Abstract
UNC-104/KIF1A transports synaptic vesicles (SVPs) along microtubule tracks in neurons. When not hauling cargo vesicles, UNC-104/KIF1A assumes to be an autoinhibited form to reduce the wasteful consumption of ATP[1][2]. This regulatory system controls the efficiency of neuronal transport; the absence of such a system leads to reduced numbers of UNC-104/KIF1A that actively transports SVPs and defects in the generation of vesicles pools and synapses[1]. In order to quantitatively understand how the number of active UNC-104 is related to vesicle pool formation and synapse creation[3], we observed the distribution and motility of fluorescent-labelled SVPs in C.
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