Hsf1 and the molecular chaperone Hsp90 support a ‘rewiring stress response’ leading to an adaptive cell size increase in chronic stress

Author:

Maiti Samarpan1ORCID,Bhattacharya Kaushik1,Wider Diana1,Hany Dina12,Panasenko Olesya3,Bernasconi Lilia1,Hulo Nicolas4ORCID,Picard Didier1ORCID

Affiliation:

1. Département de Biologie Moléculaire et Cellulaire, Université de Genève

2. On leave from: Department of Pharmacology and Therapeutics, Faculty of Pharmacy, Pharos University in Alexandria

3. BioCode: RNA to Proteins Core Facility, Département de Microbiologie et Médecine Moléculaire, Faculté de Médecine, Université de Genève

4. Institute of Genetics and Genomics of Geneva, Université de Genève

Abstract

Cells are exposed to a wide variety of internal and external stresses. Although many studies have focused on cellular responses to acute and severe stresses, little is known about how cellular systems adapt to sublethal chronic stresses. Using mammalian cells in culture, we discovered that they adapt to chronic mild stresses of up to two weeks, notably proteotoxic stresses such as heat, by increasing their size and translation, thereby scaling the amount of total protein. These adaptations render them more resilient to persistent and subsequent stresses. We demonstrate that Hsf1, well known for its role in acute stress responses, is required for the cell size increase, and that the molecular chaperone Hsp90 is essential for coupling the cell size increase to augmented translation. We term this translational reprogramming the ‘rewiring stress response’, and propose that this protective process of chronic stress adaptation contributes to the increase in size as cells get older, and that its failure promotes aging.

Funder

Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung

Canton de Genève

Publisher

eLife Sciences Publications, Ltd

Subject

General Immunology and Microbiology,General Biochemistry, Genetics and Molecular Biology,General Medicine,General Neuroscience

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