Differences in vesicle movement across treatment and control groups in LLC-Pk1 cells can be explained by nocodazole’s depolymerizing effect on tubulin structure. In the control group, the integrity of the microtubule structure remained intact, enabling vesicles to bind their receptors to microtubule tracks. This then allowed for motor proteins to hydrolyze ATP, producing movement across the microtubule. Though much of this movement is similar in displacement, the data indicates an outlier. This outlier however was still chosen to be presented to exemplify the jerky nature of endosome saltation movement across microtubules, due to occasional detachments of endosome to microtubule. Nocodazole treated cells exhibited low average displacement of vesicles due to the depolymerization of tubulin, which did not allow receptors on the vesicle surface to bind and travel across tubulin structures. Because of this, endosomes remained suspended in the luminal space of the cell, slowly migrating to lysosomes in the interior to be degraded.
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