Sumoylation of Smc5 Promotes Error-free Bypass at Damaged Replication Forks.
DNA damage tolerance
DNA replication
Mms21
Mph1
Nse2
SUMO
Smc5
chromosome
fork regression
yeast
Journal
Cell reports
ISSN: 2211-1247
Titre abrégé: Cell Rep
Pays: United States
ID NLM: 101573691
Informations de publication
Date de publication:
03 12 2019
03 12 2019
Historique:
received:
09
04
2019
revised:
25
09
2019
accepted:
29
10
2019
entrez:
5
12
2019
pubmed:
5
12
2019
medline:
29
9
2020
Statut:
ppublish
Résumé
Replication of a damaged DNA template can threaten the integrity of the genome, requiring the use of various mechanisms to tolerate DNA lesions. The Smc5/6 complex, together with the Nse2/Mms21 SUMO ligase, plays essential roles in genome stability through undefined tasks at damaged replication forks. Various subunits within the Smc5/6 complex are substrates of Nse2, but we currently do not know the role of these modifications. Here we show that sumoylation of Smc5 is targeted to its coiled-coil domain, is upregulated by replication fork damage, and participates in bypass of DNA lesions. smc5-KR mutant cells display defects in formation of sister chromatid junctions and higher translesion synthesis. Also, we provide evidence indicating that Smc5 sumoylation modulates Mph1-dependent fork regression, acting synergistically with other pathways to promote chromosome disjunction. We propose that sumoylation of Smc5 enhances physical remodeling of damaged forks, avoiding the use of a more mutagenic tolerance pathway.
Identifiants
pubmed: 31801080
pii: S2211-1247(19)31456-1
doi: 10.1016/j.celrep.2019.10.123
pii:
doi:
Substances chimiques
Cell Cycle Proteins
0
SMC5 protein, S cerevisiae
0
Saccharomyces cerevisiae Proteins
0
DNA
9007-49-2
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
3160-3172.e4Subventions
Organisme : Wellcome Trust
ID : 100955
Pays : United Kingdom
Informations de copyright
Copyright © 2019 The Author(s). Published by Elsevier Inc. All rights reserved.