Sensing of the non-essential amino acid tyrosine governs the response to protein restriction in Drosophila.


Journal

Nature metabolism
ISSN: 2522-5812
Titre abrégé: Nat Metab
Pays: Germany
ID NLM: 101736592

Informations de publication

Date de publication:
07 2022
Historique:
received: 03 12 2021
accepted: 15 06 2022
entrez: 25 7 2022
pubmed: 26 7 2022
medline: 28 7 2022
Statut: ppublish

Résumé

The intake of dietary protein regulates growth, metabolism, fecundity and lifespan across various species, which makes amino acid (AA)-sensing vital for adaptation to the nutritional environment. The general control nonderepressible 2 (GCN2)-activating transcription factor 4 (ATF4) pathway and the mechanistic target of rapamycin complex 1 (mTORC1) pathway are involved in AA-sensing. However, it is not fully understood which AAs regulate these two pathways in living animals and how they coordinate responses to protein restriction. Here we show in Drosophila that the non-essential AA tyrosine (Tyr) is a nutritional cue in the fat body necessary and sufficient for promoting adaptive responses to a low-protein diet, which entails reduction of protein synthesis and mTORC1 activity and increased food intake. This adaptation is regulated by dietary Tyr through GCN2-independent induction of ATF4 target genes in the fat body. This study identifies the Tyr-ATF4 axis as a regulator of the physiological response to a low-protein diet and sheds light on the essential function of a non-essential nutrient.

Identifiants

pubmed: 35879463
doi: 10.1038/s42255-022-00608-7
pii: 10.1038/s42255-022-00608-7
doi:

Substances chimiques

Amino Acids 0
Activating Transcription Factor 4 145891-90-3
Tyrosine 42HK56048U
Mechanistic Target of Rapamycin Complex 1 EC 2.7.11.1
Protein Serine-Threonine Kinases EC 2.7.11.1

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

944-959

Informations de copyright

© 2022. The Author(s), under exclusive licence to Springer Nature Limited.

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Auteurs

Hina Kosakamoto (H)

Department of Genetics, Graduate School of Pharmaceutical Sciences, The University of Tokyo, Bunkyo-ku, Tokyo, Japan.
RIKEN Center for Biosystems and Dynamics Research, Kobe, Japan.
Life Science Center for Survival Dynamics, Tsukuba Advanced Research Alliance (TARA), University of Tsukuba, Tsukuba, Japan.

Naoki Okamoto (N)

Life Science Center for Survival Dynamics, Tsukuba Advanced Research Alliance (TARA), University of Tsukuba, Tsukuba, Japan.

Hide Aikawa (H)

Department of Genetics, Graduate School of Pharmaceutical Sciences, The University of Tokyo, Bunkyo-ku, Tokyo, Japan.

Yuki Sugiura (Y)

Department of Biochemistry, Keio University School of Medicine, Shinjuku-ku, Tokyo, Japan.

Makoto Suematsu (M)

Department of Biochemistry, Keio University School of Medicine, Shinjuku-ku, Tokyo, Japan.

Ryusuke Niwa (R)

Life Science Center for Survival Dynamics, Tsukuba Advanced Research Alliance (TARA), University of Tsukuba, Tsukuba, Japan.

Masayuki Miura (M)

Department of Genetics, Graduate School of Pharmaceutical Sciences, The University of Tokyo, Bunkyo-ku, Tokyo, Japan.

Fumiaki Obata (F)

Department of Genetics, Graduate School of Pharmaceutical Sciences, The University of Tokyo, Bunkyo-ku, Tokyo, Japan. fumiaki.obata@riken.jp.
RIKEN Center for Biosystems and Dynamics Research, Kobe, Japan. fumiaki.obata@riken.jp.
Life Science Center for Survival Dynamics, Tsukuba Advanced Research Alliance (TARA), University of Tsukuba, Tsukuba, Japan. fumiaki.obata@riken.jp.
Laboratory of Molecular Cell Biology and Development, Graduate School of Biostudies, Kyoto University, Kyoto, Japan. fumiaki.obata@riken.jp.

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