Figure 6.
Gene-signature analysis shows a shift in pooled RNA-seq expression profiles from a progenitor-like state in WT HSPCs to pro–B-cell commitment in Gabbr1−/−mutant HSPCs. Gene signatures are defined by data from Miyai et al,42 and false discovery rate (FDR) of gene-signature enrichment is shown as red bars for WT HSPCs and turquoise bars for Gabbr1−/− mutant HSPCs. (A) Gene signatures from in vitro B-cell differentiation show a progressive shift from early B-lineage markers in WT HSPCs (red text), to a mix of signatures in “transition” stage (green text), and finally to pro–B-cell commitment signatures in Gabbr1−/− mutant HSPCs (blue text). (B) This same pattern is mirrored in the gene signatures of sorted LMPPs, CLPs, and pro-B cells. (C) Diagram showing the shift in expression profiles between WT and Gabbr1−/− mutant HSPCs.

Gene-signature analysis shows a shift in pooled RNA-seq expression profiles from a progenitor-like state in WT HSPCs to pro–B-cell commitment in Gabbr1−/−mutant HSPCs. Gene signatures are defined by data from Miyai et al,42  and false discovery rate (FDR) of gene-signature enrichment is shown as red bars for WT HSPCs and turquoise bars for Gabbr1−/− mutant HSPCs. (A) Gene signatures from in vitro B-cell differentiation show a progressive shift from early B-lineage markers in WT HSPCs (red text), to a mix of signatures in “transition” stage (green text), and finally to pro–B-cell commitment signatures in Gabbr1−/− mutant HSPCs (blue text). (B) This same pattern is mirrored in the gene signatures of sorted LMPPs, CLPs, and pro-B cells. (C) Diagram showing the shift in expression profiles between WT and Gabbr1−/− mutant HSPCs.

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