We favour this last hypothesis since deregulation of chromatin packing affected the response to N-signalling.
Chromatin architectural proteins interact with nucleosomes to modulate chromatin accessibility and higher-order chromatin structure.
A range of chromatin modifications suppress their transcription, including histone modifications and altered chromatin packing.
The degree of chromatin packing is dynamically regulated and can be either heterochromatic (densely packed chromatin, transcriptionally repressed) or euchromatic (accessible chromatin, transcriptionally active).
The DCSR pairs represent the locations of imbalances of chromatin accessibility between alleles and are ideal to reveal chromatin motifs that may directly modulate chromatin accessibility.
TEs can be transcriptionally silenced by DNA methylation and repressive chromatin formation, involving modifications of histone tails and altered chromatin packing [ 12, 44, 45].
These can be considered as reporters for genomic presence and accessibility to transcriptional machinery (for instance, due to chromatin packing).
However, due to insertion in regions with different chromatin packing, the integrated proviral DNA results in varying transgene expression levels.
The results could also help researchers to understand how the BRG1 protein organises chromatin packing in other cell types.
Cells utilize two distinct mechanisms to modulate chromatin dynamics during DNA repair.
