Edward A. Freeman
Title: Associate Professor
Office: ISHS 205
Phone: (585) 385-7289
Education: Ph.D., University of South Carolina
M.A., Kent State University
B.S., Ohio University
Areas of Interest: Reproductive endocrinology; endocrine disruptors and the impact on oocyte biology
Using environmental pollutants, termed endocrine disruptors, students working in the Freeman lab focus their studies on zebrafish ovarian follicle maturation and or primordial germ cell migration. These studies are aimed at providing a more detailed understanding of the role of environmental pollutants on reproductive cell biology both in the adult and the developing embryo from a widely used vertebrate developmental biology model.
BIOL 120C - General Biology: Genes, Cells, Evolution
BIOL 127L - General Biology Lab
BIOL 128C - General Zoology
BIOL 349 - Junior Seminar
BIOL 310 - Reproductive Biology
BIOL 425 - Endocrinology
The focus of my basic science research program is to determine the effects of endocrine disruptors on reproductive cells. Specifically, I study ovarian follicular maturation in the adult and germ cell migration during early embryonic development; both lines of experimentation utilize zebrafish (a vertebrate model heavily used in developmental biology and genetics). Endocrine disruptors (EDs) are prominent in the environment as herbicides, pesticides, plasticizers and numerous other agents. These compounds have been shown to negatively impact both wildlife and human populations, often through binding to steroid receptors. Because of their potential to bind steroid receptors these compounds are particularly disruptive to the tightly controlled mechanisms of neural and reproductive development as well as adult neural, thyroid and reproductive function.
As human females approach menopause there is an increasing chance of conceiving children with chromosomal anomalies such as too many (e.g. Down Syndrome, trisomy 21) or too few (e.g. Turner Syndrome, monosomy X [XO]) copies of a specific chromosome. This is called the maternal age affect; the mechanism(s) that underlie the maternal age affect are not known. However, the condition is thought to be caused by a failure of normal chromosome congression and segregation during reproductive cell division. In experimental animals there is no naturally occurring maternal age affect which has made study of the human condition challenging. However, when animals are exposed to chemicals that alter their normal endocrine environment (for example, certain EDs) their reproductive cells can present a phenotype nearly identical to the human maternal age effect. This demonstrates that EDs can be used as research tools to induce cellular changes in the controlled laboratory setting. Therefore, exposure of animal models to EDs with concurrent studies that access the impact(s) of ED exposure on cellular activities may provide insight into what changes are occurring in reproductive cells from aging human females. The goal of this line of experimentation is to determine the impact of EDs on zebrafish oocyte biology.
A related project involves the generation of a transgenic zebrafish line that will allow for the direct microscopic visualization of the meiotic spindle following exposure of the zebrafish follicle to specific EDs. Students in my lab have identified various EDs that alter follicular maturation rates which suggests these EDs may have an impact on meiotic spindle assembly or chromosome organization on the meiotic spindle. Only with direct visualization can this affect be verified. Following the generation of transgenic zebrafish we hope to demonstrate that zebrafish follicles cultured in the presence of specific EDs have meiotic defects that mimic the human maternal age effect. This will provide strong support for the use of specific EDs in future studies as we attempt to tease apart changes in cellular signaling and activity associated with ED exposure.
A complimentary line of investigation aimed at studying primordial germ cell migration in the presence of EDs will begin in the fall of 2010. Because primordial germ cells express steroid receptors, migrate along a chemical gradient (morphogen gradient), and must respond to chemical cues in their local environment, the presence of EDs is predictably problematic to proper migration patterns. This work will follow up on published work demonstrating negative effects of insecticides and detergent precursors on early germ cell migration. This work is important in the context of species sustainability and preservation in the presence of ever increasing aquatic and terrestrial pollution levels.
- Freeman, E. The Design and Implementation of an Effective Career Orientation Course for Undergraduate Science Majors. Biosciene, accepted pending revisions, June 2010.
- Valentino, L. and Freeman, E. Career Center, Faculty, Alumni Build Mock Interview Program Together: A collaboration between career center and faculty yields benefits for all. NACE Journal. 2010, pp. 29-32.
- Freeman, E. and Lynd-Balta, E. Developing Information Literacy Skills Early in an Undergraduate Curriculum. The Journal of College Teaching. 2010, Vol 58, pp. 109-115.
- Johnson, M., Freeman, E., Gardner, D., and Hunt, P. Oxidative Metabolism of Pyruvate is Required for Meiotic Maturation of Oocytes In-Vivo. Biology of Reproduction. 2007, Vol. 77 (1), pp. 2-8.
- Susiarjo, M., Hassold, T., Freeman, E., and Hunt, P. Bisphenol A Exposure In Utero Disrupts Early Oogenesis in the Mouse. PLoS Genet. 2007, Vol. 3(1):e5.
- Freeman, E., Jani, P., and Millette, C. Expression and Potential Function of Rho Family Small G Proteins in Cells of the Mammalian Seminiferous Epithelium. Cell Communication and Adhesion 2002, Vol. 9(4), 189-204.