Graduate School of Frontier Biosciences, Osaka University


Colloquium 192

Speaker Joanne Y. Yew (Assistant Professor, University of Hawaii at Manoa)
Title Microbiome Control of Oogenesis
Speaker Shinichi Kawaguchi (Assistant Professor, Germline Biology Group)
Title Drosophila Meiosis Arrest Female protein-1 (dMarf1) is essential for the oocyte maturation
Date Wed., July 18, 2018, 12:15~13:00
Place 2F Seminar room, BioSystems Building
Host Shinichi Kawaguchi (Assistant Professor, Germline Biology Group)
Tel: 06-6879-7974
E-mail: shinkawa[at]

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Microbiome Control of Oogenesis

One of the major scientific discoveries of the past decade has been the realization that the microbial world plays a significant role in our health and physiology. Without a microbiome (i.e., microbial partners that live in all organisms), an animal’s fertility is significantly compromised. Little is known, however, about how the microbiome supports and enhances host fertility. In this talk, I will introduce an experimental paradigm using Drosophila that will allow us to determine how the microbiome modulates host fertility at the cellular and molecular level. Preliminary studies reveal that gut microbiota boost female oogenesis by inhibiting cell death in the ovaries and changing the lipid composition of the host.

Drosophila Meiosis Arrest Female protein-1 (dMarf1) is essential for the oocyte maturation

dMarf1 is a Drosophila homolog of the mouse MARF1 (Meiosis Arrest Female Protein-1). They are highly conserved and share the functional domains (RRM and OST/Lotus domains). In mouse, MARF1 is required to resume the meiosis arrested in mature oocyte. But, its molecular mechanism remains to be elucidated. We analyzed the molecular function of dMarf1. dMarf1 expressed in the late stage of oogenesis and accumulated in the oocyte. Embryo lacking the functional dMarf1 could not enter the mitotic division, suggesting that the transition from meiosis and mitosis was compromised in KO mutant. We have identified several molecular factors that are affected by dMarf1 KO and propose the possible signaling pathway that the dMarf1 is involved in.