E2F4 is essential for normal erythrocyte maturation and neonatal viability

Patrick O. Humbert, Catherine Rogers, Soula Ganiatsas, Rebecca L. Landsberg, Jeffrey M. Trimarchi, Savita Dandapani, Carlo Brugnara, Susan Erdman, Mark Schrenzel, Roderick T. Bronson, Jacqueline A. Lees

Research output: Contribution to journalArticlepeer-review

155 Scopus citations


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.

Original languageEnglish
Pages (from-to)281-291
Number of pages11
JournalMolecular Cell
Issue number2
StatePublished - 2000
Externally publishedYes


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