Aberrant activation of p53 due to loss of MDM2 or MDMX causes early lens dysmorphogenesis.

ABSTRACT: Although forming a heterodimer or heterooligomer is essential for MDM2 and MDMX to fully control p53 during early embryogenesis, deletion of either MDM2 or MDMX in specific tissues using the loxp-Cre system reveals phenotypic diversity during organ morphogenesis, which can be completely rescued by loss of p53, suggesting the spatiotemporal independence and specificity of the regulation of p53 by MDM2 and MDMX. In this study, we investigated the role of the MDM2-MDMX-p53 pathway in the developing lens that is a relatively independent region integrating cell proliferation, differentiation and apoptosis. Using the mice expressing Cre recombinase specifically in the lens epithelial cells (LECs) beginning at E9.5, we demonstrated that deletion of either MDM2 or MDMX induces apoptosis of LEC and

SUBMITTER: Zhang Y 

PROVIDER: S-EPMC5393629 | biostudies-literature | 2014 Dec

REPOSITORIES: biostudies-literature