| First Author | Sano T | Year | 2023 |
| Journal | Genes (Basel) | Volume | 14 |
| Issue | 8 | PubMed ID | 37628583 |
| Mgi Jnum | J:360125 | Mgi Id | MGI:7797501 |
| Doi | 10.3390/genes14081531 | Citation | Sano T, et al. (2023) Impaired Repopulating Ability of Uhrf2(-/-) Hematopoietic Progenitor Cells in Mice. Genes (Basel) 14(8) |
| abstractText | UHRF proteins catalyze the ubiquitination of target proteins and are involved in regulating gene expression. Some studies reported a reduced expression of UHRF2 in acute leukemia cells, but the role of UHRF2 in hematopoiesis remains unknown. Here, we generated Uhrf2(-/-) mice to clarify the role of UHRF2 deletion in hematopoiesis. Compared to Uhrf2(+/+) mice, Uhrf2(-/-) mice showed no differences in complete blood counts, as well as bone marrow (BM) findings and spleen weights. Proportions of cells in progenitor fractions in BM were comparable between Uhrf2(+/+) mice and Uhrf2(-/-) mice. However, in competitive repopulation assays with BM transplants (BMT), the proportions of Uhrf2(-/-) cells were decreased relative to Uhrf2(+/+) cells in all lineages. After the second BMT, Uhrf2(-/-) neutrophils were few, while 20-30% of Uhrf2(-/-) T cells and B cells were still detected. RNA sequencing showed downregulation of some genes associated with stem-cell function in Uhrf2(-/-) hematopoietic stem/progenitor cells (HSPCs). Interestingly, trimethylated histone H3 lysine 9 was increased in Uhrf2(-/-) HSPCs in a cleavage under targets and tagmentation assay. While UHRF2 deletion did not cause hematologic malignancy or confer a growth advantage of HSPCs, our results suggest that UHRF2 may play a role in the regulation of hematopoiesis. |
