Sigma Factor σ ^E in Mycobacterium tuberculosis

et al. 2008

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The extracytoplasmic factor (ECF) sigma factor E is one of the most studied sigma factors of Mycobacterium tuberculosis. It has been shown to be involved in virulence as well as in survival under conditions of high temperature, alkaline pH, and exposure to detergents and oxidative stress. Unlike many ECF sigma factors, E does not directly regulate the transcription of its own gene. Two promoters have been identified upstream of the sigE gene; one is regulated by the two-component system MprAB, while the other has been shown to be H dependent. In this paper, we further characterize the regulation of E by identifying its anti-sigma factor and a previously unknown promoter. Finally, we show that sigE can be translated from three different translational start codons, depending on the promoter used. Taken together, our data demonstrate that E not only is subjected to complex transcriptional regulation but is also controlled at the translational and posttranslational levels.Sigma factors are interchangeable RNA polymerase (RNAP) subunits allowing recognition of specific promoter sequences. They are often subjected to both transcriptional and posttranslational regulation (11,12). One of the bestcharacterized Mycobacterium tuberculosis sigma factors, E (29), has been shown to be induced during growth in human macrophages (8,30) and in response to various stress conditions, such as detergent-mediated surface stress, alkaline pH, heat shock, and oxidative stress (10,18,21,28). An M. tuberculosis mutant lacking sigE was shown to be more sensitive to several environmental stresses (22), had reduced growth in both macrophages and dendritic cells (7,22), and was severely attenuated in a mouse model of infection (2,19). Interestingly, dendritic cells infected with the sigE mutant strain secrete larger amounts of interleukin 10 than those infected with the wild-type parental strain, suggesting that the lack of a functional E leads to a different interaction of the bacterium with the immune system (7). Two promoters have been described for sigE transcription. The first one was recently shown to be regulated by the twocomponent system MprAB in response to surface stress and exposure to alkaline pH (10, 26). Its transcriptional start point (TSP) corresponds to the first nucleotide of the putative E translation start codon, as annotated in the TubercuList (http: //genolist.pasteur.fr/TubercuList/). The second one has a clear H consensus sequence and is responsible for the H -dependent induction of sigE after heat shock and exposure to diamide both in M. tuberculosis (28) and in Mycobacterium leprae (34). Surprisingly, it is located 63 bp inside the putative E coding region, leading some investigators to hypothesize that the actual annotation could be wrong (34). Moreover, the Rv1222 gene, the gene located immediately downstream of sigE, has been proposed to encode a member of the zincassociated anti-sigma factor (ZAS) family, based on the typical HXXXCXXC motif found in its sequence (25). The members of the ZAS family are proteins ...

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Section: Discussionmentioning

confidence: 67%

Evidence of Complex Transcriptional, Translational, and Posttranslational Regulation of the Extracytoplasmic Function Sigma Factor σ ^E in Mycobacterium tuberculosis

et al. 2008

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“…The corresponding band was not detected in comparable samples obtained from the ⌬-H mutant. It has previously been reported that the expression of Rv2745c is controlled by E (14,51). The inability of the ⌬-H mutant to induce the expression of E likely results in the lack of induction of the Rv2745c gene.…”

Section: Resultsmentioning

confidence: 97%

Functional Genomics Reveals Extended Roles of the Mycobacterium tuberculosis Stress Response Factor σ ^H

2009

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Mycobacterium tuberculosis is one of the most successful pathogens of humankind. During infection, M. tuberculosis must cope with and survive against a variety of different environmental conditions. Sigma factors likely facilitate the modulation of the pathogen's gene expression in response to changes in its extracellular milieu during infection. sigma(H), an alternate sigma factor encoded by the M. tuberculosis genome, is induced by thiol-oxidative stress, heat shock, and phagocytosis. In response to these conditions, sigma(H) induces the expression of sigma(B), sigma(E), and the thioredoxin regulon. In order to more effectively characterize the transcriptome controlled by sigma(H), we studied the long-term effects of the induction of sigma(H) on global transcription in M. tuberculosis. The M. tuberculosis isogenic mutant of sigma(H) (Delta-sigma(H)) is more susceptible to diamide stress than wild-type M. tuberculosis. To study the long-term effects of sigma(H) induction, we exposed both strains to diamide, rapidly washed it away, and resumed culturing in diamide-free medium (post-diamide stress culturing). Analysis of the effects of sigma(H) induction in this experiment revealed a massive temporal programming of the M. tuberculosis transcriptome. Immediately after the induction of sigma(H), genes belonging to the functional categories "virulence/detoxification" and "regulatory proteins" were induced in large numbers. Fewer genes belonging to the "lipid metabolism" category were induced, while a larger number of genes belonging to this category were downregulated. sigma(H) caused the induction of the ATP-dependent clp proteolysis regulon, likely mediated by a transcription factor encoded by Rv2745c, several members of the mce1 virulence regulon, and the sulfate acquisition/transport network.

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“…A potential candidate was sigB, since sigB contains a sigE-dependent promoter (17,32) and because sigB levels are decreased in a sigE mutant during logarithmic growth, SDS-mediated stress (17), and hypoxia (Fig. 2D).…”

Section: Resultsmentioning

confidence: 99%

“…The figure shows the regulatory interactions revealed in the present work. The sigE-sigB interaction is taken from the literature (17,32). The colors of the ovals containing the gene names represent gene classes in the network structure as follows: black, global regulators; gray, local regulators; white, effector genes.…”

Section: Acknowledgmentsmentioning

confidence: 99%

Regulation of Central Metabolism Genes of Mycobacterium tuberculosis by Parallel Feed-Forward Loops Controlled by Sigma Factor E (σ ^E )

Datta¹,

Shi²,

Bibi³

et al. 2011

J Bacteriol

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Cells respond to external stimuli through networks of regulatory interactions. The human pathogen Mycobacterium tuberculosis responds to stress encountered during infection by arresting multiplication and implementing critical metabolic changes that lead to or sustain the nonreplicative state. Much of this differentiation program is recapitulated when M. tuberculosis cultures are subjected to gradual oxygen depletion in vitro. Here we report that hypoxic induction of critical central metabolism genes in the glyoxylate shunt (icl1) and in the methylcitrate cycle (gltA1) involves both global and local regulators. The global regulators are accessory sigma factors B for icl1 and E for gltA1. The local regulators are the products of two paralogous genes mapping at positions adjacent to the corresponding effector gene or operon. We call these genes lrpI and lrpG (for local regulatory protein of icl1 and gltA1). We also found that (i) each sigma factor controls the corresponding local regulator, (ii) both global and local regulators are required for effector gene induction, and (iii) the occurrence of sigma factor control of effector gene induction is independent of its control over the corresponding local regulator. Together, these data indicate that induction of icl1 and gltA1 utilizes parallel feed-forward loops with an AND input function. Both feed-forward loops are affected by E , since this sigma factor is part of the gltA1 loop and controls sigB in the icl1 loop. Feed-forward loops may critically contribute to the cellular developmental program associated with M. tuberculosis dormancy.

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Critical Role of a Single Position in the −35 Element for Promoter Recognition by Mycobacterium tuberculosis SigE and SigH

Cited by 43 publications

References 16 publications

Evidence of Complex Transcriptional, Translational, and Posttranslational Regulation of the Extracytoplasmic Function Sigma Factor σ ^E in Mycobacterium tuberculosis

Evidence of Complex Transcriptional, Translational, and Posttranslational Regulation of the Extracytoplasmic Function Sigma Factor σ ^E in Mycobacterium tuberculosis

Functional Genomics Reveals Extended Roles of the Mycobacterium tuberculosis Stress Response Factor σ ^H

Regulation of Central Metabolism Genes of Mycobacterium tuberculosis by Parallel Feed-Forward Loops Controlled by Sigma Factor E (σ ^E )

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Critical Role of a Single Position in the −35 Element for Promoter Recognition by Mycobacterium tuberculosis SigE and SigH

Cited by 43 publications

References 16 publications

Evidence of Complex Transcriptional, Translational, and Posttranslational Regulation of the Extracytoplasmic Function Sigma Factor σ E in Mycobacterium tuberculosis

Evidence of Complex Transcriptional, Translational, and Posttranslational Regulation of the Extracytoplasmic Function Sigma Factor σ E in Mycobacterium tuberculosis

Functional Genomics Reveals Extended Roles of the Mycobacterium tuberculosis Stress Response Factor σ H

Regulation of Central Metabolism Genes of Mycobacterium tuberculosis by Parallel Feed-Forward Loops Controlled by Sigma Factor E (σ E )

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Evidence of Complex Transcriptional, Translational, and Posttranslational Regulation of the Extracytoplasmic Function Sigma Factor σ ^E in Mycobacterium tuberculosis

Evidence of Complex Transcriptional, Translational, and Posttranslational Regulation of the Extracytoplasmic Function Sigma Factor σ ^E in Mycobacterium tuberculosis

Functional Genomics Reveals Extended Roles of the Mycobacterium tuberculosis Stress Response Factor σ ^H

Regulation of Central Metabolism Genes of Mycobacterium tuberculosis by Parallel Feed-Forward Loops Controlled by Sigma Factor E (σ ^E )