Ambrus, Aaron M.Islam, Abul, 1978-Holmes, Katherine B.Moon, Nam SungLópez Bigas, NúriaBenevolenskaya, Elizaveta V.Frolov, Maxim V.2015-11-252015-11-252013Ambrus AM, Islam AB, Holmes KB, Moon NS, Lopez-Bigas N, Benevolenskaya EV et al. Loss of dE2F compromises mitochondrial function. Developmental cell. 2013; 27(4):438-51. DOI: 10.1016/j.devcel.2013.10.0021534-5807http://hdl.handle.net/10230/25226E2F/DP transcription factors regulate cell proliferation and apoptosis. Here, we investigated the mechanism of the resistance of Drosophila dDP mutants to irradiation-induced apoptosis. Contrary to the prevailing view, this is not due to an inability to induce the apoptotic transcriptional program, because we show that this program is induced; rather, this is due to a mitochondrial dysfunction of dDP mutants. We attribute this defect to E2F/DP-dependent control of expression of mitochondria-associated genes. Genetic attenuation of several of these E2F/DP targets mimics the dDP mutant mitochondrial phenotype and protects against irradiation-induced apoptosis. Significantly, the role of E2F/DP in the regulation of mitochondrial function is conserved between flies and humans. Thus, our results uncover a role of E2F/DP in the regulation of mitochondrial function and demonstrate that this aspect of E2F regulation is critical for the normal induction of apoptosis in response to irradiation.application/pdfeng© Elsevier This is the published version of an article http://dx.doi.org/10.1016/j.devcel.2013.10.002 that appeared in the journal Developmental Cell. It is published in an Open Archive under an Elsevier user license. Details of this licence are available here: http://www.elsevier.com/about/open-access/open-access-policies/oa-license-policy/elsevier-user-licenseADN -- DanyDrosòfilainfo:eu-repo/semantics/articlehttp://dx.doi.org/10.1016/j.devcel.2013.10.002info:eu-repo/semantics/openAccess