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. 2021 Mar 17;35(11):3232–3244. doi: 10.1038/s41375-021-01212-6

Fig. 1. SAMD9 and SAMD9L alter hematopoietic cell proliferation, differentiation, and cell cycle.

Fig. 1

A The experimental model of lentivirus-mediated overexpression of SAMD9, SAMD9L, and their mutations SAMD9-E1136Q, SAMD9L-H880Q, -W1180R, and -R1281K, in cord blood human CD34+ or Samd9l and Samd9l-W1171R in HSPCs cells from Samd9l−/− mice. B Colony forming units (CFU-C) showing the total number of colonies from CD34+ (n = 4) (left) and Samd9l−/− HSPCs (n = 3) (right) transduced with GFP vector control (MIG), SAMD9, SAMD9L, or the indicated pathogenic mutations. Statistics: one-way ANOVA with Bonferroni-correction (ns not significant; **p < 0.01). Error bars indicate standard error of the mean for three biological replicates compared to GFP vector control. C Flow cytometric analysis showing the percentage of EdU incorporation in Samd9l−/− HSPCs (n = 3) transduced with SAMD9L or Samd9l or their mutations. Statistics: one-way ANOVA with Bonferroni-correction (ns not significant, *p < 0.05, **p < 0.01). Error bars indicate standard error of the mean from three or more biological replicates compared to GFP vector control.