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First published online 19 January 2005
doi: 10.1242/dev.01601


Development 132, 817-828 (2005)
Published by The Company of Biologists 2005


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Lunatic fringe null female mice are infertile due to defects in meiotic maturation

Katherine L. Hahn1,4, Joshua Johnson2,*, Brian J. Beres2,4, Sheena Howard3,4 and Jeanne Wilson-Rawls1,2,4,{dagger}

1 Molecular and Cellular Graduate Program, Arizona State University, Tempe, AZ 85284-4501, USA
2 Biology Graduate Program, Arizona State University, Tempe, AZ 85284-4501, USA
3 Minority Access to Research Careers (MARC) Program at ASU, Arizona State University, Tempe, AZ 85284-4501, USA
4 School of Life Sciences, Box 4501, Arizona State University, Tempe, AZ 85284-4501, USA

{dagger} Author for correspondence (e-mail: nrawls{at}imap4.asu.edu)

Accepted 1 December 2004

We have demonstrated that Notch genes are expressed in developing mammalian ovarian follicles. Lunatic fringe is an important regulator of Notch signaling. In this study, data are presented that demonstrate that radical fringe and lunatic fringe are expressed in the granulosa cells of developing follicles. Lunatic fringe null female mice were found to be infertile. Histological analysis of the lunatic fringe-deficient ovary demonstrated aberrant folliculogenesis. Furthermore, oocytes from these mutants did not complete meiotic maturation. This is a novel observation because this is the first report describing a meiotic defect that results from mutations in genes that are expressed in the somatic granulosa cells and not the oocytes. This represents a new role for the Notch signaling pathway and lunatic fringe in mammalian folliculogenesis.

Key words: Lunatic fringe, Notch, Ovary, Follicle, Meiosis, Fertility




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