A global role for KLF1 in erythropoiesis revealed by ChIP-seq in primary erythroid cells

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Figure 4.
Figure 4.

KLF1 acts primarily as a direct activator of target genes and not exclusively via promoter regions. (A) Each of the genes from the Hodge et al. (2006) expression profiling study were classified as “down-regulated” in Klf1−/−, “up-regulated” in Klf1−/−, or nonresponsive, when compared with WT expression. The plot shown represents the fraction of regions in the genes from each of these groups containing a KLF1 ChIP-seq peak binned into categories as shown in the cartoon underneath where the size of the promoter and 3′ region are each 2 kb. Each error bar represents the 95% confidence interval for the given fraction, assuming the number of regions with a peak follows a binomial distribution with N equal to the number of regions of that class. Note genes consisting of a single exon do not contribute to the intragenic region calculation. (B) A plot describing the relationship between fold change in expression in Klf1−/− fetal liver compared with WT for genes that are “bound” by KLF1 within the gene or 2 kb on either side. The down-regulated in Klf1−/− fetal liver gene set is shown (i.e., genes represented by maroon bars in A). The genes represented by some of the points are shown for clarity.

This Article

  1. Genome Res. 20: 1052-1063

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