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Erythropoietin (EPO) is a key regulator of erythropoiesis. The embryonic liver is the main site of erythropoietin synthesis, after which the kidney takes over. The adult liver retains the ability to express EPO, and we discovered here new players of this transcription, distinct from the classical hypoxia-inducible factor pathway. In mice, genetically invalidated in hepatocytes for the chromatin remodeler  Arid1a , and for  Apc , the major silencer of Wnt pathway, chromatin was more accessible and histone marks turned into active ones at the  Epo  downstream enhancer. Activating β-catenin signaling increased binding of Tcf4/β-catenin complex and upregulated its enhancer function. The loss of  Arid1a  together with β-catenin signaling, resulted in cell-autonomous  EPO  transcription in mouse and human hepatocytes. In mice with  Apc-Arid1a  gene invalidations in single hepatocytes, Epo de novo synthesis led to its secretion, to splenic erythropoiesis and to dramatic erythrocytosis. Thus, we identified new hepatic  EPO  regulation mechanism stimulating erythropoiesis.

ARID1A loss in adult hepatocytes activates β-catenin-mediated erythropoietin transcription