Figure 1
Figure 1. Loss of SRF induces the expansion of stem cells and their multipotent progenitors. (A) Relative expression of Srf in hematopoietic organs and sorted hematopoietic populations from control mice (n = 2) analyzed by qRT-PCR. Expression levels are normalized to Gapdh and results are expressed relative to the level of Srf expression in NIH3T3 fibroblasts (set to 1). (B) Experimental outline of Srf deletion. (C) Table of the hematologic parameters, BM cellularity, and spleen weight for each genotype 5 weeks post-pIpC treatment. Values shown are mean ± SEM (n = 11-13 per group, *P < .05, **P < .01, ***P < .001 by Mann-Whitney test). (D) In vitro colony assays. BM (2 × 104), spleen (2 × 105), and peripheral blood (PB,5 × 105) cells were plated in methylcellulose medium and scored for CFU-Cs (combined scoring for BFU-Es, CFU-GMs, and CFU-GEMMs) after 7 days. Values shown are mean ± SEM (n = 10 per genotype, **P < .01). (E) Representative FACS profile of LSKs and their subpopulations (LT-HSCs, ST-HSCs, MPPs) in the BM of Srf+/+;Mx1-Cre and SrfΔ/Δ;Mx1-Cre mice 5 weeks after pIpC treatment. (F) Time course analyses of dynamic changes in LSKs (left) and their subpopulations (right) after pIpC injection. Values shown are mean ± SEM (n = 4 for each genotype at 4, 5, 10, and 20 days, and n = 10 at 35 days, *P < .05 and **P < .01 by Mann-Whitney test). (G) Quantification of the percentage of CD150+CD48-CD244- cells in the LSK compartment of Srf+/+;Mx1-Cre and SrfΔ/Δ;Mx1-Cre mice 5 weeks after pIpC treatment. Values shown are mean ± SEM (n = 4 per genotype, *P < .05 by Mann-Whitney test). For box-and-whisker plots, midline indicates the median value; upper and lower edges of the box plot are the 75th and 25th percentiles.

Loss of SRF induces the expansion of stem cells and their multipotent progenitors. (A) Relative expression of Srf in hematopoietic organs and sorted hematopoietic populations from control mice (n = 2) analyzed by qRT-PCR. Expression levels are normalized to Gapdh and results are expressed relative to the level of Srf expression in NIH3T3 fibroblasts (set to 1). (B) Experimental outline of Srf deletion. (C) Table of the hematologic parameters, BM cellularity, and spleen weight for each genotype 5 weeks post-pIpC treatment. Values shown are mean ± SEM (n = 11-13 per group, *P < .05, **P < .01, ***P < .001 by Mann-Whitney test). (D) In vitro colony assays. BM (2 × 104), spleen (2 × 105), and peripheral blood (PB,5 × 105) cells were plated in methylcellulose medium and scored for CFU-Cs (combined scoring for BFU-Es, CFU-GMs, and CFU-GEMMs) after 7 days. Values shown are mean ± SEM (n = 10 per genotype, **P < .01). (E) Representative FACS profile of LSKs and their subpopulations (LT-HSCs, ST-HSCs, MPPs) in the BM of Srf+/+;Mx1-Cre and SrfΔ/Δ;Mx1-Cre mice 5 weeks after pIpC treatment. (F) Time course analyses of dynamic changes in LSKs (left) and their subpopulations (right) after pIpC injection. Values shown are mean ± SEM (n = 4 for each genotype at 4, 5, 10, and 20 days, and n = 10 at 35 days, *P < .05 and **P < .01 by Mann-Whitney test). (G) Quantification of the percentage of CD150+CD48-CD244- cells in the LSK compartment of Srf+/+;Mx1-Cre and SrfΔ/Δ;Mx1-Cre mice 5 weeks after pIpC treatment. Values shown are mean ± SEM (n = 4 per genotype, *P < .05 by Mann-Whitney test). For box-and-whisker plots, midline indicates the median value; upper and lower edges of the box plot are the 75th and 25th percentiles.

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