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EzrA Contributes to the Regulation of Cell Size in Staphylococcus aureus

EzrA is a negative regulator of FtsZ in Bacillus subtilis, involved in the coordination between cell growth and cell division and in the control of the cell elongation–division cycle. We have now studied the role of the Staphylococcus aureus homologue of the B. subtilis EzrA protein and shown that i...

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Autores principales: Jorge, Ana M., Hoiczyk, Egbert, Gomes, João P., Pinho, Mariana G.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Public Library of Science 2011
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3215724/
https://www.ncbi.nlm.nih.gov/pubmed/22110668
http://dx.doi.org/10.1371/journal.pone.0027542
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author Jorge, Ana M.
Hoiczyk, Egbert
Gomes, João P.
Pinho, Mariana G.
author_facet Jorge, Ana M.
Hoiczyk, Egbert
Gomes, João P.
Pinho, Mariana G.
author_sort Jorge, Ana M.
collection PubMed
description EzrA is a negative regulator of FtsZ in Bacillus subtilis, involved in the coordination between cell growth and cell division and in the control of the cell elongation–division cycle. We have now studied the role of the Staphylococcus aureus homologue of the B. subtilis EzrA protein and shown that it is not essential for cell viability. EzrA conditional and null mutants have an overall increase of the average cell size, compared to wild type strains. In the larger ezrA mutant S. aureus cells, cell division protein FtsZ and the cell wall synthesizing Penicillin Binding Proteins (PBPs) are not properly localized. This suggests that there may be a maximum cell diameter that allows formation of a Z-ring capable of recruiting the other components of the divisome and of driving cytokinesis. We propose that the major role of EzrA in S. aureus is in cell size homeostasis.
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spelling pubmed-32157242011-11-21 EzrA Contributes to the Regulation of Cell Size in Staphylococcus aureus Jorge, Ana M. Hoiczyk, Egbert Gomes, João P. Pinho, Mariana G. PLoS One Research Article EzrA is a negative regulator of FtsZ in Bacillus subtilis, involved in the coordination between cell growth and cell division and in the control of the cell elongation–division cycle. We have now studied the role of the Staphylococcus aureus homologue of the B. subtilis EzrA protein and shown that it is not essential for cell viability. EzrA conditional and null mutants have an overall increase of the average cell size, compared to wild type strains. In the larger ezrA mutant S. aureus cells, cell division protein FtsZ and the cell wall synthesizing Penicillin Binding Proteins (PBPs) are not properly localized. This suggests that there may be a maximum cell diameter that allows formation of a Z-ring capable of recruiting the other components of the divisome and of driving cytokinesis. We propose that the major role of EzrA in S. aureus is in cell size homeostasis. Public Library of Science 2011-11-14 /pmc/articles/PMC3215724/ /pubmed/22110668 http://dx.doi.org/10.1371/journal.pone.0027542 Text en Jorge et al. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.
spellingShingle Research Article
Jorge, Ana M.
Hoiczyk, Egbert
Gomes, João P.
Pinho, Mariana G.
EzrA Contributes to the Regulation of Cell Size in Staphylococcus aureus
title EzrA Contributes to the Regulation of Cell Size in Staphylococcus aureus
title_full EzrA Contributes to the Regulation of Cell Size in Staphylococcus aureus
title_fullStr EzrA Contributes to the Regulation of Cell Size in Staphylococcus aureus
title_full_unstemmed EzrA Contributes to the Regulation of Cell Size in Staphylococcus aureus
title_short EzrA Contributes to the Regulation of Cell Size in Staphylococcus aureus
title_sort ezra contributes to the regulation of cell size in staphylococcus aureus
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3215724/
https://www.ncbi.nlm.nih.gov/pubmed/22110668
http://dx.doi.org/10.1371/journal.pone.0027542
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