Yes, this part was obvious! What I meant with those bit-flips was the exponentially small probability of a sudden discrete transition. Why could accidental transitions like this not accumulate? Because they are selected against fast enough? I wouldn’t expect those epigenetic marks to have enough redundancy to reliably last to the end of an organisms’ lifetime, because methylated cytosine is prone to deaminate (which is why CG is the least frequent 2-mer at a ~1% frequency, rather than the ~6.25% you’d expect on baseline). I am confused how the equilibrium works here, but it seems like mutational load could explain why organisms who rely on methylating cytosine have less CG’s than would be useful to maintain epigenetic information. Things would be different in organisms that don’t rely so heavily on methylating cytosine.
Yes, this part was obvious! What I meant with those bit-flips was the exponentially small probability of a sudden discrete transition. Why could accidental transitions like this not accumulate? Because they are selected against fast enough? I wouldn’t expect those epigenetic marks to have enough redundancy to reliably last to the end of an organisms’ lifetime, because methylated cytosine is prone to deaminate (which is why CG is the least frequent 2-mer at a ~1% frequency, rather than the ~6.25% you’d expect on baseline). I am confused how the equilibrium works here, but it seems like mutational load could explain why organisms who rely on methylating cytosine have less CG’s than would be useful to maintain epigenetic information. Things would be different in organisms that don’t rely so heavily on methylating cytosine.