The chromatin accessibility landscape of primary human cancers, M. R. Corces et al., Science 362, eaav1898 (2018). DOI: 10.1126/science.aav1898
This is a recently published paper in Science. Because I am not studying this sort of things, it's hard for me to understand some of those authors' opinions.
The Fig. 4A describes the concept the authors used to identify transcription factor occupancy from ATAC-seq data. In the paper, they say "TF binding to DNA protects the protein-DNA binding site from transposition while the displacement or depletion of one or more nucleosomes creates high DNA accessibility in the immediate flanking sequence". Here I think I can understand it correctly: (1) TF binds to this region, and then (2) it blocks Tn5 binding, so (3) consequently there is a deep notch of ATAC-seq signal, and (4) this notch region tells us where a TF binds to.
Later near the end of this article, the authors said:
(1) For example, if a noncoding somatic mutation causes the generation of a TF binding site, this mutation could lead to an increase in chromatin accessibility in cis and a concomitant increase in the observed frequency of the mutant allele in ATACseq as compared with that in WGS (Fig. 7A). (2) Similarly, a mutation that inactivates a TF binding site can lead to a decrease in chromatin accessibility and a concomitant decrease in the observed frequency of the mutant allele.
From Fig. 4A we've known that when TF binds to DNA, the ATAC-seq signal plummets. However, the authors now say the generation of TF binding site increases chromatin accessibility. How could this be possible? Doesn't the generation of TF binding site make chromatin inaccessible?