Phosphatidylethanolamine positively regulates autophagy and longevity

Patrick Rockenfeller(University of Graz), Michal Koska(University of Graz), Federico Pietrocola(Inserm), Nadège Minois(University of St Andrews), Oskar Knittelfelder(University of Graz), Valentina Sica(Inserm), Joakim Franz(University of Graz), Didac Carmona‐Gutiérrez(University of Graz), Guido Kroemer(Délégation Paris 5), Frank Madeo(BioTechMed-Graz)
Cell Death and Differentiation
January 9, 2015
Cited by 268Open Access
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Abstract

Autophagy is a cellular recycling program that retards ageing by efficiently eliminating damaged and potentially harmful organelles and intracellular protein aggregates. Here, we show that the abundance of phosphatidylethanolamine (PE) positively regulates autophagy. Reduction of intracellular PE levels by knocking out either of the two yeast phosphatidylserine decarboxylases (PSD) accelerated chronological ageing-associated production of reactive oxygen species and death. Conversely, the artificial increase of intracellular PE levels, by provision of its precursor ethanolamine or by overexpression of the PE-generating enzyme Psd1, significantly increased autophagic flux, both in yeast and in mammalian cell culture. Importantly administration of ethanolamine was sufficient to extend the lifespan of yeast (Saccharomyces cerevisiae), mammalian cells (U2OS, H4) and flies (Drosophila melanogaster). We thus postulate that the availability of PE may constitute a bottleneck for functional autophagy and that organismal life or healthspan could be positively influenced by the consumption of ethanolamine-rich food.


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