Sumoylation of Smc5 Promotes Error-free Bypass at Damaged Replication Forks | Zendy

Mariel Zapatka | Zendy; Irene Pociño-Merino | Zendy; Hayat HeluaniGahete | Zendy; Marcelino Bermúdez-López | Zendy; Marc Tarrés | Zendy; Eva Ibars | Zendy; Roger Solé-Soler | Zendy; Pilar Gutiérrez-Escribano | Zendy; Sonia Apostolova | Zendy; Cèlia Casas | Zendy; Luís Aragón | Zendy; Ralf Erik Wellinger | Zendy; Neus Colomina | Zendy; Jordi TorresRosell | Zendy

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Sumoylation of Smc5 Promotes Error-free Bypass at Damaged Replication Forks

Author(s) -

Mariel Zapatka,

Irene Pociño-Merino,

Hayat HeluaniGahete,

Marcelino Bermúdez-López,

Marc Tarrés,

Eva Ibars,

Roger Solé-Soler,

Pilar Gutiérrez-Escribano,

Sonia Apostolova,

Cèlia Casas,

Luís Aragón,

Ralf Erik Wellinger,

Neus Colomina,

Jordi TorresRosell

Publication year - 2019

Publication title -

cell reports

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 6.264

H-Index - 154

eISSN - 2639-1856

pISSN - 2211-1247

DOI - 10.1016/j.celrep.2019.10.123

Subject(s) - sumo protein , sister chromatids , microbiology and biotechnology , postreplication repair , biology , dna replication , dna repair , dna damage , genetics , dna , nucleotide excision repair , chromosome , ubiquitin , gene

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.

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