Altered in vivo gene expression and splicing caused by Srsf2^P95H/+. (A) Volcano plot of differential gene expression in BM lin⁻cKit⁺eYFP⁺ cells isolated 20 weeks after tamoxifen cessation (n = 3 per genotype). (B-C) Pathway enrichment using Quantitative Set Analysis for Gene Expression analysis of data set from panel A. (D) Analysis of abnormal splicing events by type (BM lin⁻cKit⁺eYFP⁺ cells; 20 weeks after tamoxifen cessation; n = 3 per genotype). (E) Plots of inclusion events of cassette exons and mutually exclusive exons in the WT and knock-in (KI) samples. Gray dots = <5% difference between genotypes; blue dots = P < .05 and >5% difference between genotypes; red dots = q < 0.05 and >5% difference between genotypes. (F) Ptprc/Cd45 isoform at the transcript (left) and protein level of the CD45RB isoform on splenocytes from R26-CreER Srsf2^+/+ and R26-CreER Srsf2^P95H/+ animals. Polymerase chain reaction (PCR) or quantitative PCR analysis of indicated alternative splicing of the indicated transcripts in WT and KI samples from either splenocytes from R26-CreER tamoxifen treated animals (G) or tamoxifen-treated Hoxb8-immortalized myeloid progenitors (H) (n = 2 per genotype per sample type). Data expressed as normalized fold inclusion rate of the cassette exon compared with the exclusion product (WT ratio normalized to 1). FC, fold change; FDR, false discovery rate.