Cellular Barcoding Links B-1a B Cell Potential to a Fetal Hematopoietic Stem Cell State at the Single-Cell Level

Research output: Contribution to journalArticle

Bibtex

@article{a12a38e8c2994a988150c3a94fac36e5,
title = "Cellular Barcoding Links B-1a B Cell Potential to a Fetal Hematopoietic Stem Cell State at the Single-Cell Level",
abstract = "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.",
author = "Kristiansen, {Trine A.} and {Jaensson Gyllenb{\"a}ck}, Elin and Alya Zriwil and Tomas Bj{\"o}rklund and Daniel, {Jeremy A.} and Ewa Sitnicka and Shamit Soneji and David Bryder and Joan Yuan",
year = "2016",
doi = "10.1016/j.immuni.2016.07.014",
language = "English",
volume = "45",
pages = "346--357",
journal = "Immunity",
issn = "1074-7613",
publisher = "Cell Press",
number = "2",

}