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http://hdl.handle.net/2445/178988
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DC Field | Value | Language |
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dc.contributor.author | Joy, Jery | - |
dc.contributor.author | Barrio, Lara | - |
dc.contributor.author | Santos Tapia, Celia | - |
dc.contributor.author | Romão, Daniela | - |
dc.contributor.author | Giakoumakis, Nikolaos Nikiforos | - |
dc.contributor.author | Clemente Ruiz, Marta | - |
dc.contributor.author | Milán, Marco | - |
dc.date.accessioned | 2021-07-12T11:32:04Z | - |
dc.date.available | 2022-07-02T05:10:19Z | - |
dc.date.issued | 2021-07-02 | - |
dc.identifier.issn | 1534-5807 | - |
dc.identifier.uri | http://hdl.handle.net/2445/178988 | - |
dc.description.abstract | Aneuploidy, an unbalanced number of chromosomes, is highly deleterious at the cellular level and leads to senescence, a stress-induced response characterized by permanent cell-cycle arrest and a well-defined associated secretory phenotype. Here, we use a Drosophila epithelial model to delineate the pathway that leads to the induction of senescence as a consequence of the acquisition of an aneuploid karyotype. Whereas aneuploidy induces, as a result of gene dosage imbalance, proteotoxic stress and activation of the major protein quality control mechanisms, near-saturation functioning of autophagy leads to compromised mitophagy, accumulation of dysfunctional mitochondria, and the production of radical oxygen species (ROS). We uncovered a role of c-Jun N-terminal kinase (JNK) in driving senescence as a consequence of dysfunctional mitochondria and ROS. We show that activation of the major protein quality control mechanisms and mitophagy dampens the deleterious effects of aneuploidy, and we identify a role of senescence in proteostasis and compensatory proliferation for tissue repair. | ca |
dc.format.extent | 67 p. | - |
dc.format.mimetype | application/pdf | - |
dc.language.iso | eng | ca |
dc.relation.isformatof | Reproducció del document publicat a: https://doi.org/10.1016/j.devcel.2021.06.009 | - |
dc.relation.ispartof | Developmental Cell, 2021, vol. 56, num. 14, p. 2043-2058.e7 | - |
dc.relation.uri | https://doi.org/10.1016/j.devcel.2021.06.009 | - |
dc.rights | cc-by-nc-nd (c) Elsevier, 2021 | - |
dc.rights.uri | http://creativecommons.org/licenses/by-nc-nd/3.0/es/ | * |
dc.source | Articles publicats en revistes (Institut de Recerca Biomèdica (IRB Barcelona)) | - |
dc.subject.classification | Drosòfila | - |
dc.subject.classification | Autofàgia | - |
dc.subject.classification | Envelliment | - |
dc.subject.classification | Cromosomes | - |
dc.subject.other | Drosophila | - |
dc.subject.other | Autophagy | - |
dc.subject.other | Aging | - |
dc.subject.other | Chromosomes | - |
dc.title | Proteostasis failure and mitochondrial dysfunction leads to aneuploidy-induced senescence | ca |
dc.type | info:eu-repo/semantics/article | ca |
dc.date.updated | 2021-07-12T10:31:47Z | - |
dc.rights.accessRights | info:eu-repo/semantics/openAccess | - |
dc.identifier.idimarina | 6519885 | - |
Appears in Collections: | Articles publicats en revistes (Institut de Recerca Biomèdica (IRB Barcelona)) |
Files in This Item:
File | Description | Size | Format | |
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12541_6519885_jery_et_al_dev_cel_2021.pdf | 5.23 MB | Adobe PDF | View/Open |
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