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.

• This report represents the work of one or more WPI undergraduate students submitted to the faculty as evidence of completion of a degree requirement. WPI routinely publishes these reports on its website without editorial or peer review.

Creator

• Gagnon, James Alan

Publisher

• Worcester Polytechnic Institute

Identifier

• 03D176M

Advisor

• Adams, David S.

Year

• 2003

Date created

• 2003-01-01

Resource type

• Major Qualifying Project

Major

• Biology & Biotechnology

Rights statement

• In Copyright