ArticlePLoS pathogens2015
Disruption of an M. tuberculosis membrane protein causes a magnesium-dependent cell division defect and failure to persist in mice.
Article in PLoS pathogens, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 34 citations in OpenAlex.
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- Insights into the molecular determinants involved inVirulence · 2021Review
- Point mutation in the stop codon ofMicrobiology (Reading, England) · 2021Article
- HigB1 Toxin inFrontiers in microbiology · 2021Article
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- Rv0954 Is a Member of the Mycobacterial Cell Division Complex.Frontiers in microbiology · 2021Article
- Review
- The endogenous galactofuranosidase GlfH1 hydrolyzes mycobacterial arabinogalactan.The Journal of biological chemistry · 2020Article
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- Lineage-Specific Proteomic Signatures in theFrontiers in microbiology · 2020Article
- Involvement of Transcription Elongation Factor GreA inFrontiers in microbiology · 2020Article
- Development and Optimization of Chromosomally-Integrated FluorescentFrontiers in microbiology · 2020Article
- PersistenteLife · 2019Article
- Inhibition of CorA-Dependent Magnesium Homeostasis Is Cidal in Mycobacterium tuberculosis.Antimicrobial agents and chemotherapy · 2019Article
- Article
- Discovery and Structure-Activity-Relationship Study of N-Alkyl-5-hydroxypyrimidinone Carboxamides as Novel Antitubercular Agents Targeting Decaprenylphosphoryl-β-d-ribose 2'-Oxidase.Journal of medicinal chemistry · 2018Article
- Targeting Phenotypically Tolerant Mycobacterium tuberculosis.Microbiology spectrum · 2017Review
- Mycobacterium tuberculosis Thioredoxin Reductase Is Essential for Thiol Redox Homeostasis but Plays a Minor Role in Antioxidant Defense.PLoS pathogens · 2016Article
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
Abstract
The identification of Mycobacterium tuberculosis genes necessary for persistence in vivo provides insight into bacterial biology as well as host defense strategies. We show that disruption of M. tuberculosis membrane protein PerM (Rv0955) resulted in an IFN-γ-dependent persistence defect in chronic mouse infection despite the mutant's near normal growth during acute infection. The perM mutant required increased magnesium for replication and survival; incubation in low magnesium media resulted in cell elongation and lysis. Transcriptome analysis of the perM mutant grown in reduced magnesium revealed upregulation of cell division and cell wall biosynthesis genes, and live cell imaging showed PerM accumulation at the division septa in M. smegmatis. The mutant was acutely sensitive to β-lactam antibiotics, including specific inhibitors of cell division-associated peptidoglycan transpeptidase FtsI. Together, these data implicate PerM as a novel player in mycobacterial cell division and pathogenesis, and are consistent with the hypothesis that immune activation deprives M. tuberculosis of magnesium.
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