SMC is recruited to oriC by ParB and promotes chromosome segregation in Streptococcus pneumoniae.

Détails

ID Serval
serval:BIB_8461B14D48C3
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
SMC is recruited to oriC by ParB and promotes chromosome segregation in Streptococcus pneumoniae.
Périodique
Molecular Microbiology
Auteur⸱e⸱s
Minnen A., Attaiech L., Thon M., Gruber S., Veening J.W.
ISSN
1365-2958 (Electronic)
ISSN-L
0950-382X
Statut éditorial
Publié
Date de publication
2011
Peer-reviewed
Oui
Volume
81
Numéro
3
Pages
676-688
Langue
anglais
Résumé
Segregation of replicated chromosomes is an essential process in all organisms. How bacteria, such as the oval-shaped human pathogen Streptococcus pneumoniae, efficiently segregate their chromosomes is poorly understood. Here we show that the pneumococcal homologue of the DNA-binding protein ParB recruits S. pneumoniae condensin (SMC) to centromere-like DNA sequences (parS) that are located near the origin of replication, in a similar fashion as was shown for the rod-shaped model bacterium Bacillus subtilis. In contrast to B. subtilis, smc is not essential in S. pneumoniae, and Δsmc cells do not show an increased sensitivity to gyrase inhibitors or high temperatures. However, deletion of smc and/or parB results in a mild chromosome segregation defect. Our results show that S. pneumoniae contains a functional chromosome segregation machine that promotes efficient chromosome segregation by recruitment of SMC via ParB. Intriguingly, the data indicate that other, as of yet unknown mechanisms, are at play to ensure proper chromosome segregation in this organism.
Mots-clé
Bacterial Proteins/genetics, Bacterial Proteins/metabolism, Cell Cycle Proteins/genetics, Cell Cycle Proteins/metabolism, Chromosome Segregation, Chromosomes, Bacterial/metabolism, DNA-Binding Proteins/metabolism, Gene Deletion, Origin Recognition Complex, Protein Binding, Streptococcus pneumoniae/enzymology, Streptococcus pneumoniae/genetics
Pubmed
Web of science
Open Access
Oui
Création de la notice
17/08/2016 10:52
Dernière modification de la notice
20/08/2019 15:44
Données d'usage