| First Author | Kristiansen TA | Year | 2016 |
| Journal | Immunity | Volume | 45 |
| Issue | 2 | Pages | 346-57 |
| PubMed ID | 27533015 | Mgi Jnum | J:301604 |
| Mgi Id | MGI:6140644 | Doi | 10.1016/j.immuni.2016.07.014 |
| Citation | Kristiansen TA, et al. (2016) Cellular Barcoding Links B-1a B Cell Potential to a Fetal Hematopoietic Stem Cell State at the Single-Cell Level. Immunity 45(2):346-57 |
| abstractText | Hematopoietic stem cells (HSCs) undergo a functional switch in neonatal mice hallmarked by a decrease in self-renewing divisions and entry into quiescence. Here, we investigated whether the developmental attenuation of B-1a cell output is a consequence of a shift in stem cell state during ontogeny. Using cellular barcoding for in vivo single-cell fate analyses, we found that fetal liver definitive HSCs gave rise to both B-1a and B-2 cells. Whereas B-1a potential diminished in all HSCs with time, B-2 output was maintained. B-1a and B-2 plasticity could be reinitiated in a subset of adult HSCs by ectopic expression of the RNA binding protein LIN28B, a key regulator of fetal hematopoiesis, and this coincided with the clonal reversal to fetal-like elevated self-renewal and repopulation potential. These results anchor the attenuation of B-1a cell output to fetal HSC behavior and demonstrate that the developmental decline in regenerative potential represents a reversible HSC state. |
