Abstract
The exact molecular mechanism underlying erythroblast enucleation has been a fundamental biological question for decades. In this study, we found that miR‐144/451 critically regulated erythroid differentiation and enucleation. We further identified CAP1, a G‐actin‐binding protein, as a direct target of miR‐144/451 in these processes. During terminal erythropoiesis, CAP1 expression declines along with gradually increased miR‐144/451 levels. Enforced CAP1 up‐regulation inhibits the formation of contractile actin rings in erythroblasts and prevents their terminal differentiation and enucleation. Our findings reveal a negative regulatory role of CAP1 in miR‐144/451‐mediated erythropoiesis and thus shed light on how microRNAs fine‐tune terminal erythroid development through regulating actin dynamics.
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