ArticleNature communications2023
Sequestration of histidine kinases by non-cognate response regulators establishes a threshold level of stimulation for bacterial two-component signaling.
Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 18 citations in OpenAlex.
- Intratumoral Mycobacterium abscessus promotes cytidine deaminase mutagenesis in non-small cell lung cancer.Signal transduction and targeted therapy · 2026Article
- Tamoxifen inhibits histidine kinases ofMicrobiology spectrum · 2026Article
- Multiple input-multiple output (MIMO) designs in two-component signalling systems of Mycobacterium tuberculosis.FEMS microbiology reviews · 2026Review
- The BaeS/BaeR two-component system enhancesFrontiers in cellular and infection microbiology · 2026Article
- Untangling the Complexity of Two-Component Signal Transduction in Bacteria.Microorganisms · 2025Review
- Mycobacterial MutT1-mediated dephosphorylation of the sensor histidine kinases reveals a new link in the regulation of the two-component signaling.Nucleic acids research · 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
- An Evolutionary Paradigm Favoring Cross Talk between Bacterial Two-Component Signaling Systems.mSystems · 2022Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Bacterial two-component systems (TCSs) consist of a sensor histidine kinase (HK) that perceives a specific signal, and a cognate response regulator (RR) that modulates the expression of target genes. Positive autoregulation improves TCS sensitivity to stimuli, but may trigger disproportionately large responses to weak signals, compromising bacterial fitness. Here, we combine experiments and mathematical modelling to reveal a general design that prevents such disproportionate responses: phosphorylated HKs (HK~Ps) can be sequestered by non-cognate RRs. We study five TCSs of Mycobacterium tuberculosis and find, for all of them, non-cognate RRs that show higher affinity than cognate RRs for HK~Ps. Indeed, in vitro assays show that HK~Ps preferentially bind higher affinity non-cognate RRs and get sequestered. Mathematical modelling indicates that this sequestration would introduce a 'threshold' stimulus strength for eliciting responses, thereby preventing responses to weak signals. Finally, we construct tunable expression systems in Mycobacterium bovis BCG to show that higher affinity non-cognate RRs suppress responses in vivo.
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