Cellular Barcoding Links B-1a B Cell Potential to a Fetal Hematopoietic Stem Cell State at the Single-Cell Level
Kristiansen, Trine A. LU ; Jaensson Gyllenbäck, Elin LU ; Zriwil, Alya LU ; Björklund, Tomas LU ; Daniel, Jeremy A. ; Sitnicka, Ewa LU ; Soneji, Shamit LU ; Bryder, David LU and Yuan, Joan LU
(2016)
In Immunity
45(2).
p.346-357
- 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... (More)
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.
(Less)
- author
- Kristiansen, Trine A.
LU
; Jaensson Gyllenbäck, Elin
LU
; Zriwil, Alya
LU
; Björklund, Tomas
LU
; Daniel, Jeremy A.
; Sitnicka, Ewa
LU
; Soneji, Shamit
LU
; Bryder, David
LU
and Yuan, Joan
LU
- organization
- publishing date
- 2016
- type
- Contribution to journal
- publication status
- published
- subject
- in
- Immunity
- volume
- 45
- issue
- 2
- pages
- 12 pages
- publisher
- Cell Press
- external identifiers
-
- pmid:27533015
- wos:000382267300016
- scopus:85002548279
- ISSN
- 1074-7613
- DOI
- 10.1016/j.immuni.2016.07.014
- language
- English
- LU publication?
- yes
- id
- a12a38e8-c299-4a98-8150-c3a94fac36e5
- date added to LUP
- 2016-12-30 13:53:48
- date last changed
- 2024-04-05 12:25:33
@article{a12a38e8-c299-4a98-8150-c3a94fac36e5,
abstract = {{<p>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.</p>}},
author = {{Kristiansen, Trine A. and Jaensson Gyllenbäck, Elin and Zriwil, Alya and Björklund, Tomas and Daniel, Jeremy A. and Sitnicka, Ewa and Soneji, Shamit and Bryder, David and Yuan, Joan}},
issn = {{1074-7613}},
language = {{eng}},
number = {{2}},
pages = {{346--357}},
publisher = {{Cell Press}},
series = {{Immunity}},
title = {{Cellular Barcoding Links B-1a B Cell Potential to a Fetal Hematopoietic Stem Cell State at the Single-Cell Level}},
url = {{http://dx.doi.org/10.1016/j.immuni.2016.07.014}},
doi = {{10.1016/j.immuni.2016.07.014}},
volume = {{45}},
year = {{2016}},
}