Polyunsaturated fatty acids and p38-MAPK link metabolic reprogramming to cytoprotective gene expression during dietary restriction.


Journal

Nature communications
ISSN: 2041-1723
Titre abrégé: Nat Commun
Pays: England
ID NLM: 101528555

Informations de publication

Date de publication:
25 09 2020
Historique:
received: 27 08 2019
accepted: 02 09 2020
entrez: 26 9 2020
pubmed: 27 9 2020
medline: 21 10 2020
Statut: epublish

Résumé

The metabolic state of an organism instructs gene expression modalities, leading to changes in complex life history traits, such as longevity. Dietary restriction (DR), which positively affects health and life span across species, leads to metabolic reprogramming that enhances utilisation of fatty acids for energy generation. One direct consequence of this metabolic shift is the upregulation of cytoprotective (CyTP) genes categorized in the Gene Ontology (GO) term of "Xenobiotic Detoxification Program" (XDP). How an organism senses metabolic changes during nutritional stress to alter gene expression programs is less known. Here, using a genetic model of DR, we show that the levels of polyunsaturated fatty acids (PUFAs), especially linoleic acid (LA) and eicosapentaenoic acid (EPA), are increased following DR and these PUFAs are able to activate the CyTP genes. This activation of CyTP genes is mediated by the conserved p38 mitogen-activated protein kinase (p38-MAPK) pathway. Consequently, genes of the PUFA biosynthesis and p38-MAPK pathway are required for multiple paradigms of DR-mediated longevity, suggesting conservation of mechanism. Thus, our study shows that PUFAs and p38-MAPK pathway function downstream of DR to help communicate the metabolic state of an organism to regulate expression of CyTP genes, ensuring extended life span.

Identifiants

pubmed: 32978396
doi: 10.1038/s41467-020-18690-4
pii: 10.1038/s41467-020-18690-4
pmc: PMC7519657
doi:

Substances chimiques

Caenorhabditis elegans Proteins 0
Fatty Acids, Unsaturated 0
eicosapentaenoic acid ethyl ester 6GC8A4PAYH
Linoleic Acid 9KJL21T0QJ
Eicosapentaenoic Acid AAN7QOV9EA
Protein Serine-Threonine Kinases EC 2.7.11.1
drl-1 protein, C elegans EC 2.7.11.1
p38 Mitogen-Activated Protein Kinases EC 2.7.11.24

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

4865

Subventions

Organisme : NIH HHS
ID : P40 OD010440
Pays : United States

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Auteurs

Manish Chamoli (M)

Molecular Aging Laboratory, National Institute of Immunology, Aruna Asaf Ali Marg, New Delhi, 110067, India.
Buck Institute for Research on Aging, 8001 Redwood Blvd., Novato, CA, 94945, USA.

Anita Goyala (A)

Molecular Aging Laboratory, National Institute of Immunology, Aruna Asaf Ali Marg, New Delhi, 110067, India.

Syed Shamsh Tabrez (SS)

Molecular Aging Laboratory, National Institute of Immunology, Aruna Asaf Ali Marg, New Delhi, 110067, India.
Department of Molecular Genetics of Ageing, Max Planck Institute for Biology of Ageing, Cologne, 50931, Germany.

Atif Ahmed Siddiqui (AA)

Molecular Aging Laboratory, National Institute of Immunology, Aruna Asaf Ali Marg, New Delhi, 110067, India.

Anupama Singh (A)

Molecular Aging Laboratory, National Institute of Immunology, Aruna Asaf Ali Marg, New Delhi, 110067, India.

Adam Antebi (A)

Department of Molecular Genetics of Ageing, Max Planck Institute for Biology of Ageing, Cologne, 50931, Germany.
Cologne Excellence Cluster on Cellular Stress Responses in Aging Associated Diseases, University of Cologne, Cologne, 50931, Germany.

Gordon J Lithgow (GJ)

Buck Institute for Research on Aging, 8001 Redwood Blvd., Novato, CA, 94945, USA.

Jennifer L Watts (JL)

School of Molecular Biosciences, Washington State University, Pullman, WA, 99164-7520, USA.

Arnab Mukhopadhyay (A)

Molecular Aging Laboratory, National Institute of Immunology, Aruna Asaf Ali Marg, New Delhi, 110067, India. arnab@nii.ac.in.

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