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Omics · study · 2026

Cell Membrane Maintenance by PhoP is Critical for Methyylglyoxal Resistance in Mycobacterium tuberculosis

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The human pathogen Mycobacterium tuberculosis primarily infects macrophages.

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Upon activation by IFNγ, infected macrophages produce higher levels of methylglyoxal, a toxic aldehyde. Mycobacterium tuberculosis defense mechanisms against aldehydes have not been elucidated.

A transposon mutagenesis screen identified 22 loci required for resistance to methylglyoxal, one of which was phoP. The attenuated phoP mutant was even more attenuated in mice that accumulate MG. Secondary mutations in the fatty acid β-oxidation genes fadE25 or fixB restored methylglyoxal resistance to a phoP mutant by restoring the membrane barrier that is compromised in a phoP mutant.

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Analysis of transcriptional responses to methylglyoxal suggests that phoP mutants are unable to appropriately respond to methylglyoxal-induced stress. Together, our data suggest that the major virulence factor PhoP is essential for Mycobacterium tuberculosis resistance to methylglyoxal toxicity in vivo.

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Life Sciences
Provenance · 1 source records, 6 field assertions
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NCBI GEOGSE29770414 d agoJSON v1
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access_levelsource · NCBI GEOconnector:ncbi_geo@1.0.0
concepts[field].local:field:life-sciencesmapping · NCBI GEOconnector:ncbi_geo@1.0.0
concepts[method].geo_series_type:expression-profiling-by-high-throughput-sequencingsource · NCBI GEOconnector:ncbi_geo@1.0.0/gdstype
descriptionsource · NCBI GEOconnector:ncbi_geo@1.0.0/summary
publication_datesource · NCBI GEOconnector:ncbi_geo@1.0.0
titlesource · NCBI GEOconnector:ncbi_geo@1.0.0/title