A developmental checkpoint directs metabolic remodelling as a strategy against starvation in Drosophila.


Journal

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

Informations de publication

Date de publication:
10 2020
Historique:
received: 14 04 2020
accepted: 07 09 2020
pubmed: 14 10 2020
medline: 31 12 2020
entrez: 13 10 2020
Statut: ppublish

Résumé

Steroid hormones are crucial regulators of life-stage transitions during development in animals. However, the molecular mechanisms by which developmental transition through these stages is coupled with optimal metabolic homeostasis remains poorly understood. Here, we demonstrate through mathematical modelling and experimental validation that ecdysteroid-induced metabolic remodelling from resource consumption to conservation can be a successful life-history strategy to maximize fitness in Drosophila larvae in a fluctuating environment. Specifically, the ecdysteroid-inducible protein ImpL2 protects against hydrolysis of circulating trehalose following pupal commitment in larvae. Stored glycogen and triglycerides in the fat body are also conserved, even under fasting conditions. Moreover, pupal commitment dictates reduced energy expenditure upon starvation to maintain available resources, thus negotiating trade-offs in resource allocation at the physiological and behavioural levels. The optimal stage-specific metabolic shift elucidated by our predictive and empirical approaches reveals that Drosophila has developed a highly controlled system for ensuring robust development that may be conserved among higher-order organisms in response to intrinsic and extrinsic cues.

Identifiants

pubmed: 33046910
doi: 10.1038/s42255-020-00293-4
pii: 10.1038/s42255-020-00293-4
doi:

Substances chimiques

Drosophila Proteins 0
Ecdysteroids 0
ImpL2 protein, Drosophila 0
Insulin-Like Growth Factor Binding Proteins 0
Triglycerides 0
Glycogen 9005-79-2

Types de publication

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

Langues

eng

Sous-ensembles de citation

IM

Pagination

1096-1112

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Auteurs

Takayuki Yamada (T)

Laboratory for Growth Control Signaling, RIKEN Center for Biosystems Dynamics Research (BDR), Kobe, Japan.

Ken-Ichi Hironaka (KI)

Laboratory for Growth Control Signaling, RIKEN Center for Biosystems Dynamics Research (BDR), Kobe, Japan.
Department of Biological Sciences, Graduate School of Science, University of Tokyo, Tokyo, Japan.

Okiko Habara (O)

Laboratory for Growth Control Signaling, RIKEN Center for Biosystems Dynamics Research (BDR), Kobe, Japan.

Yoshihiro Morishita (Y)

Laboratory for Developmental Morphogeometry, RIKEN BDR, Kobe, Japan.

Takashi Nishimura (T)

Laboratory for Growth Control Signaling, RIKEN Center for Biosystems Dynamics Research (BDR), Kobe, Japan. takashi.nishimura@riken.jp.

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