GlmR (PA5550) is a DeoR-family transcriptional repressor of Pseudomonas aeruginosa, with an N-terminal DeoR-type helix-turn-helix DNA-binding domain and a C-terminal DeoR sensor domain of the NagB/RpiA fold that in related regulators binds a sugar-phosphate effector. The gene lies between the glmS and glmU homologues, and GlmR represses transcription of the adjacent glmS (glucosamine-6-phosphate synthase), which supplies precursors for peptidoglycan and lipopolysaccharide. A glmR transposon mutant is hypersusceptible to many antibiotics and shows filamentous cells, loss of motility and reduced stress tolerance. Its effector ligand is unknown.
| GO Term | Evidence | Action | Reason |
|---|---|---|---|
| GO:0000987 cis-regulatory region sequence-specific DNA binding | IBA GO_REF:0000033 | ACCEPT | Summary: IBA from PTN000769142, seeded by E. coli DeoR and GlpR. Reason: Operator binding is the conserved mechanism of DeoR-family repressors, and GlmR carries the DeoR HTH domain and represses glmS transcription. Supporting Evidence: PMID:14982774 We showed that GlmR represses the transcription of the adjacent glmS homologue (PA5549) in P. aeruginosa, possibly affecting the pool of precursors for peptidoglycan and LPS synthesis. |
| GO:0003677 DNA binding | IEA GO_REF:0000104 | TOO GENERAL | Summary: Generic DNA binding from UniRule. Reason: Entailed by GO:0000987 cis-regulatory region sequence-specific DNA binding (is_a GO:0003677), accepted above. |
| GO:0003700 DNA-binding transcription factor activity | IEA GO_REF:0000002 | TOO GENERAL | Summary: InterPro2GO from the DeoR HTH signatures. Reason: Entailed by GO:0098531 ligand-modulated transcription factor activity (is_a GO:0003700), accepted below. |
| GO:0006351 DNA-templated transcription | IEA GO_REF:0000104 | MODIFY | Summary: UniRule transcription term for a transcription factor. Reason: A repressor regulates transcription rather than carrying it out; the supported process is negative regulation of DNA-templated transcription. Proposed replacements: negative regulation of DNA-templated transcription |
| GO:0006355 regulation of DNA-templated transcription | IBA GO_REF:0000033 | TOO GENERAL | Summary: IBA from PTN000769142, seeded by seven DeoR-family regulators (E. coli GlpR and SrlR IDA, DeoR, AgaR, YciT and L. lactis LacR IMP, CsqR IEP) and the PseudoCAP IMP on Q9HT24 itself (expected, not circular). The IBD stands without this seed. Reason: Correct, but entailed by GO:0045892 negative regulation of DNA-templated transcription, accepted below. |
| GO:0006355 regulation of DNA-templated transcription | IEA GO_REF:0000120 | TOO GENERAL | Summary: Combined IEA. Reason: Entailed by GO:0045892, accepted below; consistent with the IBA row. |
| GO:0032885 regulation of polysaccharide biosynthetic process | IMP PMID:14982774 Selection of an antibiotic-hypersusceptible mutant of Pseudo... | MARK AS OVER ANNOTATED | Summary: PseudoCAP row from the glmR mutant study. The abstract reports glmS repression and says it is "possibly" affecting peptidoglycan and LPS precursor pools; it reports no measurement of polysaccharide synthesis. Reason: GlmR's demonstrated action is repression of glmS transcription. An effect on polysaccharide biosynthesis is an inference about downstream metabolism that the abstract states only as a possibility. Full text not read. Supporting Evidence: PMID:14982774 We showed that GlmR represses the transcription of the adjacent glmS homologue (PA5549) in P. aeruginosa, possibly affecting the pool of precursors for peptidoglycan and LPS synthesis. |
| GO:0045724 positive regulation of cilium assembly | IMP PMID:14982774 Selection of an antibiotic-hypersusceptible mutant of Pseudo... | REMOVE | Summary: PseudoCAP row. A cilium is a eukaryotic organelle by GO definition, so the term cannot apply to a bacterium. The observation behind it is loss of motility in a pleiotropic glmR mutant. Reason: Taxonomically impossible term; a bacterial-flagellum term would also be an indirect phenotype, since no flagellar target of GlmR is reported. Supporting Evidence: PMID:14982774 The drug supersusceptibility of 19A was accompanied by loss of motility, reduced resistance to osmotic and heat shock stress, and impaired growth at low temperatures. |
| GO:0045892 negative regulation of DNA-templated transcription | IMP PMID:14982774 Selection of an antibiotic-hypersusceptible mutant of Pseudo... | ACCEPT | Summary: PseudoCAP seed row. The abstract states GlmR represses transcription of the adjacent glmS homologue. Seed verdict SOUND; this descendant term supports the PTN000769142 node term. Reason: Direct finding of the paper, consistent with a DeoR-family repressor. Supporting Evidence: PMID:14982774 We showed that GlmR represses the transcription of the adjacent glmS homologue (PA5549) in P. aeruginosa, possibly affecting the pool of precursors for peptidoglycan and LPS synthesis. |
| GO:0098531 ligand-modulated transcription factor activity | IBA GO_REF:0000033 | ACCEPT | Summary: IBA from PTN000769142, seeded by E. coli FucR. Reason: DeoR-family regulators sense sugar-phosphate effectors through the C-terminal DeoRC domain, which GlmR has. The GlmR effector is unknown, so the term describes the family mechanism rather than a measured ligand. |
| GO:2000147 positive regulation of cell motility | IMP PMID:14982774 Selection of an antibiotic-hypersusceptible mutant of Pseudo... | REMOVE | Summary: PseudoCAP row. The abstract reports loss of motility together with filamentous cells, stress sensitivity and cold-sensitive growth, a pleiotropic envelope phenotype. Reason: Indirect phenotype of a pleiotropic mutant; GlmR's only reported target is glmS, and no regulation of motility genes is described in the abstract. Supporting Evidence: PMID:14982774 Light microscopy of the mutant strain revealed abnormal morphology characterized by large, filamentous cells. |
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Download this section (compressed HTML)Q: What effector does the GlmR DeoRC domain bind (for example glucosamine-6-phosphate or another amino-sugar phosphate), and does it relieve repression of glmS?
Q: Are the antibiotic hypersusceptibility and filamentation of the glmR mutant caused by glmS overexpression, or by other GlmR targets?
Experiment: Map the GlmR operator in the glmS promoter by EMSA and footprinting, and screen amino-sugar phosphates for release of GlmR from DNA.
Experiment: Test whether deleting or down-regulating glmS in the glmR mutant restores antibiotic resistance, cell shape and motility.
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