Jeffrey Mason Graduate Student (Ph.D program) Major Professor: Dr. Gary B. Anderson   Phone: (530) 752-7544 FAX: ( 530)752-0175 E-Mail: jbmason@ucdavis.edu

Education

B.S., Animal Science, University of California, Davis,1999
M.S., Animal Science, University of California, Davis,2001
Ph.D., Molecular, Cellular and Integrative Physiology with a Designated Emphasis in Reproductive Biology, University of California, Davis (In Progress)

Project:  

Title: Investigating the Perturbations Observed in Clone Murine Concepti

Description: A growing number of reports have documented the adverse effects of in vitro manipulation and culture of mammalian embryos on postimplantation growth and development. The in vitro-production of morphologically normal preimplantation embryos does not guarantee that their postimplantation development will be normal. It is therefore appropriate to understand the precise nature of culture and manipulation-induced abnormalities and to investigate the causal mechanisms involved. Aberrant fetal growth is observed in most mammalian species studied and can arise as a consequence of different in vitro interventions. The phenotypic consequences of culture and manipulation of preimplantation embryos, and their frequency of occurrence, are extremely diverse. Extensive documentation exists on abnormalities that arise as a consequence of in vitro-manipulation of murine embryos. Fetal and/or placental overgrowth is commonly reported for in vitro-manipulated murine embryos with clone concepti displaying the more severe perturbations.

A prominent morphological abnormality commonly found among histologically examined cloned placentae is expansion of the spongiotrophoblast layer, with an increased number of glycogen cells and enlarged spongiotrophoblast cells. Spongiotrophoblast cells differentiate from polar trophectoderm cells, which in turn have differentiated from trophectoderm cells.

These and other similar findings are the foundation on which I base my hypothesis that perturbations in the trophectoderm are the origin of fetal and placental overgrowth. To test this hypothesis effectively, I will separate inner cell mass (ICM) and trophectoderm influences by employing separate cellular origins for the ICM and trophectoderm. To accomplish this, different genetic strains of experimental animals, and ICM and trophectoderm of different developmental potential will be employed.