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. 2015 Dec 15;29(24):2603–2616. doi: 10.1101/gad.267633.115

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© 2015 Kadri et al.; Published by Cold Spring Harbor Laboratory Press

This article is distributed exclusively by Cold Spring Harbor Laboratory Press for the first six months after the full-issue publication date (see http://genesdev.cshlp.org/site/misc/terms.xhtml). After six months, it is available under a Creative Commons License (Attribution-NonCommercial 4.0 International), as described at http://creativecommons.org/licenses/by-nc/4.0/.

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Figure 5. — Male mice bearing Gata1^S310A alleles die from hemolytic anemia after inhibition of IGF-1R signaling by PPP. (A) Hematopoietic indices of Gata1 (WT/Y) and Gata1^S310A (KI/Y) male mice after 20 d of PPP treatment. (HGB) Hemoglobin concentrations (after separating RBCs from plasma); (HCT) hematocrit; (MCV) mean corpuscular volume; (MCHC) mean corpuscular hemoglobin concentration. (B) Gata1 and Gata1^S310A peripheral blood smears on days 10 and 20 of PPP treatment (630×). (C) Electron microscopy of erythrocytes described in B. (Bottom left) Estimation of the percentage of acanthocyte and echinocyte RBCs on day 10. (Bottom right) Enlarged echinocyte Gata1^S310A RBC. Bar, 5 μm. (D) Centrifuged microhematocrit capillaries. (E) Spectroscopic analysis of hemoglobin in the plasma. (F) Manual quantification of hemoglobin of washed RBCs and serum in Gata1 and Gata1^S310A peripheral blood and of urine of the same mice after 20 d of PPP treatment, as assessed by Drabkin's method. n = 3 per group.