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. 2017 May 26;7:2467. doi: 10.1038/s41598-017-02655-7

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© The Author(s) 2017

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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The EGFR^C329R mutant impairs erythroid differentiation in the human TF1.8 erythroleukemia cell line. (a) Dot plots representative of CD235a (glycophorin A, erythroid marker) and CD13 (myeloid marker) surface expression on TF1.8/MIG, TF1.8/EGFR and TF1.8/C329R cells on day 5 of culture with GM-CSF (5 ng/mL), EPO (5 U/mL) or rhEGF (0.5 ng/mL or 10 ng/mL). (b) Percentage of cells in gates (a) or (c) (identified in (Fig. 3a) in GM-CSF culture (top panel), and plotted over a 7 day time-course for EPO (middle panels) or EGF (bottom panel) containing cultures. Points represent mean ± SE of 3 independent experiments. T-test *P < 0.05, **P < 0.01 (MIG vs. C329R). (c) Schematics of temporal acquisition of mutations (originating from a WT stem/progenitor cell) as determined from genotyping of individual BFU-E colonies plated from PBMNC. The percentage of each clone in PBMNC is shown.