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The Polycomb group gene  Bmi1  is essential for the proliferation of neural and hematopoietic stem cells. Much remains to be learned about the pathways involved in the severe hematopoietic phenotype observed in  Bmi1  homozygous mutant mice except for the fact that loss of  p53  or concomitant loss of  p16 Ink4a   and  p19 Arf   functions achieves only a partial rescue. Here we report the identification of E4F1, an inhibitor of cellular proliferation, as a novel BMI1-interacting partner in hematopoietic cells. We provide evidence that  Bmi1  and  E4f1  genetically interact in the hematopoietic compartment to regulate cellular proliferation. Most importantly, we demonstrate that reduction of  E4f1  levels through RNA interference mediated knockdown is sufficient to rescue the clonogenic and repopulating ability of  Bmi1  −/−  hematopoietic cells up to 3 mo post-transplantation. Using cell lines and MEF, we also demonstrate that INK4A/ARF and p53 are not essential for functional interaction between  Bmi1  and  E4f1 . Together, these findings identify E4F1 as a key modulator of BMI1 activity in primitive hematopoietic cells.

E4F1: a novel candidate factor for mediating BMI1 function in primitive hematopoietic cells