Abstract：
: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.
journal_name
Cell Repjournal_title
Cell reportsauthors
Zapatka M,Pociño-Merino I,Heluani-Gahete H,Bermúdez-López M,Tarrés M,Ibars E,Solé-Soler R,Gutiérrez-Escribano P,Apostolova S,Casas C,Aragon L,Wellinger R,Colomina N,Torres-Rosell Jdoi
10.1016/j.celrep.2019.10.123subject
Has Abstractpub_date
2019-12-03 00:00:00pages
3160-3172.e4issue
10issn
2211-1247pii
S2211-1247(19)31456-1journal_volume
29pub_type
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