Fig. 2: Fully reconstituted CMG exhibits two different motion types.
From: Nucleotide binding halts diffusion of the eukaryotic replicative helicase during activation
a Position vs. time plots of dCas9LD555 spots; (inset) distribution of instantaneous velocities coming from the CPA fits of dCas9LD555 spots; red lines show the instantaneous velocity cutoff (5σdCas9) used to separate CMG spots in b and c into static or mobile; CPA fits are not shown for clarity. b, c Position vs. time plots of CMG spots in the b presence of ATP or c absence of nucleotide; CPA fits are plotted in black, static traces are shown in light gray. d Ratio of static CMG traces in the presence of ATP (Nspots = 43), absence of nucleotide (Nspots = 36), and static dCas9 (Nspots = 23) traces; error bars show the standard error of proportion. e Frequency of consecutive CPA segments with the same direction for CMG spots in the presence of ATP (Nmobile spots = 29) or absence of nucleotide (Nmobile spots = 15); inset diagrams illustrate expected segment directions of a unidirectionally moving spot (top) or a diffusive spot (bottom); error bars show the standard error of proportion. f (left panel) Idealized examples of MSD vs. delay time τ plots with an anomalous coefficients α < 1 (red), α = 1 (yellow), and α > 1 (green); (right panel) diagrams illustrating the types of CMG motion corresponding to each of these three cases: constrained diffusion (α << 1), free diffusion (α ≈ 1) or unidirectional motion (α > >1). g, h Fraction of mobile CMG traces classified into different motion types in the g presence of ATP or h absence of nucleotide; error bars show the standard error of proportion.
