Evidence map›Paper›PMID 20061478›Full record

ArticleJournal of bacteriology2010

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

Mark J White, Hongjun He, Renee M Penoske, Sally S Twining, Thomas C Zahrt

Abstract read
In one paragraph

Article in Journal of bacteriology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
2.1field-weighted citation impact, top 13% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

35 citing papers in PubMed, 60 citations in OpenAlex.

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  13. Physiological and Transcriptional Responses ofFrontiers in microbiology · 2020
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Mark J WhiteDepartment of Microbiology and Molecular Genetics and Center for Biopreparedness and Infectious Diseases, Medical College of Wisconsin, 8701 Watertown Plank Road, Milwaukee, Wisconsin 53226-0509, USA.
Hongjun He
Renee M Penoske
Sally S Twining
Thomas C Zahrt
Medical College of Wisconsin · US

Funding

M.tuberculosis Genes Regulating Persistent InfectionR01AI051669 · NIAID · MEDICAL COLLEGE OF WISCONSIN · PI ZAHRT, THOMAS C. · 2001 to 2011
$3.5M
Proteases in the CorneaR01EY012731 · NEI · MEDICAL COLLEGE OF WISCONSIN · PI TWINING, SALLY S. · 1999 to 2011
$2.1M
NEI NIH HHS R01 EY012731NIAID NIH HHS R01 AI051669NIAID NIH HHS R01 AI51669
6 · The paper itself

Abstract

Currently, one-third of the world's population is believed to be latently infected with Mycobacterium tuberculosis. The mechanisms by which M. tuberculosis establishes latent infection remain largely undefined. mprAB encodes a two-component signal transduction system required by M. tuberculosis for aspects of persistent infection. MprAB regulates a large and diverse group of genetic determinants in response to membrane stress, including the extracytoplasmic function (ECF) sigma factor sigE and the HtrA-like serine protease pepD. Recent studies have demonstrated that PepD functions as both a protease and chaperone in vitro. In addition, inactivation of pepD alters the virulence of M. tuberculosis in a mouse model system of infection. Here, we demonstrate that PepD plays an important role in the stress response network of Mycobacterium mediated through MprAB and SigE. In particular, we demonstrate that the protease activity of PepD requires the PDZ domain, in addition to the catalytic serine at position 317. pepD expression initiates from at least three promoters in M. tuberculosis, including one that is regulated by SigE and is located upstream of the mprA coding sequence. Deletion of pepD or mprAB in Mycobacterium smegmatis and M. tuberculosis alters the stress response phenotypes of these strains, including increasing sensitivity to SDS and cell wall antibiotics and upregulating the expression of stress-responsive determinants, including sigE. Taking these data together, we hypothesize that PepD utilizes its PDZ domain to recognize and process misfolded proteins at the cell membrane, leading to activation of the MprAB and SigE signaling pathways and subsequent establishment of a positive feedback loop that facilitates bacterial adaptation.

Indexed as

AnimalsBacterial ProteinsGene Expression ProfilingGene Expression Regulation, BacterialMycobacterium tuberculosisOligonucleotide Array Sequence AnalysisPromoter Regions, GeneticSignal TransductionStress, PhysiologicalTranscription, GeneticBacterial Proteins

Identifiers

PMID20061478
PMCPMC2832534
OpenAlexW2171702377

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.