Faculty Advisor

Adams, David S.


Mdm2 is the primary regulator of the p53 tumor suppressor. In order to bypass early embryonic lethality of Mdm2 deletion, we utilized a conditional Mdm2 allele to study Mdm2 loss during development. The tissue-specific deletion of Mdm2 during embroyogenesis by a Cre recombinase transgene under transcriptional control of the Collagen Type 1- 3.6kb promoter results in severe caudal defects as a result of transgene activation as early as E6.5 in the developing embryo. Transgene activation was associated with an increase in apoptosis in the affected region of the embryo. Remarkably, transgene activation in connective and skeletal tissue later in development did not result in increased apoptosis in these tissues; in fact, skin and bone tissue developed normally without Mdm2. Instead, osteoprogenitor cells exhibited delayed differentiation. These results suggest that Mdm2 loss does not always result in cell death, and may, in certain cell types, influence differentiation.


Worcester Polytechnic Institute

Date Accepted

January 2003


Biology and Biotechnology

Project Type

Major Qualifying Project


Restricted-WPI community only

Advisor Department

Biology and Biotechnology