Electron Transport Chain Remodeling by GSK3 during Oogenesis Connects Nutrient State to Reproduction

Matthew H. Sieber, Michael B. Thomsen, Allan C. Spradling

Research output: Contribution to journalArticle

34 Citations (Scopus)

Abstract

Summary Reproduction is heavily influenced by nutrition and metabolic state. Many common reproductive disorders in humans are associated with diabetes and metabolic syndrome. We characterized the metabolic mechanisms that support oogenesis and found that mitochondria in mature Drosophila oocytes enter a low-activity state of respiratory quiescence by remodeling the electron transport chain (ETC). This shift in mitochondrial function leads to extensive glycogen accumulation late in oogenesis and is required for the developmental competence of the oocyte. Decreased insulin signaling initiates ETC remodeling and mitochondrial respiratory quiescence through glycogen synthase kinase 3 (GSK3). Intriguingly, we observed similar ETC remodeling and glycogen uptake in maturing Xenopus oocytes, suggesting that these processes are evolutionarily conserved aspects of oocyte development. Our studies reveal an important link between metabolism and oocyte maturation.

Original languageEnglish (US)
Pages (from-to)420-432
Number of pages13
JournalCell
Volume164
Issue number3
DOIs
StatePublished - Jan 28 2016

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Glycogen Synthase Kinase 3
Oogenesis
Electron Transport
Nutrients
Oocytes
Reproduction
Glycogen
Food
Mitochondria
Nutrition
Medical problems
Metabolism
Insulin
Xenopus
Mental Competency
Drosophila

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)

Cite this

Electron Transport Chain Remodeling by GSK3 during Oogenesis Connects Nutrient State to Reproduction. / Sieber, Matthew H.; Thomsen, Michael B.; Spradling, Allan C.

In: Cell, Vol. 164, No. 3, 28.01.2016, p. 420-432.

Research output: Contribution to journalArticle

Sieber, Matthew H. ; Thomsen, Michael B. ; Spradling, Allan C. / Electron Transport Chain Remodeling by GSK3 during Oogenesis Connects Nutrient State to Reproduction. In: Cell. 2016 ; Vol. 164, No. 3. pp. 420-432.
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