ArticlePLoS pathogens2021
NAD+ pool depletion as a signal for the Rex regulon involved in Streptococcus agalactiae virulence.
Article in PLoS pathogens, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 16 citations in OpenAlex.
- Article
- The LiaFSR-SpxA2 regulatory axis governs bile salt resistance and virulence in Group BVirulence · 2026Article
- Structure-Informed Prioritization of Phytochemical Antistreptococcal Candidates: Integrated Molecular Docking and In Vitro Proof-of-Concept Validation AgainstCurrent issues in molecular biology · 2026Article
- Versatile NTP recognition and domain fusions expand the functional repertoire of the ParB-CTPase fold beyond chromosome segregation.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- c-di-GMP regulates bacterial NAD biosynthesis via targeting the transcriptional repressor NadR.mBio · 2025Article
- Systematic analysis of the glucose-PTS inApplied and environmental microbiology · 2025Article
- The invasive GAS puzzle in Italy: genomic insights from a hospital cohort in a fragmented surveillance landscape.Frontiers in cellular and infection microbiology · 2025Article
- Butyrate enhancesJournal of bacteriology · 2023Article
- Structural Basis of Redox-Sensing Transcriptional Repressor Rex with Cofactor NADInternational journal of molecular sciences · 2022Article
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Authors and funding
13 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In many Gram-positive bacteria, the redox-sensing transcriptional repressor Rex controls central carbon and energy metabolism by sensing the intra cellular balance between the reduced and oxidized forms of nicotinamide adenine dinucleotide; the NADH/NAD+ ratio. Here, we report high-resolution crystal structures and characterization of a Rex ortholog (Gbs1167) in the opportunistic pathogen, Streptococcus agalactiae, also known as group B streptococcus (GBS). We present structures of Rex bound to NAD+ and to a DNA operator which are the first structures of a Rex-family member from a pathogenic bacterium. The structures reveal the molecular basis of DNA binding and the conformation alterations between the free NAD+ complex and DNA-bound form of Rex. Transcriptomic analysis revealed that GBS Rex controls not only central metabolism, but also expression of the monocistronic rex gene as well as virulence gene expression. Rex enhances GBS virulence after disseminated infection in mice. Mechanistically, NAD+ stabilizes Rex as a repressor in the absence of NADH. However, GBS Rex is unique compared to Rex regulators previously characterized because of its sensing mechanism: we show that it primarily responds to NAD+ levels (or growth rate) rather than to the NADH/NAD+ ratio. These results indicate that Rex plays a key role in GBS pathogenicity by modulating virulence factor gene expression and carbon metabolism to harvest nutrients from the host.
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