PcdA promotes orthogonal division plane selection in Staphylococcus aureus.


Journal

Nature microbiology
ISSN: 2058-5276
Titre abrégé: Nat Microbiol
Pays: England
ID NLM: 101674869

Informations de publication

Date de publication:
28 Oct 2024
Historique:
received: 17 10 2023
accepted: 30 08 2024
medline: 29 10 2024
pubmed: 29 10 2024
entrez: 29 10 2024
Statut: aheadofprint

Résumé

The bacterial pathogen, Staphylococcus aureus, grows by dividing in two alternating orthogonal planes. How these cell division planes are positioned correctly is not known. Here we used chemical genetic screening to identify PcdA as a division plane placement factor. Molecular biology and imaging approaches revealed non-orthogonal division plane selection for pcdA mutant bacteria. PcdA is a structurally and functionally altered member of the McrB AAA+ NTPase family, which are often found as restriction enzyme subunits. PcdA interacts with the tubulin-like divisome component, FtsZ, and the structural protein, DivIVA; it also localizes to future cell division sites. PcdA multimerization, localization and function are NTPase activity-dependent. We propose that the DivIVA/PcdA complex recruits unpolymerized FtsZ to assemble along the proper cell division plane. Although pcdA deletion did not affect S. aureus growth in several laboratory conditions, its clustered growth pattern was disrupted, sensitivity to cell-wall-targeting antibiotics increased and virulence in mice decreased. We propose that the characteristic clustered growth pattern of S. aureus, which emerges from dividing in alternating orthogonal division planes, might protect the bacterium from host defences.

Identifiants

pubmed: 39468247
doi: 10.1038/s41564-024-01821-8
pii: 10.1038/s41564-024-01821-8
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Subventions

Organisme : U.S. Department of Health & Human Services | National Institutes of Health (NIH)
ID : Intramural Research Program

Informations de copyright

© 2024. This is a U.S. Government work and not under copyright protection in the US; foreign copyright protection may apply.

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Auteurs

Félix Ramos-León (F)

Laboratory of Molecular Biology, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA.

Brandon R Anjuwon-Foster (BR)

Laboratory of Molecular Biology, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA.

Vivek Anantharaman (V)

National Center for Biotechnology Information, National Library of Medicine, National Institutes of Health, Bethesda, MD, USA.

Taylor B Updegrove (TB)

Laboratory of Molecular Biology, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA.

Colby N Ferreira (CN)

Department of Cell and Molecular Biology, University of Rhode Island, Kingston, RI, USA.

Amany M Ibrahim (AM)

Department of Microbiology, Howard Taylor Ricketts Laboratory, University of Chicago, Lemont, IL, USA.

Chin-Hsien Tai (CH)

Laboratory of Molecular Biology, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA.

Michael J Kruhlak (MJ)

Laboratory of Cancer Biology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA.

Dominique M Missiakas (DM)

Department of Microbiology, Howard Taylor Ricketts Laboratory, University of Chicago, Lemont, IL, USA.

Jodi L Camberg (JL)

Department of Cell and Molecular Biology, University of Rhode Island, Kingston, RI, USA.

L Aravind (L)

National Center for Biotechnology Information, National Library of Medicine, National Institutes of Health, Bethesda, MD, USA.

Kumaran S Ramamurthi (KS)

Laboratory of Molecular Biology, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA. ramamurthiks@mail.nih.gov.

Classifications MeSH