Viable Gata2 deficient mice exhibit T cell development independent of adult definitive hematopoiesis.

Gata2 is indispensable for hematopoiesis, with knockout mice typically exhibiting embryonic lethality attributed to severe anemia and defective hematopoietic stem cell (HSC) development. Intriguingly, we obtained viable adult Gata2-/- mice harboring a 17-nucleotide deletion in exon 2, which displayed intact T-cell development despite a significantly reduced bone marrow HSC pool. While mutant HSCs exhibited attenuated lymphoid potential, they retained partial myeloid reconstitution capacity. Single-cell transcriptomic analysis revealed compensatory upregulation of key hematopoietic regulators, including Fos and Klf6, in Gata2-deficient HSCs. Comprehensive profiling further demonstrated preservation of the complete T-cell hierarchy, including all major subsets, in Gata2 mutant mice. These findings provide evidence that Gata2 knockout mice may be viable, and T-cell development may proceed independently of definitive hematopoiesis.