| First Author | Sakamoto H | Year | 2015 |
| Journal | Stem Cells | Volume | 33 |
| Issue | 2 | Pages | 479-90 |
| PubMed ID | 25329760 | Mgi Jnum | J:223579 |
| Mgi Id | MGI:5659782 | Doi | 10.1002/stem.1855 |
| Citation | Sakamoto H, et al. (2015) Determining c-Myb protein levels can isolate functional hematopoietic stem cell subtypes. Stem Cells 33(2):479-90 |
| abstractText | The transcription factor c-Myb was originally identified as a transforming oncoprotein encoded by two avian leukemia viruses. Subsequently, through the generation of mouse models that affect its expression, c-Myb has been shown to be a key regulator of hematopoiesis, including having critical roles in hematopoietic stem cells (HSCs). The precise function of c-Myb in HSCs although remains unclear. We have generated a novel c-myb allele in mice that allows direct observation of c-Myb protein levels in single cells. Using this reporter line we demonstrate that subtypes of HSCs can be isolated based upon their respective c-Myb protein expression levels. HSCs expressing low levels of c-Myb protein (c-Myb(low) HSC) appear to represent the most immature, dormant HSCs and they are a predominant component of HSCs that retain bromodeoxyuridine labeling. Hematopoietic stress, induced by 5-fluorouracil ablation, revealed that in this circumstance c-Myb-expressing cells become critical for multilineage repopulation. The discrimination of HSC subpopulations based on c-Myb protein levels is not reflected in the levels of c-myb mRNA, there being no more than a 1.3-fold difference comparing c-Myb(low) and c-Myb(high) HSCs. This illustrates how essential it is to include protein studies when aiming to understand the regulatory networks that control stem cell behavior. |
