ArticleMolecular microbiology2017
Suppression and synthetic-lethal genetic relationships of ΔgpsB mutations indicate that GpsB mediates protein phosphorylation and penicillin-binding protein interactions in Streptococcus pneumoniae D39.
Article in Molecular microbiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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47 citing papers in PubMed, 82 citations in OpenAlex.
- Pneumococcal S protein coordinates cell wall modification and repair to resist host antimicrobials.Nature microbiology · 2026Article
- Streptococcus pneumoniae S protein activates PBP1a to regulate peptidoglycan remodelling and cell division.Nature microbiology · 2026Article
- Article
- tRNA Modification Landscapes in Streptococci: Shared Losses and Clade-Specific Adaptations.bioRxiv : the preprint server for biology · 2025Article
- EzrA promotes Z-ring formation through interaction of its QNR motif with FtsA.Journal of bacteriology · 2025Article
- Glycosylation of serine/threonine-rich intrinsically disordered regions of membrane-associated proteins in streptococci.Nature communications · 2025Article
- GpsB interacts with FtsZ in multiple species and may serve as an accessory Z-ring anchor.Molecular biology of the cell · 2025Article
- GpsB Coordinates StkP Signaling as a PASTA Kinase Adaptor in Streptococcus pneumoniae Cell Division.Journal of molecular biology · 2024Article
- Signal recognition particle RNA is critical for genetic competence and virulence ofJournal of bacteriology · 2024Article
- Dynamic Protein Phosphorylation inMicroorganisms · 2024Article
- Multisite Phosphorylation Regulates GpsB Function in Cephalosporin Resistance of Enterococcus faecalis.Journal of molecular biology · 2023Article
- Negative regulation of MurZ and MurA underlies the essentiality of GpsB- and StkP-mediated protein phosphorylation in Streptococcus pneumoniae D39.Molecular microbiology · 2023Article
- Mslar: Microbial synthetic lethal and rescue database.PLoS computational biology · 2023Review
- The roles of GpsB and DivIVA inFrontiers in microbiology · 2023Article
- A multiomics analysis of direct interkingdom dynamics between influenza A virus and Streptococcus pneumoniae uncovers host-independent changes to bacterial virulence fitness.PLoS pathogens · 2022Article
- GpsB Promotes PASTA Kinase Signaling and Cephalosporin Resistance inJournal of bacteriology · 2022Article
- Roles of RodZ and class A PBP1b in the assembly and regulation of the peripheral peptidoglycan elongasome in ovoid-shaped cells of Streptococcus pneumoniae D39.Molecular microbiology · 2022Article
- Regulatory cross-talk supports resistance to Zn intoxication in Streptococcus.PLoS pathogens · 2022Article
- GpsB Coordinates Cell Division and Cell Surface Decoration by Wall Teichoic Acids in Staphylococcus aureus.Microbiology spectrum · 2022Article
- Amoxicillin-resistanteLife · 2022Article
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14 authors at 3 institutions in 4 countries.
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Abstract
GpsB regulatory protein and StkP protein kinase have been proposed as molecular switches that balance septal and peripheral (side-wall like) peptidoglycan (PG) synthesis in Streptococcus pneumoniae (pneumococcus); yet, mechanisms of this switching remain unknown. We report that ΔdivIVA mutations are not epistatic to ΔgpsB division-protein mutations in progenitor D39 and related genetic backgrounds; nor is GpsB required for StkP localization or FDAA labeling at septal division rings. However, we confirm that reduction of GpsB amount leads to decreased protein phosphorylation by StkP and report that the essentiality of ΔgpsB mutations is suppressed by inactivation of PhpP protein phosphatase, which concomitantly restores protein phosphorylation levels. ΔgpsB mutations are also suppressed by other classes of mutations, including one that eliminates protein phosphorylation and may alter division. Moreover, ΔgpsB mutations are synthetically lethal with Δpbp1a, but not Δpbp2a or Δpbp1b mutations, suggesting GpsB activation of PBP2a activity. Consistent with this result, co-IP experiments showed that GpsB complexes with EzrA, StkP, PBP2a, PBP2b and MreC in pneumococcal cells. Furthermore, depletion of GpsB prevents PBP2x migration to septal centers. These results support a model in which GpsB negatively regulates peripheral PG synthesis by PBP2b and positively regulates septal ring closure through its interactions with StkP-PBP2x.
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