Musashi-2 controls cell fate, lineage bias, and TGF-β signaling in HSCs
Deering, Raquel P.
Lengner, Christopher J.
Kharas, Michael G.Note: Order does not necessarily reflect citation order of authors.
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CitationPark, S., R. P. Deering, Y. Lu, P. Tivnan, S. Lianoglou, F. Al-Shahrour, B. L. Ebert, et al. 2014. “Musashi-2 controls cell fate, lineage bias, and TGF-β signaling in HSCs.” The Journal of Experimental Medicine 211 (1): 71-87. doi:10.1084/jem.20130736. http://dx.doi.org/10.1084/jem.20130736.
AbstractHematopoietic stem cells (HSCs) are maintained through the regulation of symmetric and asymmetric cell division. We report that conditional ablation of the RNA-binding protein Msi2 results in a failure of HSC maintenance and engraftment caused by a loss of quiescence and increased commitment divisions. Contrary to previous studies, we found that these phenotypes were independent of Numb. Global transcriptome profiling and RNA target analysis uncovered Msi2 interactions at multiple nodes within pathways that govern RNA translation, stem cell function, and TGF-β signaling. Msi2-null HSCs are insensitive to TGF-β–mediated expansion and have decreased signaling output, resulting in a loss of myeloid-restricted HSCs and myeloid reconstitution. Thus, Msi2 is an important regulator of the HSC translatome and balances HSC homeostasis and lineage bias.
Citable link to this pagehttp://nrs.harvard.edu/urn-3:HUL.InstRepos:12717470
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