| First Author | Byon JC | Year | 2014 |
| Journal | Exp Hematol | Volume | 42 |
| Issue | 10 | Pages | 852-6.e1 |
| PubMed ID | 24971698 | Mgi Jnum | J:230155 |
| Mgi Id | MGI:5755573 | Doi | 10.1016/j.exphem.2014.06.004 |
| Citation | Byon JC, et al. (2014) Deletion of Dicer in late erythroid cells results in impaired stress erythropoiesis in mice. Exp Hematol 42(10):852-6.e1 |
| abstractText | MicroRNAs (miRNAs) have been shown to influence erythroid lineage commitment and differentiation; however, our knowledge of miRNA function in terminal erythropoiesis remains limited. To address this issue, we generated a novel animal model, where the miRNA-processing enzyme, Dicer, is selectively inactivated in erythropoietin receptor positive erythroid cells beginning with CFU-e/proerythroblast cells. This results in significant depletion of all miRNAs from the proerythroblast stage onwards, with one exception, miR-451, which is processed by Ago2 in a Dicer-independent manner. We observed that mature Dicer-dependent miRNAs, like miR-451, are dispensable under steady-state conditions, but these mutants have an impaired response to stress erythropoiesis, as demonstrated by a delay in recovery from anemia. This defect was specific to later maturing erythroid cells, as progenitor numbers were unaffected. In addition to generating a novel mouse model to study miRNA function in late erythroid cells, we conclude that miRNAs (both Dicer-dependent and independent) act primarily to regulate the optimal response to stress among late erythroid cells. |
