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Adenosine-to-inosine RNA editing by ADAR1 is essential for normal murine erythropoiesis

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Seeburg,  Peter H.
Department of Molecular Neurobiology, Max Planck Institute for Medical Research, Max Planck Society;

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Citation

Liddicoat, B. J., Hartner, J. C., Piskol, R., Ramaswami, G., Chalka, A. M., Kingsley, P. D., et al. (2016). Adenosine-to-inosine RNA editing by ADAR1 is essential for normal murine erythropoiesis. Experimental Hematology, 44(10), 947-963. doi:10.1016/j.exphem.2016.06.250.


Cite as: http://hdl.handle.net/11858/00-001M-0000-002C-B282-6
Abstract
Adenosine deaminases that act on RNA (ADARs) convert adenosine residues to inosine in doublestranded RNA. In vivo, ADAR1 is essential for the maintenance of hematopoietic stem/progenitors. Whether other hematopoietic cell types also require ADAR1 has not been assessed. Using erythroid- and myeloid-restricted deletion of Adar1, we demonstrate that ADAR1 is dispensable for myelopoiesis but is essential for normal erythropoiesis. Adar1-deficient erythroid cells display a profound activation of innate immune signaling and high levels of cell death. No changes in microRNAlevels were found inADAR1-deficient erythroid cells. Using an editing-deficient allele, we demonstrate thatRNA editing is the essential function ofADAR1 during erythropoiesis.Mapping of adenosine-to-inosine editing in purified erythroid cells identified clusters of hyperedited adenosines located in long 3’-untranslated regions of erythroid-specific transcripts and these are ADAR1-specific editing events. ADAR1-mediated RNA editing is essential for normal erythropoiesis.