Fig. 9

Up-regulation of canonical Wnt signaling rescues Gfi1b-deficient phenotypes in HSCs and MKs. a, b Lineage depleted Gfi1b WT/KO BM cells were taken into culture under the indicated concentrations of Wnt3A. MKs and HSCs CD41^low/CD9^low were quantified by FACS at day seven post Tamoxifen injection, n = 5 GFI1b WT and five GFI1B KO mice. c Gfi1b KO MKs spreading on fibronectin-coated matrices is rescued by Wnt3A treatment. d MK roundness index plotted as bean plot. Upper part: spreading of Gfi1b KO MKs on Fibronectin coated matrices is rescued by Wnt3A treatment at increasing concentrations. Lower part: spreading of WT MKs on Fibronectin coated matrices is abrogated by Wnt3A treatment at increasing concentrations. (*p < 0.05, **p < 0.001, ***p < 0.0001 on a Mann–Whitney U-test, colored horizontal line shows median, n values for upper part are, in order from left to right: 39, 46, 95, 83, 91, 111, and 87. n values for lower part are, in order from left to right: 39, 120, 89, 108, 86, and 81). Each horizontal short line represents one individual cell. e Proposed model: Gfi1b interacts with β-catenin and regulates Wnt signaling in HSCs and MKs. Deletion of Gfi1b alters the balance between canonical and non-canonical Wnt signaling leading to expansion of HSCs and MKs and impaired MKs spreading on Fibronectin coated matrix