Article
Sumoylation of Smc5 Promotes Error-free Bypass at Damaged Replication Forks
Author/s | Zapatka, Mariel
Pociño Merino, Irene Heluani Gahete, Hayat Bermúdez López, Marcelino Tarrés, Marc Ibars, Eva Solé Soler, Roger Gutiérrez Escribano, Pilar Apostolova, Sonia Casas, Celia Aragon, Luis Wellinger, Ralf Erik ![]() ![]() ![]() ![]() ![]() ![]() ![]() Colomina, Neus Torres Rosell, Jordi |
Department | Universidad de Sevilla. Departamento de Genética |
Date | 2019 |
Published in |
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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 ... 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. |
Funding agencies | Ministerio de Ciencia, Innovación y Universidades (MICINN). España |
Project ID. | BFU2015-71308-P
![]() PGC2018-097796-B-I00 ![]() |
Citation | Zapatka, M., Pociño Merino, I., Heluani Gahete, H., Bermúdez López, M., Tarrés, M., Ibars, E.,...,Torres Rosell, J. (2019). Sumoylation of Smc5 Promotes Error-free Bypass at Damaged Replication Forks. Cell Reports, 20 (10), 3160-3172. |
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