Figure 6
Figure 6. Transcriptomics analysis by RNA-seq identified several potential mediators of BAF53a function in the hemopoietic stem/progenitor cell compartment. (A) Functional Gene Ontology-term analysis of BAF53a-regulated genes in Sca1+ Lin− BM cells as determined using the Ingenuity Pathway Analysis software (Content Version 12710793; release date: 2012-05-07). Transcripts exhibiting a > 2-fold difference in expression were used in this analysis. See supplemental Table 4 for list of most significantly misregulated genes. (B) Quantitative PCR analyses of potential mediators of BAF53a function in HSC-enriched Sca1+Lin− BM cells mice (3 independent pairs of WT and BAF53a-deficient mice; referred to as A, B, and C). For FL cell analysis, E14.5 BAF53a+/+, BAF53afl/+, and BAF53afl/fl FL cells were infected with retroviruses expressing Cre and GFP. Efficiency of deletion in GFP+ sorted cells was evaluated at 95% by PCR (data not shown). Values are mean ± SD of 3 independent replicates. ΔCT values for each gene were determined relative to HPRT in each population. RQ values represent the relative expression of each gene in BAF53a-deficient cells over control cells after HPRT normalization. Supplemental Table 7 contains a list of oligonucleotides and probes. Supplemental Table 8 contains numerical values. (C) Schematic representation of BAF53a regulated genes in HSC-enriched Sca1+Lin− BM cells as identified by RNA-seq. Genes down-regulated (≥ 2-fold) in the absence of BAF53a appear in green and up-regulated genes (≥ 2-fold) are in red.

Transcriptomics analysis by RNA-seq identified several potential mediators of BAF53a function in the hemopoietic stem/progenitor cell compartment. (A) Functional Gene Ontology-term analysis of BAF53a-regulated genes in Sca1+ Lin BM cells as determined using the Ingenuity Pathway Analysis software (Content Version 12710793; release date: 2012-05-07). Transcripts exhibiting a > 2-fold difference in expression were used in this analysis. See supplemental Table 4 for list of most significantly misregulated genes. (B) Quantitative PCR analyses of potential mediators of BAF53a function in HSC-enriched Sca1+Lin BM cells mice (3 independent pairs of WT and BAF53a-deficient mice; referred to as A, B, and C). For FL cell analysis, E14.5 BAF53a+/+, BAF53afl/+, and BAF53afl/fl FL cells were infected with retroviruses expressing Cre and GFP. Efficiency of deletion in GFP+ sorted cells was evaluated at 95% by PCR (data not shown). Values are mean ± SD of 3 independent replicates. ΔCT values for each gene were determined relative to HPRT in each population. RQ values represent the relative expression of each gene in BAF53a-deficient cells over control cells after HPRT normalization. Supplemental Table 7 contains a list of oligonucleotides and probes. Supplemental Table 8 contains numerical values. (C) Schematic representation of BAF53a regulated genes in HSC-enriched Sca1+Lin BM cells as identified by RNA-seq. Genes down-regulated (≥ 2-fold) in the absence of BAF53a appear in green and up-regulated genes (≥ 2-fold) are in red.

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