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. 2019 Mar 20;10:1270. doi: 10.1038/s41467-019-09273-z

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© The Author(s) 2019

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 1 — Loss of Gfi1b in MKs and HCSs causes their expansion and mobilization into the blood. a Schematic of Tamoxifen injections; mice were analyzed by FACS at day 10 following the first injection. b, c Quantification of Gfi1b WT/KO MKs and HSCs in lineage negative depleted BM and blood (n = 3 mice per group). d Schematic of in vitro analysis of Gfi1b WT/KO HSCs and MKs expansion. e MKs and HSCs (CD41^low/CD9^low) were taken into culture and were quantified by FACS at day six (day seven post Tamoxifen injection, n = 3 mice per group). f, g Loss of Gfi1b leads to impaired MKs spreading on Fibronectin coated matrix as quantified by calculating their roundness index (n = 70 Gfi1b wt/flox cells and 220 Gfi1b flox/flox cells). (*p < 0.05, **p < 0.001, ***p < 0.0001 on a Welch corrected t-test, error bars show s.d)