The hypoxia response pathway promotes PEP carboxykinase and gluconeogenesis in C. elegans.


Journal

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

Informations de publication

Date de publication:
18 10 2022
Historique:
received: 12 07 2021
accepted: 05 10 2022
entrez: 18 10 2022
pubmed: 19 10 2022
medline: 21 10 2022
Statut: epublish

Résumé

Actively dividing cells, including some cancers, rely on aerobic glycolysis rather than oxidative phosphorylation to generate energy, a phenomenon termed the Warburg effect. Constitutive activation of the Hypoxia Inducible Factor (HIF-1), a transcription factor known for mediating an adaptive response to oxygen deprivation (hypoxia), is a hallmark of the Warburg effect. HIF-1 is thought to promote glycolysis and suppress oxidative phosphorylation. Here, we instead show that HIF-1 can promote gluconeogenesis. Using a multiomics approach, we reveal the genomic, transcriptomic, and metabolomic landscapes regulated by constitutively active HIF-1 in C. elegans. We use RNA-seq and ChIP-seq under aerobic conditions to analyze mutants lacking EGL-9, a key negative regulator of HIF-1. We integrate these approaches to identify over two hundred genes directly and functionally upregulated by HIF-1, including the PEP carboxykinase PCK-1, a rate-limiting mediator of gluconeogenesis. This activation of PCK-1 by HIF-1 promotes survival in response to both oxidative and hypoxic stress. Our work identifies functional direct targets of HIF-1 in vivo, comprehensively describing the metabolome induced by HIF-1 activation in an organism.

Identifiants

pubmed: 36257965
doi: 10.1038/s41467-022-33849-x
pii: 10.1038/s41467-022-33849-x
pmc: PMC9579151
doi:

Substances chimiques

Transcription Factors 0
Oxygen S88TT14065
Hypoxia-Inducible Factor 1, alpha Subunit 0

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

6168

Subventions

Organisme : NIGMS NIH HHS
ID : R01 GM101972
Pays : United States
Organisme : NIGMS NIH HHS
ID : R35 GM124976
Pays : United States
Organisme : Foundation for the National Institutes of Health (Foundation for the National Institutes of Health, Inc.)
ID : R01GM101972

Commentaires et corrections

Type : CommentIn
Type : CommentIn

Informations de copyright

© 2022. The Author(s).

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Auteurs

Mehul Vora (M)

The Waksman Institute, Rutgers The State University of New Jersey, Piscataway, NJ, 08854, USA.

Stephanie M Pyonteck (SM)

The Waksman Institute, Rutgers The State University of New Jersey, Piscataway, NJ, 08854, USA.

Tatiana Popovitchenko (T)

The Waksman Institute, Rutgers The State University of New Jersey, Piscataway, NJ, 08854, USA.

Tarmie L Matlack (TL)

The Waksman Institute, Rutgers The State University of New Jersey, Piscataway, NJ, 08854, USA.

Aparna Prashar (A)

The Department of Genetics, Rutgers The State University of New Jersey, Piscataway, NJ, 08854, USA.

Nanci S Kane (NS)

The Waksman Institute, Rutgers The State University of New Jersey, Piscataway, NJ, 08854, USA.

John Favate (J)

The Department of Genetics, Rutgers The State University of New Jersey, Piscataway, NJ, 08854, USA.

Premal Shah (P)

The Department of Genetics, Rutgers The State University of New Jersey, Piscataway, NJ, 08854, USA.

Christopher Rongo (C)

The Waksman Institute, Rutgers The State University of New Jersey, Piscataway, NJ, 08854, USA. crongo@waksman.rutgers.edu.
The Department of Genetics, Rutgers The State University of New Jersey, Piscataway, NJ, 08854, USA. crongo@waksman.rutgers.edu.

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