Figure 6.
A model of differential enhancer and silencer sensitivity to CRX mutants. Silencers, with higher predicted CRX occupancy, engage in effector domain–mediated homotypic interactions that permit CRX to remain bound even when the DBD is weakened by the p.R90W variant. The p.E168d2 variant lacks most of the effector domain and cannot engage in these interactions. Enhancers have lower CRX predicted occupancy and engage in fewer homotypic interactions.
