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I’m trying to understand how a specific transcription factor I’m working with actually locates its binding site on the DNA amidst all the nucleosomes. The literature says it can sometimes recruit chromatin remodelers, but in my assays it seems to just sit in solution unless I use heavily digested chromatin.

I’ve seen roughly the same thing in my hands. the TF would sit in solution until chromatin was loosened a bit, then you could spot some binding. When we used more intact chromatin, it barely moved. it felt like the site was only available for a split second and the factor didn’t stay put.

Sometimes I wonder if what we measure is binding vs access. In one batch we varied salt and a few co factors and the signal would pop, then vanish, as if the nucleosome landscape kept shifting under it. it’s like the factor is trying to peek through a door that’s almost always closed.

I worry we’re chasing the remodeler angle too much. in my setup the remodelers are scarce or not recruited, so the TF never gets a real chance. heavy digestion might give something that looks like binding but isn’t what happens in cells.

Do you think the real bottleneck is accessibility rather than the sequence?

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