Loss of dE2F compromises mitochondrial function

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dc.contributor.author	Ambrus, Aaron M.
dc.contributor.author	Islam, Abul, 1978-
dc.contributor.author	Holmes, Katherine B.
dc.contributor.author	Moon, Nam Sung
dc.contributor.author	López Bigas, Núria
dc.contributor.author	Benevolenskaya, Elizaveta V.
dc.contributor.author	Frolov, Maxim V.
dc.date	2013
dc.identifier.citation	Ambrus 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): 438-451. DOI 10.1016/j.devcel.2013.10.002
dc.identifier.citation	1534-5807
dc.identifier.citation	http://dx.doi.org/10.1016/j.devcel.2013.10.002
dc.identifier.uri	http://hdl.handle.net/10230/25226
dc.format	application/pdf
dc.language.iso	eng
dc.publisher	Elsevier
dc.relation	Developmental cell. 2013; 27(4): 438-451
dc.rights	info:eu-repo/semantics/openAccess
dc.rights	© 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-license
dc.subject	ADN -- Dany
dc.subject	Drosòfila
dc.title	Loss of dE2F compromises mitochondrial function
dc.type	info:eu-repo/semantics/article
dc.type	info:eu-repo/semantics/publishedVersion
dc.description.abstract	E2F/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.

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