Evidence map›Paper›PMID 21592957›Full record

ArticleThe Journal of biological chemistry2011

Inactivation of tesA reduces cell wall lipid production and increases drug susceptibility in mycobacteria.

Sivagami Sundaram Chavadi, Uthamaphani R Edupuganti, Olivia Vergnolle, Itrat Fatima, Shaneen M Singh, Clifford E Soll, Luis E N Quadri

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.6field-weighted citation impact, top 11% 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

28 citing papers in PubMed, 58 citations in OpenAlex.

  1. Article
  2. Article
  3. Drug resistantbioRxiv : the preprint server for biology · 2024
    Article
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  5. Article
  6. Drug-resistant strains ofFrontiers in cellular and infection microbiology · 2023
    Review
  7. Pathogens (Basel, Switzerland) · 2022
    Article
  8. Article
  9. Article
  10. Mycobacterial fatty acid catabolism is repressed by FdmR to sustain lipogenesis and virulence.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  11. Evolution of Drug-ResistantFrontiers in microbiology · 2021
    Review
  12. Article
  13. Article
  14. Article
  15. Underestimated Manipulative Roles ofFrontiers in immunology · 2019
    Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
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

7 authors at 3 institutions in 1 country.

Sivagami Sundaram ChavadiBiology Department, Brooklyn College (City University of New York), Brooklyn, New York 11210, USA.
Uthamaphani R Edupuganti
Olivia Vergnolle
Itrat Fatima
Shaneen M Singh
Clifford E Soll
Luis E N Quadri
City University of New York · USBrooklyn College · USHunter College · US

Funding

Mycobacterial PDIM/PGL: synthesis pathway and inhibitionR01AI069209 · NIAID · WEILL MEDICAL COLL OF CORNELL UNIV · PI QUADRI, LUIS E · 2006 to 2010
$1.6M
MALDI-TOF MASS SPECT SYST: GENOMIC SCREENING OF KAMPOS10RR022649 · NCRR · HUNTER COLLEGE · PI SOLL, CLIFF · 2005 to 2005
$409k
NCRR NIH HHS S10 RR022649NIAID NIH HHS R01 AI069209NIAID NIH HHS R01AI069209
6 · The paper itself

Abstract

Phthiocerol dimycocerosates (PDIMs) and phenolic glycolipids (PGLs) are structurally related lipids noncovalently bound to the outer cell wall layer of Mycobacterium tuberculosis, Mycobacterium leprae, and several opportunistic mycobacterial human pathogens. PDIMs and PGLs are important effectors of virulence. Elucidation of the biosynthesis of these complex lipids will not only expand our understanding of mycobacterial cell wall biosynthesis, but it may also illuminate potential routes to novel therapeutics against mycobacterial infections. We report the construction of an in-frame deletion mutant of tesA (encoding a type II thioesterase) in the opportunistic human pathogen Mycobacterium marinum and the characterization of this mutant and its corresponding complemented strain control in terms of PDIM and PGL production. The growth and antibiotic susceptibility of these strains were also probed and compared with the parental wild-type strain. We show that deletion of tesA leads to a mutant that produces only traces of PDIMs and PGLs, has a slight growth yield increase and displays a substantial hypersusceptibility to several antibiotics. We also provide a robust model for the three-dimensional structure of M. marinum TesA (TesAmm) and demonstrate that a Ser-to-Ala substitution in the predicted catalytic Ser of TesAmm renders a mutant that recapitulates the phenotype of the tesA deletion mutant. Overall, our studies demonstrate a critical role for tesA in mycobacterial biology, advance our understanding of the biosynthesis of an important group of polyketide synthase-derived mycobacterial lipids, and suggest that drugs aimed at blocking PDIM and/or PGL production might synergize with antibiotic therapy in the control of mycobacterial infections.

Indexed as

Anti-Bacterial AgentsCell WallDrug DesignDrug Resistance, BacterialFatty Acid SynthasesGene DeletionGlycolipidsHumansLipidsMycobacteriumMycobacterium InfectionsThiolester HydrolasesAnti-Bacterial AgentsFatty Acid SynthasesGlycolipidsLipidsphthiocerol dimycocerosatethioesterase IIThiolester Hydrolases

Identifiers

PMID21592957
PMCPMC3137037
OpenAlexW2088587521

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.