Distinct roles of Deinococcus radiodurans RecFOR and RecA in DNA transformation.
Deinococcus radiodurans
RecA
RecFOR
Transformation
Journal
Biochemical and biophysical research communications
ISSN: 1090-2104
Titre abrégé: Biochem Biophys Res Commun
Pays: United States
ID NLM: 0372516
Informations de publication
Date de publication:
04 06 2019
04 06 2019
Historique:
received:
27
03
2019
accepted:
04
04
2019
pubmed:
18
4
2019
medline:
23
6
2020
entrez:
18
4
2019
Statut:
ppublish
Résumé
RecFOR and RecA are key recombination factors in Deinococcus radiodurans, a bacterium that possesses robust DNA repair capability and is also naturally transformable. While RecFOR functioning as a RecA loader during DNA repair has been established, their relative roles in transformation need further exploration. Here, we constructed recFOR and recA deletion mutants of D. radiodurans, and investigated the effect of these mutations on DNA transformation. recA deletion causes defects in both plasmid and chromosomal transformation. However, it was found that recFOR is not involved in chromosomal transformation, and that only recO and recR mutations compromise plasmid transformation. How recO, recR and recA mutations influence plasmid transformation was further examined by complementation plasmids. Interestingly, the transformation process remains defective in the recA mutant, but gets restored in the recO and recR mutants. This indicates that unlike RecA, RecOR may not be essential for DNA uptake. Therefore, we provide evidence that RecFOR is dispensable for RecA to protect incoming exogenous DNA and to catalyze recombination during transformation. Instead, RecO and RecR are likely to promote later steps in plasmid transformation.
Identifiants
pubmed: 30992133
pii: S0006-291X(19)30664-3
doi: 10.1016/j.bbrc.2019.04.042
pii:
doi:
Substances chimiques
Bacterial Proteins
0
Rec A Recombinases
EC 2.7.7.-
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
740-745Informations de copyright
Copyright © 2019 Elsevier Inc. All rights reserved.