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A lost binding site may have been replaced with a new, species-specific binding site - i.e. binding site turnover.
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Therefore, true binding sites may have SNPs less frequently than the non-binding sites.
Alternatively we cannot rule out that sequence divergence in these samples at primer binding sites may have prevented amplification.
As with the failed attempt to amplify nuDNA from the two relatively recent specimens, an explanation may simply be that sequence divergence in the problematic samples at the primer binding sites may have prevented amplification.
Similarly, some of the annotated binding sites may have been used to construct the PSFM models that we use in our analysis and that in turn can introduce an optimistic bias into our results.
The nucleosome binding sites may have a different distribution between introns and exons in plant genes compared to human genes and this may be a specificity of plant introns favouring the establishment of open chromatin configurations which are typical of genes with high EB.
Therefore, the expression of silMUT, missing these binding sites, may have a similar effect.
These binding sites may have low sequence specificities, but their binding affinities can be complemented by high structure specificities.
Thus, identified SNPs in the binding sites may have no influence on the binding site integrity and therefore will not affect transcription factor binding and gene expression.
Here, we test the hypothesis that evolutionary divergence of miRNAs and/or their binding sites may have contributed to the diversification of species (Plasterk 2006).
To assess whether at the inversion breakpoints crucial factor binding sites may have been disrupted, we made another series of inversion constructs (Fig. 2A) called Flip49 and Flip49+REP3A.
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