ArticleNature communications2024
Lsr2 acts as a cyclic di-GMP receptor that promotes keto-mycolic acid synthesis and biofilm formation in mycobacteria.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 34 citations in OpenAlex.
- Cyclic di-GMP directly reprograms the multidrug resistance machinery via UspG-mediated sequestration of RamR in Klebsiella.PLoS pathogens · 2026Article
- The Cyclic Di-GMP Receptor HpoR Modulates Mycobacterial Multidrug Susceptibility by Regulating IniBAC-Mediated Envelope Permeability.Microorganisms · 2026Article
- Article
- Actinobacteria TFDB: An integrated view of transcription factors in Actinobacteria.Engineering microbiology · 2026Article
- Orn-mediated c-di-GMP regulates the CRISPR-Cas system to confer stress response in Mycobacterium tuberculosis.Nucleic acids research · 2026Article
- The virulence regulator Rv3425 mediates stress adaptation and promotes intracellular survival of Mycobacterium tuberculosis avirulent strain.Archives of microbiology · 2026Article
- Molecular Kaleidoscope of Nucleoid-Associated Proteins Regulatory Network and Chromosome Architecture in Mycobacterium Tuberculosis.Current microbiology · 2026Review
- Exploring the evolutionary divergence of cyclic di-nucleotide signaling in diverse mycobacterial species.Archives of microbiology · 2026Article
- Intracellular glutamine fluctuates with nitrogen availability and regulatesJournal of bacteriology · 2025Article
- Cyclic-di-GMP interferes with DNA-MucR-DNA bridging to derepress genes targeted by the xenogeneic silencer MucR.Nucleic acids research · 2025Article
- c-di-GMP regulates bacterial NAD biosynthesis via targeting the transcriptional repressor NadR.mBio · 2025Article
- Cold Shock Proteins Balance Biofilm-Associated Antibiotic Resistance and Oxidative Vulnerability in Mycobacteria.Microorganisms · 2025Article
- c-di-GMP does not bind H-NS, nor inhibits H-NS binding DNA.Nature communications · 2025Article
- Reply to: "c-di-GMP does not bind H-NS, nor inhibits H-NS binding DNA".Nature communications · 2025Article
- NapR Regulates the Expression of Phosphoserine Aminotransferase SerC to Modulate Biofilm Formation and Resistance to Serine Stress of Mycobacteria.International journal of molecular sciences · 2025Article
- Crosstalk between cyclic-di-guanosine monophosphate and the sensor kinase MtrB regulates MtrA-dependent genes, bacterial growth, biofilm formation and lysosomal trafficking ofMicrobiology (Reading, England) · 2025Article
- Post-translational modifications of the nucleoid protein H-NS: sites, mechanisms, and regulatory cues.FEMS microbiology reviews · 2025Review
- Deciphering tuberculosis: lysosome-centric insights into pathogenesis and therapies.Frontiers in cellular and infection microbiology · 2025Review
- Mycobacterial Biofilm: Mechanisms, Clinical Problems, and Treatments.International journal of molecular sciences · 2024Review
- HadBD dehydratase from Mycobacterium tuberculosis fatty acid synthase type II: A singular structure for a unique function.Protein science : a publication of the Protein Society · 2024Article
Corrections and comments
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cyclic di-GMP (c-di-GMP) is a second messenger that promotes biofilm formation in several bacterial species, but the mechanisms are often unclear. Here, we report that c-di-GMP promotes biofilm formation in mycobacteria in a manner dependent on the nucleoid-associated protein Lsr2. We show that c-di-GMP specifically binds to Lsr2 at a ratio of 1:1. Lsr2 upregulates the expression of HadD, a (3R)-hydroxyacyl-ACP dehydratase, thus promoting the synthesis of keto-mycolic acid and biofilm formation. Thus, Lsr2 acts as a c-di-GMP receptor that links the second messenger's function to lipid synthesis and biofilm formation in mycobacteria.
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Registered trials
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.