Figure 2

ATAC-seq was performed on human lymphoblastoid cells and half of each sample was left untreated (green) and the other half was treated with anti-mt CRISPR (purple). (a) Representative genomic region (hg38, chr2:74,425,417–74,586,546) showing read counts (usable reads) in 5 replicate pairs (DT) at the same sequencing depth of 21.9 M reads. Differences between treated and untreated samples were minimal, indicating that the treatment did not damage the samples. (b) ATAC-seq reads in the mitochondrial chromosome and in a 16.5 kb region of chromosome 9 around the SYF promoter (same as Fig. 1). For each condition, all samples were pooled together and 227 M reads were sampled. (c) Treated samples yielded 1.7-fold fewer mitochondrial reads compared to untreated samples. (d) Accordingly, the number of unique, non-mitochondrial (usable) reads was 1.7-fold higher in treated samples than in their untreated counterparts. (e) At the same sequencing depth, 1.6-fold more peaks were called in the treated samples. Only 6 data points are shown because the treated halves of samples 18 and 19 (same batch) had only 14.5 M and 9.8 M reads each and were combined for improved peak calling. (f) Anti-mt CRISPR-treated samples shared a similar number of peaks with treated replicates and untreated samples. The top 20,000 peaks of each sample were used in this analysis. Comparison of peaks at the read count level also supports that peaks from treated samples do not substantially differ from untreated samples. Fold-differences were calculated on the medians. (c–e): all samples normalized to 21.9 M sequenced reads.