So you’re saying that the persistent epigenetic modification is a change in the “equilibrium state” of a potentially methylated location?
Does this mean that the binding affinity of the location is the property that changes? i.e. all else being equal, a location with high affinity will be methylated much more often than a location with low affinity, because the methyl groups will tend to stick harder or longer in the high affinity location.
But if that’s the case, it seems like there still must be some persistent structural feature responsible for setting the binding affinity to high or low...
So you’re saying that the persistent epigenetic modification is a change in the “equilibrium state” of a potentially methylated location?
Yes.
Does this mean that the binding affinity of the location is the property that changes?
Not quite, it would most likely be a change in concentrations of enzymes or cofactors or whatever which methylate/demethylate the specific site (or some set of specific sites), rather than a change in the site itself.
So you’re saying that the persistent epigenetic modification is a change in the “equilibrium state” of a potentially methylated location?
Does this mean that the binding affinity of the location is the property that changes? i.e. all else being equal, a location with high affinity will be methylated much more often than a location with low affinity, because the methyl groups will tend to stick harder or longer in the high affinity location.
But if that’s the case, it seems like there still must be some persistent structural feature responsible for setting the binding affinity to high or low...
Yes.
Not quite, it would most likely be a change in concentrations of enzymes or cofactors or whatever which methylate/demethylate the specific site (or some set of specific sites), rather than a change in the site itself.