Hello. My name is Vincenzo Pirrotta,
and this is part two of our talk about Polycomb Epigenetic Mechanisms.
As we have seen,
a more useful way to look at polycomb group activities,
is to think of them as involved in dynamic processes.
And in particular, a polycomb complex like PRC2.
PRC2 target all chromatin,
not just polycomb group target sites,
where it is found stably bound.
PRC2 in fact has clearly untargeted functions.
If we look at histone H3 methylation at lysine 27 in the whole genome.
It is clear that most of the activity of PRC2 is not to
trimethylate but to dimethylate lysine 27 of histone H3.
It appears that PRC2 acts on most of the nucleosomes in the genome.
There is only a small percentage of histone H3 that remains unmethylated and note that
a small amount at any one time is acetylated at lysine
27 and therefore cannot be methylated at that position.
Chromatin immunoprecipitation and sequencing, so ChIP-seq,
so-called allows us to map where these different states have methylation
are in the genome relative to the genes and the activity of these genes.
The sites where polycomb protein is bound representing
PRC1 or polycomb target genes are also regions that contain histone H3 trimethylation.
Instead, dimethylation of lysine 27 is found almost everywhere,
particularly in genomic regions that are not transcriptionally active,
intergenic regions or genes that are weakly or not at all transcribed.
So this is in fact, most of the genome.
Monomethylation of lysine 27 is found at
actively transcribed genes which are indicated
here by the presence of RNA polymerase, Pol II.
And monomethylation is probably an intermediate of dimethylation or remethylation.