Pathogenic hyperactivation of mTORC1 by cytoplasmic EP300 in Hutchinson-Gilford progeria syndrome

Lucille Ferret; Guido Kroemer; Mojgan Djavaheri-Mergny

doi:10.15698/cst2024.04.295

Pathogenic hyperactivation of mTORC1 by cytoplasmic EP300 in Hutchinson-Gilford progeria syndrome

Cell Stress. 2024 Apr 30:8:51-55. doi: 10.15698/cst2024.04.295. eCollection 2024.

Authors

Lucille Ferret^{1

2

3}, Guido Kroemer^{1

2

4}, Mojgan Djavaheri-Mergny^{1

2}

Affiliations

¹ Centre de Recherche des Cordeliers, INSERM UMRS 1138, Sorbonne Université, Université Paris Cité, Équipe labellisée par la Ligue contre le Cancer, Institut universitaire de France, Paris, France.
² Metabolomics and Cell Biology Platforms, Institut Gustave Roussy, Villejuif, France.
³ Faculté de Médecine, Université de Paris Saclay, Paris, France.
⁴ Institut du Cancer Paris CARPEM, Department of Biology, Hôpital Européen Georges Pompidou, AP-HP, Paris, France.

Abstract

In a recent issue in Nature Cell Biology, Sung Min Son et al. unveil a novel layer in the regulation of the mTORC1/autophagy axis by EP300 which can undergo nucleocytoplasmic shuttling in response to alterations in nutrient availability. The study highlights that, in Hutchinson-Gilford progeria syndrome, overabundant cytoplasmic EP300 results in mTORC1 hyperactivation and impaired autophagy, potentially contributing to premature and accelerated aging.

Keywords: EP300; MTORC1; aging; autophagy.

Publication types

Comment