Figure 5. Repaired rings close faster and catch up with uncut control rings. (A) Perimeter versus time plot of four cut rings with initial perimeters of 41, 36, 30, and 26 µm. The dashed portion of colored lines corresponds to time points from 0 to ∼22 s, for which part of the measured perimeter corresponds to the outline of cortical myosinNMY-2::GFP labeling. The mean perimeter for uncut rings is in black, with gray lines indicating the 95% CI (data as in Fig. S1 C). Arrows indicate moment of laser cut. (B) Normalized ratio of perimeter change over time after cut (n = 15; see Fig. S1 F and Materials and methods for details). Colored lines represent individual examples, and the black line shows the mean. The dashed lines indicate normalized ratios of 1 and 1.35 (mean of normalized velocities >1 over the time period of 22–55 s after the laser cut). The gray area represents the 95% CI of the mean curve. (C) Time required for cut rings to catch up with the perimeter of uncut rings plotted against initial perimeter (n = 21; R2 = 0.59 and r = 0.76; P < 0.0001). (D) Normalized myosin fluorescence intensity levels plotted against time after cut for rings with initial perimeters between 16 and 42 µm (see Fig. S3 A for method). Black dots represent mean intensities (see Materials and methods for details) with 95% CI error bars; gray circles represent individual measurements. (E) An increase in constriction velocity proportional to the gap size can be explained by the contractile unit model. When a ring is cut, the plasma membrane retracts at the site of the cut, and contractile units (green) assemble de novo at nucleation sites (green circles) distributed along the plasma membrane. This increases the total number of units in the ring and the overall velocity of constriction after gap repair relative to uncut control rings. We propose that subsequent myosin hyperaccumulation (thick green line) transiently increases tension locally along the new units and promotes faster shortening of the repaired ring, leading to an overall higher constriction velocity than expected by serial incorporation of new units.
Figure 5.

Repaired rings close faster and catch up with uncut control rings. (A) Perimeter versus time plot of four cut rings with initial perimeters of 41, 36, 30, and 26 µm. The dashed portion of colored lines corresponds to time points from 0 to ∼22 s, for which part of the measured perimeter corresponds to the outline of cortical myosinNMY-2::GFP labeling. The mean perimeter for uncut rings is in black, with gray lines indicating the 95% CI (data as in Fig. S1 C). Arrows indicate moment of laser cut. (B) Normalized ratio of perimeter change over time after cut (n = 15; see Fig. S1 F and Materials and methods for details). Colored lines represent individual examples, and the black line shows the mean. The dashed lines indicate normalized ratios of 1 and 1.35 (mean of normalized velocities >1 over the time period of 22–55 s after the laser cut). The gray area represents the 95% CI of the mean curve. (C) Time required for cut rings to catch up with the perimeter of uncut rings plotted against initial perimeter (n = 21; R2 = 0.59 and r = 0.76; P < 0.0001). (D) Normalized myosin fluorescence intensity levels plotted against time after cut for rings with initial perimeters between 16 and 42 µm (see Fig. S3 A for method). Black dots represent mean intensities (see Materials and methods for details) with 95% CI error bars; gray circles represent individual measurements. (E) An increase in constriction velocity proportional to the gap size can be explained by the contractile unit model. When a ring is cut, the plasma membrane retracts at the site of the cut, and contractile units (green) assemble de novo at nucleation sites (green circles) distributed along the plasma membrane. This increases the total number of units in the ring and the overall velocity of constriction after gap repair relative to uncut control rings. We propose that subsequent myosin hyperaccumulation (thick green line) transiently increases tension locally along the new units and promotes faster shortening of the repaired ring, leading to an overall higher constriction velocity than expected by serial incorporation of new units.

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