6gqa
From Proteopedia
Cell division regulator S. pneumoniae GpsB
Structural highlights
Function[GPSB_STRR6] Divisome component that associates with the complex late in its assembly, after the Z-ring is formed, and is dependent on DivIC and PBP2B for its recruitment to the divisome. Together with EzrA, is a key component of the system that regulates PBP1 localization during cell cycle progression. Its main role could be the removal of PBP1 from the cell pole after pole maturation is completed. Also contributes to the recruitment of PBP1 to the division complex. Not essential for septum formation.[HAMAP-Rule:MF_02011] Publication Abstract from PubMedBacterial growth and cell division requires precise spatiotemporal regulation of the synthesis and remodelling of the peptidoglycan layer that surrounds the cytoplasmic membrane. GpsB is a cytosolic protein that affects cell wall synthesis by binding cytoplasmic mini-domains of peptidoglycan synthases to ensure their correct subcellular localisation. Here, we describe critical structural features for the interaction of GpsB with peptidoglycan synthases from three bacterial species (Bacillus subtilis, Listeria monocytogenes and Streptococcus pneumoniae) and suggest their importance for cell wall growth and viability in L. monocytogenes and S. pneumoniae. We use these structural motifs to identify novel partners of GpsB in B. subtilis and extend the members of the GpsB interactome in all three bacterial species. Our results support that GpsB functions as an adaptor protein that mediates the interaction between membrane proteins, scaffolding proteins, signalling proteins and enzymes to generate larger protein complexes at specific sites in a bacterial cell cycle-dependent manner. The cell cycle regulator GpsB functions as cytosolic adaptor for multiple cell wall enzymes.,Cleverley RM, Rutter ZJ, Rismondo J, Corona F, Tsui HT, Alatawi FA, Daniel RA, Halbedel S, Massidda O, Winkler ME, Lewis RJ Nat Commun. 2019 Jan 16;10(1):261. doi: 10.1038/s41467-018-08056-2. PMID:30651563[1] From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine. References
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