dc.creator | Galati, Elena | es |
dc.creator | Bosio, Maria C. | es |
dc.creator | Novarina, Daniele | es |
dc.creator | Chiara, Matteo | es |
dc.creator | Bernini, Giulia M. | es |
dc.creator | Mozzarelli, Alessandro M. | es |
dc.creator | García Rubio, María Luisa | es |
dc.creator | Gómez González, Belén | es |
dc.creator | Aguilera López, Andrés | es |
dc.creator | Carzaniga, Thomas | es |
dc.creator | Todisco, Marco | es |
dc.creator | Bellini, Tommaso | es |
dc.creator | Nava, Giulia M. | es |
dc.creator | Frige, Gianmaria | es |
dc.creator | Lazzaro, Federico | es |
dc.date.accessioned | 2022-01-28T16:00:41Z | |
dc.date.available | 2022-01-28T16:00:41Z | |
dc.date.issued | 2021 | |
dc.identifier.citation | Galati, E., Bosio, M.C., Novarina, D., Chiara, M., Bernini, G.M., Mozzarelli, A.M.,...,Lazzaro, F. (2021). VID22 counteracts G-quadruplex-induced genome instability. Nucleic Acids Research, 49 (22), 12785-12804. | |
dc.identifier.issn | 0305-1048 | es |
dc.identifier.issn | 1362-4962 | es |
dc.identifier.uri | https://hdl.handle.net/11441/129420 | |
dc.description.abstract | Genome instability is a condition characterized by the accumulation of genetic alterations and is a hallmark of cancer cells. To uncover new genes and cellular pathways affecting endogenous DNA damage and genome integrity, we exploited a Synthetic Genetic Array (SGA)-based screen in yeast. Among the positive genes, we identified VID22, reported to be involved in DNA double-strand break repair. vid22Δ cells exhibit increased levels of endogenous DNA damage, chronic DNA damage response activation and accumulate DNA aberrations in sequences displaying high probabilities of forming G-quadruplexes (G4-DNA). If not resolved, these DNA secondary structures can block the progression of both DNA and RNA polymerases and correlate with chromosome fragile sites. Vid22 binds to and protects DNA at G4-containing regions both in vitro and in vivo. Loss of VID22 causes an increase in gross chromosomal rearrangement (GCR) events dependent on G-quadruplex forming sequences. Moreover, the absence of Vid22 causes defects in the correct maintenance of G4-DNA rich elements, such as telomeres and mtDNA, and hypersensitivity to the G4-stabilizing ligand TMPyP4. We thus propose that Vid22 is directly involved in genome integrity maintenance as a novel regulator of G4 metabolism. | es |
dc.description.sponsorship | Associazione Italiana per la Ricerca sul Cancro (AIRC) 15631, 21806 | es |
dc.description.sponsorship | MIUR PRIN 2015- 2015SJLMB9, PRIN 2017-2017KSZZJW, PRIN2017-2017Z55KC | es |
dc.description.sponsorship | Ministerio de Economía y Competitividad BFU2016- 75058-P | es |
dc.description.sponsorship | Canadian Institutes of Health Research FDN-159913 | es |
dc.format | application/pdf | es |
dc.format.extent | 20 p. | es |
dc.language.iso | eng | es |
dc.publisher | Oxford University Press | es |
dc.relation.ispartof | Nucleic Acids Research, 49 (22), 12785-12804. | |
dc.rights | Attribution-NonCommercial-NoDerivatives 4.0 Internacional | * |
dc.rights.uri | http://creativecommons.org/licenses/by-nc-nd/4.0/ | * |
dc.title | VID22 counteracts G-quadruplex-induced genome instability | es |
dc.type | info:eu-repo/semantics/article | es |
dcterms.identifier | https://ror.org/03yxnpp24 | |
dc.type.version | info:eu-repo/semantics/publishedVersion | es |
dc.rights.accessRights | info:eu-repo/semantics/openAccess | es |
dc.contributor.affiliation | Universidad de Sevilla. Departamento de Genética | es |
dc.relation.projectID | 15631 | es |
dc.relation.projectID | 21806 | es |
dc.relation.projectID | PRIN 2015- 2015SJLMB9 | es |
dc.relation.projectID | PRIN 2017-2017KSZZJW | es |
dc.relation.projectID | PRIN2017-2017Z55KC | es |
dc.relation.projectID | BFU2016- 75058-P | es |
dc.relation.projectID | FDN-159913 | es |
dc.relation.publisherversion | https://doi.org/10.1093/nar/gkab1156 | es |
dc.identifier.doi | 10.1093/nar/gkab1156 | es |
dc.journaltitle | Nucleic Acids Research | es |
dc.publication.volumen | 49 | es |
dc.publication.issue | 22 | es |
dc.publication.initialPage | 12785 | es |
dc.publication.endPage | 12804 | es |