E2F4 is essential for normal erythrocyte maturation and neonatal viability.
Document Type
Article
Publication Date
2000
Keywords
Animals-Newborn, Cell-Cycle, Cell-Division, Craniofacial-Abnormalities, Disease-Susceptibility, DNA-Binding-Proteins, Erythrocytes, Fetal-Development, Fetal-Growth-Retardation, Mice, Mice-Knockout, Opportunistic-Infections, Recombinant-Proteins, SUPPORT-NON-U-S-GOVT, SUPPORT-U-S-GOVT-P-H-S, Transcription-Factors
First Page
281
Last Page
291
JAX Source
Mol Cell 2000 Aug; 6(2):281-91.
Abstract
The retinoblastoma protein (pRB) plays a key role in the control of normal development and proliferation through the regulation of the E2F transcription factors. We generated a mutant mouse model to assess the in vivo role of the predominant E2F family member, E2F4. Remarkably, loss of E2F4 had no detectable effect on either cell cycle arrest or proliferation. However, E2F4 was essential for normal development. E2f4-/- mice died of an increased susceptibility to opportunistic infections that appeared to result from craniofacial defects. They also displayed a variety of erythroid abnormalities that arose from a cell autonomous defect in late stage maturation. This suggests that E2F4 makes a major contribution to the control of erythrocyte development by the pRB tumor suppressor.
Recommended Citation
Humbert PO,
Rogers C,
Ganiatsas S,
Landsberg RL,
Trimarchi JM,
Dandapani S,
Brugnara C,
Erdman S,
Schrenzel M,
Bronson RT,
Lees JA.
E2F4 is essential for normal erythrocyte maturation and neonatal viability. Mol Cell 2000 Aug; 6(2):281-91.