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Citation
Robin, M., Issa, A.R., Santos, C.C., Napoletano, F., Petitgas, C., Chatelain, G., Ruby, M., Walter, L., Birman, S., Domingos, P.M., Calvi, B.R., Mollereau, B. (2019). Drosophila p53 integrates the antagonism between autophagy and apoptosis in response to stress.  Autophagy 15(5): 771--784.
FlyBase ID
FBrf0241963
Publication Type
Research paper
Abstract
The tumor suppressor TP53/p53 is a known regulator of apoptosis and macroautophagy/autophagy. However, the molecular mechanism by which TP53 regulates 2 apparently incompatible processes remains unknown. We found that Drosophila lacking p53 displayed impaired autophagic flux, higher caspase activation and mortality in response to oxidative stress compared with wild-type flies. Moreover, autophagy and apoptosis were differentially regulated by the p53 (p53B) and ΔNp53 (p53A) isoforms: while the former induced autophagy in differentiated neurons, which protected against cell death, the latter inhibited autophagy by activating the caspases Dronc, Drice, and Dcp-1. Our results demonstrate that the differential use of p53 isoforms combined with the antagonism between apoptosis and autophagy ensures the generation of an appropriate p53 biological response to stress.
PubMed ID
PubMed Central ID
PMC6526837 (PMC) (EuropePMC)
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Secondary IDs
    Language of Publication
    English
    Additional Languages of Abstract
    Parent Publication
    Publication Type
    Journal
    Abbreviation
    Autophagy
    Title
    Autophagy
    Publication Year
    2005-
    ISBN/ISSN
    1554-8627 1554-8635
    Data From Reference