As a consequence, natural selection on allele length within these loci is likely to be much weaker than for gene associated microsatellites.
In the same gene family, old introns were embedded within strong protosplice motifs which were found to be much weaker in homologous genes lacking the intron in the given position [ 123].
Among genes with no CpG islands, responsive genes were enriched in H3K4me3 chromatin marks and binding of several TFs to distal portions of promoters; however the effects of these factors were much weaker than for genes with CpG islands (Additional Files 12, 13).
And, in fact, there is a strong positive correlation between the number of SNPs a gene harbors and the maximum FST value these SNPs can reach (ρ = 0.527, p < 10-50, n = 19,074), while the correlation is much weaker with the gene-specific average FST (ρ = 0.094, p < 10-39, n = 19,074).
Although the IL2RA and IL7RA genes exert much weaker effects than the HLA-class II genes, associations of these two genes with the disease have been confirmed in several independent MS cohorts.
The expression of the last two genes was much weaker than that of the first two genes in the polycistronic cassette, suggesting that the "cleavage" efficiencies at the downstream 2A sites were lower than those at the upstream 2A sites.
However, this correlation is much weaker when limited to genes that are weakly induced (2-fold or less induction in both our data and the microarray data; r = 0.0429, P = 0.0388), and much stronger when limited to genes that are strongly induced (greater than 2-fold induction in both datasets; r = 0.5053, P = 0.002).
The challenges are the expression strength of chromosomally engineered genes under constitutive promoters is much weaker than the vector engineered genes under inducible promoters.
The same binding activity was detected for the region in front of the glcD gene, whereas the complex with the predicted binding site in front of the mraZ gene was much weaker.
For example, the profound transcriptional response upon challenge with M. luteus and the much weaker and mainly down-regulated gene response after E. coli challenge, taken together with the reported higher virulence of E. coli to An. gambiae, suggests that the potency of the immune response activated by these two bacterial species is quite different [ 27, 81].
