Stress-induced erythroid differentiation is impaired in β1Δ/Δ mice. (A) Survival curve (ctrl, n = 25; β1Δ/Δ, n = 16), splenic weight (ctrl, n = 25; β1Δ/Δ, n = 6), and splenic cellularity (ctrl, n = 25; β1Δ/Δ, n = 6). (B) Erythroid differentiation in BM and spleen. FACS profiles of CD71/TER119-labeled splenic cells (left panels in BM and spleen), and CD44/side scatter analysis of TER119+ cells from days 0 and 6 after PHZ (right panels in BM and spleen). Note the failure of β1Δ/Δ erythroid cells to advance to later maturation stages (ie, from R1 to R2 in the CD71/TER119 profiles after RBC lysis). CD44/side scatter analysis of TER119+ cells shows discreet stages of progressive maturation (from I-V) before PHZ but a significant overlap after PHZ treatment in both sets of animals. (C) Progenitors (total CFU-C, left panel; BFU-E/stress BFU-E, middle panel; and CFU-E, right panel) in spleen before and after PHZ treatment in controls and β1-deficient mice. (Stress BFU-E are shown as a proportion of total BFU-E.) Note the significant reduction of all progenitors in spleen after PHZ treatment in β1Δ/Δ mice (day 6).