| First Author | Zhao X | Year | 2020 |
| Journal | Elife | Volume | 9 |
| PubMed ID | 32820720 | Mgi Jnum | J:294998 |
| Mgi Id | MGI:6458173 | Doi | 10.7554/eLife.55360 |
| Citation | Zhao X, et al. (2020) beta-catenin and gamma-catenin are dispensable for T lymphocytes and AML leukemic stem cells. Elife 9:e55360 |
| abstractText | The beta-catenin transcriptional coregulator is involved in various biological and pathological processes; however, its requirements in hematopoietic cells remain controversial. We re-targeted the Ctnnb1 gene locus to generate a true beta-catenin-null mutant mouse strain. Ablation of beta-catenin alone, or in combination with its homologue gamma-catenin, did not affect thymocyte maturation, survival or proliferation. Deficiency in beta/gamma-catenin did not detectably affect differentiation of CD4(+)T follicular helper cells or that of effector and memory CD8(+) cytotoxic cells in response to acute viral infection. In an MLL-AF9 AML mouse model, genetic deletion of beta-catenin, or even all four Tcf/Lef family transcription factors that interact with beta-catenin, did not affect AML onset in primary recipients, or the ability of leukemic stem cells (LSCs) in propagating AML in secondary recipients. Our data thus clarify on a long-standing controversy and indicate that beta-catenin is dispensable for T cells and AML LSCs. |
