Such a subset comprising clearly distinct motifs could indicate the coordinate binding of multiple factors.
We next evaluated the performance of dCaP Test2 (dCaP-T2-all) for detecting differential binding of multiple factors in multiple conditions.
However, this is not to say that cooperative interactions do not take place, or are not important in other contexts, but rather that it is necessary to distinguish between synergistic interactions that can be explained by independent binding of multiple factors (as in our model), and those that occur as a result of pairwise interactions between TFs.
To examine this, we compared the clustering of binding sites of multiple factors studied by ChIP-seq across cell types.
Therefore, experimental analysis of the binding activities of multiple factors has served as a means of identifying crucial regulators for a specific cell type (DeVilbiss et al., 2014; Tijssen et al., 2011).
We analysed the genome-wide binding sites of multiple factors, including CTCF, ELF1, ETS1, FOSL2, GABPA, REST, EP300, SIN3AK20, SIX5,SP1, TAF1, TCF12, USF1, YY1, ZBTB33, FOXA1, ATF3, BCL33, and RNA polymeraseII(POL2) using ENCODE ChIP-Seq data from human A549 cells [ 15].
Importantly, meiotic recombination hotspots are clearly nonrandom: their locations involve DNA sequence motifs and, according to Wahls and Davidson [ 135], are determined by the combinatorial effect of the binding of multiple transcription factors at multiple transcription factor binding sites.
While we have incorporated a fairly accurate phylogenetic model, we have not incorporated into this model such effects as the non-independence of the positions in a site (e.g., the effect of di- or tri-nucleotide energy terms, also known as stacking energies), nor effects from the cooperative binding of multiple transcription factors on the ability of a factor to bind to a DNA site.
Synergistic binding of multiple transcription factors to certain combinations of binding sites is an important mechanism of achieving highly specific regulation of genes in particular cellular conditions.
How is the binding of multiple chromatin factors to the same nucleosomal surface regulated?
