Evidence map›Paper›PMID 24603869›Full record

ArticlePLoS pathogens2014

Post-translational regulation via Clp protease is critical for survival of Mycobacterium tuberculosis.

Ravikiran M Raju, Mark P Jedrychowski, Jun-Rong Wei, Jessica T Pinkham, Annie S Park, Kathryn O'Brien, German Rehren, Dirk Schnappinger, Steven P Gygi, Eric J Rubin

Abstract read
In one paragraph

Article in PLoS pathogens, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
–field-weighted citation impact
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

48 citing papers in PubMed.

  1. Article
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  5. Article
  6. Article
  7. Article
  8. Review
  9. WhiB-like proteins: Diversity of structure, function and mechanism.Biochimica et biophysica acta. Molecular cell research · 2024
    Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. The essentialScience advances · 2022
    Article
  16. Article
  17. Review
  18. Review
  19. Article
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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

10 authors.

Ravikiran M RajuDepartment of Immunology and Infectious Diseases, Harvard School of Public Health, Boston, Massachusetts, United States of America.
Mark P JedrychowskiDepartment of Cell Biology, Harvard Medical School, Boston, Massachusetts, United States of America.
Jun-Rong WeiDepartment of Immunology and Infectious Diseases, Harvard School of Public Health, Boston, Massachusetts, United States of America.
Jessica T PinkhamDepartment of Immunology and Infectious Diseases, Harvard School of Public Health, Boston, Massachusetts, United States of America.
Annie S ParkDepartment of Immunology and Infectious Diseases, Harvard School of Public Health, Boston, Massachusetts, United States of America.
Kathryn O'BrienDepartment of Microbiology and Immunology, Weill Cornell Medical College, New York, New York, United States of America.
German RehrenDepartment of Microbiology and Immunology, Weill Cornell Medical College, New York, New York, United States of America.
Dirk SchnappingerDepartment of Microbiology and Immunology, Weill Cornell Medical College, New York, New York, United States of America.
Steven P GygiDepartment of Cell Biology, Harvard Medical School, Boston, Massachusetts, United States of America.
Eric J RubinDepartment of Immunology and Infectious Diseases, Harvard School of Public Health, Boston, Massachusetts, United States of America.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Unlike most bacterial species, Mycobacterium tuberculosis depends on the Clp proteolysis system for survival even in in vitro conditions. We hypothesized that Clp is required for the physiologic turnover of mycobacterial proteins whose accumulation is deleterious to bacterial growth and survival. To identify cellular substrates, we employed quantitative proteomics and transcriptomics to identify the set of proteins that accumulated upon the loss of functional Clp protease. Among the set of potential Clp substrates uncovered, we were able to unambiguously identify WhiB1, an essential transcriptional repressor capable of auto-repression, as a substrate of the mycobacterial Clp protease. Dysregulation of WhiB1 turnover had a toxic effect that was not rescued by repression of whiB1 transcription. Thus, under normal growth conditions, Clp protease is the predominant regulatory check on the levels of potentially toxic cellular proteins. Our findings add to the growing evidence of how post-translational regulation plays a critical role in the regulation of bacterial physiology.

Indexed as

Bacterial ProteinsEndopeptidase ClpMycobacterium tuberculosisPolymerase Chain ReactionProtein Processing, Post-TranslationalProteolysisProteomicsTranscription FactorsBacterial ProteinsEndopeptidase ClpTranscription FactorsWhiB1 protein, Mycobacterium tuberculosis

Identifiers

PMID24603869
PMCPMC3946367

What OpenQuestion holds

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Registered trials

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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.