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To determine the contribution of each modification we calculated payments using current quarter instead of previous quarter data.
For each histone modification, we calculated the percentage of its total stable nucleosome-bound DNA sequence that consists of satellite II or III DNA.
In an effort to mitigate the changes in ChIP-Seq signal resulting from histone modification, we calculated the sum of the deltaH3K4me1, deltaH3K4me2, and deltaH3K4me3 signals, henceforth referred to as the deltaH3K4methyls signal.
To examine the relationship between RNAPII occupancy and chromatin modification, we calculated the PCC (r) between dynamic RNAPII occupancy of unmodified CTD, Ser5-P and Ser2/5-P and 13 histone modifications determined in our previous study [ 19].
For each histone modification, we calculated occupancy[ 32] over aligned satellite II (or III) DNA sequences, where occupancy is defined as the fraction of sequences at a position that are bound to a stable nucleosome containing that histone modification (see Methods).
Additionally, for each histone modification, we calculated its occupancy along satellite II DNA, or satellite III DNA, sequences aligned by start site — where occupancy[ 32] is defined as the fraction of sequences bound to a stable nucleosome, in this context, with the histone modification.
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To confirm the distribution profiles of histone modifications, we calculated the ratio of histone modifications (H3K4me3 and H3K9ac) to pan-H3.
To assess the spatial relationships between the arsenical-induced hypermethylation and the stem cell histone modification domains we calculated the number of hypermethylated microarray probes from CAsE-PE cells that occur within H3K27me3 or H3K9me3 stem cell domains.
In order to allow clustering of sites displaying significant evidence of ASHM by their histone-modification patterns, we calculated the degree of allelic imbalance for each individual modification at each site using a binomial test.
For each chromatin remodeler-modification pair, we calculated Pearson correlation coefficient between the above representation of each gene and its transcription rate.
To confirm the modification of the effect, we calculated the PRs of the main association per stratum of each preselected covariate and their respective 95% CI.
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