To characterize further the relationship between AML1, AML1-ETO, the co-regulators p300 and N-CoR, and epigenetic signatures, the mean tag densities for these datasets over regions (100 bp, centered on the summits of ChIP-seq peaks) bound by AML1 and/or AML1-ETO were clustered using k-means.
Average tag density profiles were calculated around TSSs after shifting tags.
Tag densities on the average profiles were determined by calculating tag density over each base pair (using a 40 bp window size) per 10 million total mapped reads.
K-means clustering was performed on ChIP-seq tag density around 3 kb regions across the TSS in R statistical software (http://www.r-project.org).org
We compared the intensity of ChIP-seq signals at rDNA to those along chromosome 12 via normalized tag density, which was calculated by dividing the mean intensity of all peaks called within rDNA by the mean intensity of all peaks called outside of rDNA on chromosome 12.
This means that we use only a part of the tag density profile when looking for binding sites.
The accuracy achieved is meter-scale with high enough reference tag density.
Next, we examined the tag density distribution across the genome.
We calculated the tag density of a genomic position as the number of tags that cover the position.
