Evidence map›Paper›PMID 16077122›Full record

ArticleJournal of bacteriology2005

Deletion of the Mycobacterium tuberculosis pknH gene confers a higher bacillary load during the chronic phase of infection in BALB/c mice.

K G Papavinasasundaram, Bosco Chan, Ji-Hae Chung, M Joseph Colston, Elaine O Davis, Yossef Av-Gay

Open access · greenAbstract read
In one paragraph

Article in Journal of bacteriology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed
4.7field-weighted citation impact, top 4% 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

63 citing papers in PubMed, 127 citations in OpenAlex.

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  14. Host- and Age-Dependent Transcriptional Changes inInternational journal of molecular sciences · 2022
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  20. The mycobacterial cell envelope - a moving target.Nature reviews. Microbiology · 2020
    Review

3 more citing papers are in PubMed but not listed here.

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

6 authors at 1 institution in 1 country.

K G PapavinasasundaramDepartment of Medicine, Division of Infectious Diseases, University of British Columbia, 2733 Heather St., Vancouver, B.C., Canada V5Z 3J5.
Bosco Chan
Ji-Hae Chung
M Joseph Colston
Elaine O Davis
Yossef Av-Gay
University of British Columbia · CA

Funding

Medical Research Council MC_U117532056
6 · The paper itself

Abstract

The role of the serine/threonine kinase PknH in the physiology and virulence of Mycobacterium tuberculosis was assessed by the construction of a pknH deletion mutant. Deletion of the pknH gene did not affect sensitivity to the antimycobacterial drug ethambutol, although it was previously thought to be involved in regulating expression of emb genes encoding arabinosyl transferases, the targets of ethambutol. Nevertheless, transcription analyses revealed that genes associated with mycobacterial cell wall component synthesis, such as emb and ini operons, are downstream substrates of the PknH signaling cascade. In vitro survival studies revealed that a mutant with a deletion of the pknH gene displayed increased resistance to acidified nitrite stress, suggesting that nitric oxide is one of the potential environmental triggers for PknH activation. The effect of pknH deletion on mycobacterial virulence was investigated in BALB/c mice. In this model, the DeltapknH mutant was found to survive and replicate to a higher bacillary load in mouse organs than its parental strain and the pknH-complemented strain. In contrast, another closely related kinase mutant, the DeltapknE mutant, obtained from the same parental strain, was not affected in its virulence phenotype. Infection of THP-1 cells or in vitro growth studies in 7H9 medium did not reveal a significant in vitro growth advantage phenotype for the DeltapknH mutant. In conclusion, we propose that the serine/threonine kinase PknH plays a role in regulating bacillary load in mouse organs to facilitate adaptation to the host environment, possibly by enabling a regulated chronic infection by M. tuberculosis.

Indexed as

Gene DeletionAnimalsAntitubercular AgentsBacterial ProteinsCell Line, TumorChronic DiseaseDrug Resistance, BacterialEthambutolGenotypeHumansMiceMice, Inbred BALB CMycobacterium tuberculosisNitritesOperonPhenotypeAntitubercular AgentsBacterial ProteinsEthambutolNitritesPknH protein, Mycobacterium tuberculosisProtein Serine-Threonine Kinases

Identifiers

PMID16077122
PMCPMC1196067
OpenAlexW2143724068

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.