Figure 7. Sox17 Deletion from Neonatal HSCs Induces Cell Death, and the Postnatal Decline in Sox17 Expression by Wild-Type HSCs Is Associated with a Transition to an Adult Phenotype.

(A and B) Sca-1⁺Lineage⁻c-kit⁺CD48⁻ HSCs isolated from the bone marrow of neonatal Mx-1-Cre⁺Sox17^fl/GFP mice 5 days after pIpC treatment exhibited normal cell-cycle distribution relative to littermate controls (A) but a 3-fold increased frequency of cells undergoing cell death (Annexin V⁺; B).

(C–F) GFP⁺ (Sox17-expressing) and GFP⁻ (Sox17-non-expressing) Sca-1⁺Lineage⁻c-kit⁺CD48⁻ HSCs were isolated from the bone marrow of 3.5 to 4 week-old Sox17^GFP/+ mice. GFP⁻ Sca-1⁺Lineage⁻c-kit⁺CD48⁻ HSCs were dividing less rapidly (D), and failed to express AA4.1 (E) or Mac-1 (F), consistent with an adult HSC phenotype. In contrast, GFP⁺ Sca-1⁺Lineage⁻c-kit⁺CD48⁻ HSCs were more rapidly dividing (D), and expressed AA4.1 (E) and Mac-1 (F), consistent with a fetal HSC phenotype.