Now let us focus on an extreme case where after a WGD there is deletion of all extra non-coding DNA and only the genes encoding the TF and its targets are left as duplicates. By virtue of the nucleotypic effect, the GSK1363089 nucleus should undergo a 2-fold volumetric shrinkage, which translates into doubling the concentration of the TF and its targets while the concentration of nsDNA will remain approximately the same. If there were only specific binding, coming back to the ancient volume while retaining double doses of TF and its GSK2118436 target sequences implies doubling the concentration of the complexes TF-sDNA. On the other hand, in presence of non-specific binding, the same amount of TF is normally shared by sDNA and nsDNA sites and the results are quite different: the higher the non-specific affinity Kns, the higher the concentration of complexes TF-sDNA formed after a hypothetical genomic shrinkage. In other words, a double amount of TF produced after genomic shrinking, for a smaller concentration of non-specific binding sites, leads to a non-linear increase in the effective TF concentration and thus in the concentration of TF-sDNA complexes. These changes in the binding of TFs to their specific targets can alter the behavior of genetic networks significantly. Consider for instance what would happen to a network involving two different factors, TF1 and TF2 that are in balance. We will assume, for simplicity, that in the steady state they both reach the same global concentration and have the same Ks. If they do not undergo non-specific binding, there will be no problem. However, if for instance TF1 binds only specifically but TF2 has substantial non-specific binding, TF2 can form as much as two times more complexes than TF1, which should perturb their balance. Again, a strategy that keeps non-specific interactions at optimal levels involves pseudogenization without deletion or replacement of deleted DNA by repetitive DNA. Mutations in COL6A1, COL6A2 and COL6A3 encoding collagen VI, cause Ullrich congenital muscular dystrophy, Bethlem myopathy and myosclerosis myopathy.