Degree Type

Honors Capstone Project

Date of Submission

Spring 5-1-2005

Capstone Advisor

Dr. Melissa Pepling

Honors Reader

Dr. Eleanor Maine

Capstone Major

Biology

Capstone College

Arts and Science

Audio/Visual Component

no

Capstone Prize Winner

no

Won Capstone Funding

no

Honors Categories

Sciences and Engineering

Subject Categories

Biology

Abstract

Although critically important to fertility and reproduction, the mechanisms controlling development of mammalian primordial germ cells into functional oocytes are poorly understood. Understanding the mechanisms that regulate oocyte development will ultimately reveal significant insights into female infertility problems in mammals, including humans. In order to decipher what mediates the formation of a functional oocyte, we are studying oogenesis in the mammalian model Mus musculus. During mouse embryonic development the oocytes develop as interconnected clusters of cells called germline cysts. Evidence suggests that in humans, oocytes are also organized into cysts. Eventually the cysts undergo programmed cell breakdown, each giving rise to at least one oocyte. In the mouse, a subset of cells in each cyst dies, with only a third of the original number of oocytes surviving. DAX-1 encodes a transcription factor that has been implicated in sex determination and gonad differentiation. Adult female mice lacking the Dax-1 gene exhibit an abnormal multiple oocyte follicle phenotype. These multiple oocyte follicles may be cysts that never completed the cyst breakdown process. To determine if Dax-1 plays a role in the process of cyst breakdown, ovaries from animals lacking Dax-1 were examined at postnatal day (PND) 7 which is just after cyst breakdown is completed. PND7 mutants had reduced cyst breakdown and reduced oocyte survival. In addition, expression of Dax-1 was examined in normal mice and was found to be present during the cyst breakdown period.

Creative Commons License

Creative Commons Attribution-Noncommercial-No Derivative Works 3.0 License
This work is licensed under a Creative Commons Attribution-Noncommercial-No Derivative Works 3.0 License.

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