Dp1 is required for extra-embryonic development.
Document Type
Article
Publication Date
2003
Keywords
Cell-Cycle-Proteins, DNA-Binding-Proteins, Fetal-Death, Gene-Expression-Regulation-Developmental, Gene-Targeting, Genes-Lethal, Mice, Mice-Knockout, Protein-p53, SUPPORT-NON-U-S-GOVT, SUPPORT-U-S-GOVT-P-H-S, Transcription-Factors, Trophoblasts
First Page
1295
Last Page
1305
JAX Source
Development 2003 Apr; 130(7):1295-1306.
Abstract
Release of E2F1/DP1 heterodimers from repression mediated by the retinoblastoma tumor suppressor (pRB) triggers cell cycle entry into S phase, suggesting that E2F1 and DP1 proteins must act in unison, either to facilitate or to suppress cell-cycle progression. In stark contrast to the milder phenotypes that result from inactivation of E2Fs, we report that loss of Dp1 leads to death in utero because of the failure of extra-embryonic development. Loss of Dp1 compromises the trophectoderm-derived tissues - specifically, the expansion of the ectoplacental cone and chorion, and endoreduplication in trophoblast giant cells. Inactivation of p53 is unable to rescue the Dp1-deficient embryonic lethality. Thus, DP1 is absolutely required for extra-embryonic development and consequently embryonic survival, consistent with E2F/DP1 normally acting to promote growth in vivo.
Recommended Citation
Kohn MJ,
Bronson RT,
Harlow E,
Dyson NJ,
Yamasaki L.
Dp1 is required for extra-embryonic development. Development 2003 Apr; 130(7):1295-1306.