In these rescue experiments, we observed reduction of reporter repression also in RIC, again probably by the effect of overexpression.
However, the change in mitochondrial transcripts of tor1 Δ strains might represent a reduction of glucose repression, which is known to induce mitochondrial transcription [ 27, 28] and mimic the effects of tor1 Δ on respiration and CLS based on our previous study [ 18].
Finally, ChIP analyses of total histones and different histone acetylation and methylation marks have shown that T3 treatment leads to the removal of core histones at the T3 target genes, and a reduction in the levels of repression histone modification marks and an increase in the levels of activation histone modification marks in the remaining nucleosomes [ 31, 88, 89, 92].
Several candidate genes in our list of validated transcripts suggest that callipyge muscle hypertrophy may be the result of a loss of repression or reduction in a negative feedback mechanism for controlling normal growth signals.
However, it is also clear that Tcl1 is not the only primary Oct3/4 target gene that controls proliferation in ES cells, because the constitutive expression of Tcl1 cannot prevent the reduction of proliferation by the repression of Oct3/4 (Figure 6E).
Finally, we asked how the lack of Pcl protein and the concomitant reduction of H3-K27 trimethylaffectaffect repression of these target genes.
Increased expression of MeCP2 resulting from reduction of miR-132-mediated repression has also been implicated in the neuroprotective response to pending ischemic injury [ 94].
Several pathways reflect the cellular response to stress following gene perturbations, and the coupling between reduction of cell growth (through repression of ribosomal functions) and changes to carbon metabolism during stress.
The reduction in repression activity of K25 and K87, since do not seem to be sumoylation sites, might be due to a different mechanism, such as alteration in DNA/protein binding.
