Missing oocyte: connecting meiotic progression and metabolism in early oogenesis

Wednesday, October 10, 2012 — Poster Session II
Noon – 2:00 p.m	Natcher Conference Center, Building 45	NICHD	DEV-12

Authors

• J.C. Reich
• Y. Wei
• W. Laursen
• M.L. Lilly

Abstract

Chromosome missegregation during female meiosis is the leading cause of miscarriages and birth defects in humans. Recent evidence suggests that many meiotic errors are downstream of defects in oocyte growth and/or the hormonal signaling pathways that drive the differentiation of the oocyte. Yet, how oocytes coordinate meiotic progression with gametogenesis remains poorly understood in metazoans. We use the molecular genetics available in the model organism Drosophila melanogaster to delineate the pathways that regulate meiotic progression during oogenesis. In previous work we identified two genes required to maintain the meiotic cycle and the oocyte fate during the extended process of oogenesis, missing oocyte (mio) and seh11. In yeast, the Mio and Seh1 proteins are components of a newly identified complex (SEA-Complex) that regulates nutritional sensing and metabolism upstream of the Target of Rapamycin signaling pathway2. Our biochemical and genetic studies indicate that the SEA-complex is conserved in metazoans and functions to regulate metabolism. This work strongly suggests that metabolic pathways influence meiotic progression and oocyte differentiation in early oogenesis.

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