Stuart A. Wallace Chair and Professor, Departments of Pathology, Molecular & Cellular Biology, and Molecular and Human Genetics; Program in Developmental Biology
Co-Director, Medical Scientist Training Program

B.A., University of Chicago, 1982
M.D., Ph.D., Washington University School of Medicine, 1989
Postdoc, Baylor College of Medicine, 1993

RESEARCH INTERESTS:

Reproductive and embryonic development are complex processes which require the coordinate interaction of multiple proteins. The overall research goals of my laboratory are directed at elucidating the critical proteins involved in both normal and abnormal reproductive development. These studies are focusing on both extragonadal regulators such as luteinizing hormone and follicle stimulating hormone and intragonadal regulators such as the inhibins, activins, and growth/differentiation factor 9 (GDF-9). These latter proteins are members of the large TGF-b's superfamily of secreted growth factors and appear to play important roles in multiple tissues as endocrine, paracrine, and autocrine mediators during both embryonic and adult development.

To characterize the roles of these proteins in mammalian reproduction and development, we have taken a systematic approach to generate standard transgenic mice as well as "knock-out" mice deficient in a number of these genes using gene targeting and embryonic stem (ES) cell technology. Analysis of the mice generated in these "gain of function" and "loss of function" experiments have revealed the critical roles of several of these proteins in mammalian reproduction, development, and oncogenesis. Initial studies to generate mice deficient in the inhibins have already demonstrated the power of this approach revealing that inhibin is a novel tumor suppressor with specificity for the gonads and the adrenal gland. Similarly, mice lacking GDF-9 have defined it as the first oocyte-derived growth factor required for somatic cell function in vivo. Current studies using these transgenic mice as in vivo tools will enable us to more fully understand the relationship of these proteins in reproduction, development, and oncogenesis.

SELECTED PUBLICATIONS:

1. Rajkovic A, Pangas SA, Ballow D, Suzumori N, Matzuk MM (2004). NOBOX deficiency disrupts early folliculogenesis and oocyte-specific gene expression. Science 305: 115-117.

2. Burns KH, Viveiros MM, Ren Y, Wang P, DeMayo F, Frail DE, Eppig JJ, Matzuk MM (2003). Roles of NPM2 in chromatin and nucleolar organization in oocytes and embryos. Science 300: 633-636.

3. Wu X, Viveiros M, Eppig JJ, Bai Y, Fitzpatrick S, Matzuk MM (2003). Zygote arrest 1 (Zar1) is a novel maternal effect gene critical for the oocyte-to-embryo transition. Nat. Genet. 33: 187-191.

4. Matzuk MM, Lamb DJ (2002). Genetic dissection of mammalian fertility pathways. Nat. Med. 8: S33-S40.

5. Matzuk MM, Burns KH, Viveiros MM, Eppig JJ (2002). Intercellular communication in the mammalian ovary: Oocytes carry the conversation. Science 296: 2178-2180.

6. Brown CW, Houston-Hawkins DE, Woodruff TK, Matzuk MM (2000). Insertion of Inhbb into the Inhba locus rescues the Inhba-null phenotype and reveals new activin functions. Nat. Genet. 25: 453-457.

7. Shou W, Aghdasi B, Armstrong DL, Guo Q, Bao S, Charng M-J, Mathews LS, Schneider MD, Hamilton SL, Matzuk MM (1998). Cardiac defects and altered ryanodine receptor function in mice lacking FKBP12. Nature 391: 489-492.

8. Kumar TR, Wang Y, Lu N, Matzuk MM (1997). Follicle stimulating hormone is required for ovarian follicle maturation but not male fertility. Nat. Genet. 15: 201-204.

9. Dong J, Albertini DF, Nishimori K, Kumar TR, Lu N, Matzuk MM (1996). Growth differentiation factor-9 is required during early folliculogenesis. Nature 383: 531-535.

For more publications, see listing on Pub Med.

CONTACT INFORMATION:

Martin M. Matzuk, M.D., Ph.D.
Department of Pathology
Baylor College of Medicine
One Baylor Plaza
Houston, Texas 77030, U.S.A.

Phone: 713-798-6451
Fax: 713-798-5833
E-mail:

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