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Publication : PLZF mutation alters mouse hematopoietic stem cell function and cell cycle progression.

First Author  Vincent-Fabert C Year  2016
Journal  Blood Volume  127
Issue  15 Pages  1881-5
PubMed ID  26941402 Mgi Jnum  J:233011
Mgi Id  MGI:5780609 Doi  10.1182/blood-2015-09-666974
Citation  Vincent-Fabert C, et al. (2016) PLZF mutation alters mouse hematopoietic stem cell function and cell cycle progression. Blood 127(15):1881-5
abstractText  Hematopoietic stem cells (HSCs) give rise to all blood populations due to their long-term self-renewal and multipotent differentiation capacities. Because they have to persist throughout an organism's life span, HSCs tightly regulate the balance between proliferation and quiescence. Here, we investigated the role of the transcription factor promyelocytic leukemia zinc finger (plzf) in HSC fate using the Zbtb16(lu/lu)mouse model, which harbors a natural spontaneous mutation that inactivates plzf. Regenerative stress revealed that Zbtb16(lu/lu)HSCs had a lineage-skewing potential from lymphopoiesis toward myelopoiesis, an increase in the long-term-HSC pool, and a decreased repopulation potential. Furthermore, oldplzf-mutant HSCs present an amplified aging phenotype, suggesting that plzf controls age-related pathway. We found that Zbtb16(lu/lu)HSCs harbor a transcriptional signature associated with a loss of stemness and cell cycle deregulation. Lastly, cell cycle analyses revealed an important role for plzf in the regulation of the G1-S transition of HSCs. Our study reveals a new role for plzf in regulating HSC function that is linked to cell cycle regulation, and positions plzf as a key player in controlling HSC homeostasis.
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