Loss of Stat5a serine-phosphorylation delays disease onset in transplanted mice. (A) Kaplan-Meier plot of cS5- vs cS5-S725A–, cS5-S779A–, and cS5-SASA–transplanted mice. GFP vector–transplanted mice were included as controls. All cS5-transplanted mice died within 10 weeks. In contrast, cS5-SASA–transplanted mice remained disease-free, and disease onset in cS5 single serine mutants was significantly delayed (***P < .001). All groups were monitored over a period of 40 weeks after which all mice were killed and analyzed (n ≥ 8). (B) WBC counts of transplanted mice at 8 weeks (left) and 32 weeks after transplantation (right). PB hematology revealed a dramatic increase in WBCs in cS5-transplanted mice after 8 weeks. By contrast, all serine mutants showed a slight increase in WBCs after 32 weeks only. (C) FACS analysis of PB for representative cS5 versus cS5-S725A–, cS5-S779A–, and cS5-SASA–transplanted mice at 8 and 32 weeks after BM transplantation. The overall number of GFP⁺ cells is displayed in the histogram. All cS5-transplanted mice were found to present with severe myelodysplasia when GFP⁺ cells were gated for lymphoid (CD3 and CD19) and myeloid (Gr-1 and Mac-1/CD11b) markers, respectively. Conversely, all serine mutants showed an increase in GFP⁺ lymphoid cells (mainly CD3⁺ cells) and in Gr-1⁺ cells.