ArticlePLoS genetics2026
Serine/threonine protein kinase phosphorylation of DosR alters target gene transcription mechanics and regulates Mycobacterium tuberculosis response to nitric oxide stress.
Article in PLoS genetics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
1 citing paper in PubMed.
- Multiple input-multiple output (MIMO) designs in two-component signalling systems of Mycobacterium tuberculosis.FEMS microbiology reviews · 2026Review
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
Successful host colonization by bacterial pathogens requires appropriate response and adaptation to environmental signals encountered during infection, with two-component systems (TCSs) and serine/threonine protein kinases (STPKs) being two important signal transduction mechanisms. Mycobacterium tuberculosis (Mtb) possesses similar numbers of STPKs (11) and TCSs (12), but if and how these two regulatory systems coordinate to enable Mtb adaptation in response to key environmental cues remains poorly understood. Here, we identify extensive interactions between STPKs and TCSs, with a subset of STPKs demonstrating interactions with multiple TCS response regulators. STPK phosphorylation of purified DosR, the response regulator of the key nitric oxide (NO)/hypoxia-responsive TCS DosRS(T), decreased its binding to target promoter DNA and its ability to activate steady-state gene transcription, in marked contrast with the opposite phenotypes observed with the activated, phospho-aspartic acid form of DosR. Strikingly, a ΔSTPK Mtb mutant exhibited increased DosR regulon transcription at lower NO levels than wild type Mtb, illustrating how STPK phosphorylation of a TCS RR may act to restrict and fine-tune conditions in which activation occurs. Together, our results support a functional relationship between STPKs and TCSs, and shed light on the mechanisms underpinning STPK-TCS interplay.
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Registered trials
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