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ELL associated factor 1 and ELL associated factor 2 (EAF1/2 factors) are reported to play important roles in tumor suppression and embryogenesis. Our previous studies showed that  eaf  factors mediated effective convergence and extension (C&E) movements and modulated mesoderm and neural patterning by regulating both non-canonical and canonical Wnt signaling in the early embryonic process. In this study, through knockdown of both  eaf1  and  eaf2  in embryos, we found that differentiation of primary erythroid cells was blocked, but hematopoietic precursor cells maintained in  eaf s morphants. Co-injection of  c-myb -MO rescued the erythroid differentiation in  eaf s morphants, as indicated by the restored expression of the erythroid-specific gene,  βe3 globin . In addition, low dosage of  c-myb  effectively blocked the  βe3 globin  expression in embryos, and did not affect the expression of markers of hematopoietic progenitor cells and other mesoderm, which was similar to the phenotypes we observed in  eaf s morphants. We also revealed that knockdown Wnt signaling by transiently inducing  dn-Tcf  in embryos at the bud stage down-regulated the increased  c-myb  to normal level and also restored  βe3 globin  expression in  eaf s morphants. Our evidence points to a novel role for  eaf  factors in controlling erythroid cell fate by regulating  c-Myb  expression through canonic Wnt signaling.

Eafs Control Erythroid Cell Fate by Regulating c-myb Expression through Wnt Signaling