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 Gene Profiles


  RV1473A is profiled in 4 experiments

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Characterization of a Clp protease gene regulator and the reaeration response in Mycobacterium tuberculosis.

Sherrid AM, et al. (2010) PLoS One 5(7):e11622

The mechanism by which mycobacteria return to a replicating state upon re-exposure to favorable conditions is not well understood. In this study, we utilized reaeration from a defined hypoxia model to characterize the adaptive response of Mycobacterium tuberculosis (MTB) following a return to favorable growth conditions. Global transcriptional analysis identified the ~100 gene Reaeration Response, induced relative ... Expand to both log-phase and hypoxic MTB. This response includes chaperones and proteases, as well as the transcription factor Rv2745c, a Clp protease gene regulator (ClgR) orthologue. During reaeration, genes repressed during hypoxia are also upregulated in a wave of transcription that includes genes crucial to transcription, translation and oxidative phosphorylation.

Each reaerating culture compared at multiple timepoints to a sample from the same culture at seven days of hypoxia. Three or more replicates at each timepoint. Hide text

View RV1473A gene profile across 32 experiments

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The enduring hypoxic response of Mycobacterium tuberculosis.

Rustad TR, et al. (2008) PLoS ONE 3(1):e1502

Background A significant body of evidence accumulated over the last century suggests a link between hypoxic microenvironments within the infected host and the latent phase of tuberculosis. Studies to test this correlation have identified the M. tuberculosis initial hypoxic response, controlled by the two-component response regulator DosR. The initial hypoxic response is completely blocked in a dosR deletion mutant. ... Expand Methodology/Principal Findings We show here that a dosR deletion mutant enters bacteriostasis in response to in vitro hypoxia with only a relatively mild decrease in viability. In the murine infection model, the phenotype of the mutant was indistinguishable from that of the parent strain. These results suggested that additional genes may be essential for entry into and maintenance of bacteriostasis. Detailed microarray analysis of oxygen starved cultures revealed that DosR regulon induction is transient, with induction of nearly half the genes returning to baseline within 24 hours. In addition, a larger, sustained wave of gene expression follows the DosR-mediated initial hypoxic response. This Enduring Hypoxic Response (EHR) consists of 230 genes significantly induced at four and seven days of hypoxia but not at initial time points. These genes include a surprising number of transcriptional regulators that could control the program of bacteriostasis. We found that the EHR is independent of the DosR-mediated initial hypoxic response, as EHR expression is virtually unaltered in the dosR mutant. Conclusions/Significance Our results suggest a reassessment of the role of DosR and the initial hypoxic response in MTB physiology. Instead of a primary role in survival of hypoxia induced bacteriostasis, DosR may regulate a response that is largely optional in vitro and in mouse infections. Analysis of the EHR should help elucidate the key regulatory factors and enzymatic machinery exploited by M. tuberculosis for long-term bacteriostasis in the face of oxygen deprivation. Hide text

View RV1473A gene profile across 35 experiments

Download gene expression data in PCL format


The enduring hypoxic response of Mycobacterium tuberculosis.

Rustad TR, et al. (2008) PLoS ONE 3(1):e1502

Background A significant body of evidence accumulated over the last century suggests a link between hypoxic microenvironments within the infected host and the latent phase of tuberculosis. Studies to test this correlation have identified the M. tuberculosis initial hypoxic response, controlled by the two-component response regulator DosR. The initial hypoxic response is completely blocked in a dosR deletion mutant. ... Expand Methodology/Principal Findings We show here that a dosR deletion mutant enters bacteriostasis in response to in vitro hypoxia with only a relatively mild decrease in viability. In the murine infection model, the phenotype of the mutant was indistinguishable from that of the parent strain. These results suggested that additional genes may be essential for entry into and maintenance of bacteriostasis. Detailed microarray analysis of oxygen starved cultures revealed that DosR regulon induction is transient, with induction of nearly half the genes returning to baseline within 24 hours. In addition, a larger, sustained wave of gene expression follows the DosR-mediated initial hypoxic response. This Enduring Hypoxic Response (EHR) consists of 230 genes significantly induced at four and seven days of hypoxia but not at initial time points. These genes include a surprising number of transcriptional regulators that could control the program of bacteriostasis. We found that the EHR is independent of the DosR-mediated initial hypoxic response, as EHR expression is virtually unaltered in the dosR mutant. Conclusions/Significance Our results suggest a reassessment of the role of DosR and the initial hypoxic response in MTB physiology. Instead of a primary role in survival of hypoxia induced bacteriostasis, DosR may regulate a response that is largely optional in vitro and in mouse infections. Analysis of the EHR should help elucidate the key regulatory factors and enzymatic machinery exploited by M. tuberculosis for long-term bacteriostasis in the face of oxygen deprivation. Hide text

View RV1473A gene profile across 17 experiments

Download gene expression data in PCL format


PepD participates in the mycobacterial stress response mediated through MprAB and SigE.

White MJ, et al. (2010) J Bacteriol 192(6):1498-510

The researchers compare total RNA from early log growth cultures of both wild type and PepD null mutant strain using microarray analysis to understand transcriptional profiles in a PepD null mutant ... Expand strain. Hide text

View RV1473A gene profile across 5 experiments

Download gene expression data in PCL format