関連する実験動画
Updated: Jan 18, 2026

Identification of Kinesin-1 Cargos Using Fluorescence Microscopy
Published on: February 14, 2016
Kinesin-1がSARM1のシナプス局在をトランスシナプス的に制御し、非対称的なニューロン多様化を促進する
Abstract:
The Caenorhabditis elegans AWC olfactory neuron pair differentiates stochastically into two distinct subtypes, default AWC OFF and induced AWC ON . A calcium signaling complex assembled by the TIR-1/SARM1 adaptor protein is transported from the AWC cell body to the axons, where it cell autonomously specifies the AWC OFF subtype through lateral signaling. UNC-104, the C. elegans homolog of the kinesin-3 motor protein KIF1A, acts non-cell autonomously in AWC ON to control the synaptic localization of the TIR-1 signaling complex in promoting AWC OFF . Here, we identify a non-cell-autonomous role of unc-116/kinesin-1 , similar to that of unc-104/kinesin-3 , in promoting AWC OFF . unc-116 mutants, similar to unc-104 mutants, enhance the 2AWC ON phenotype of a hypomorphic tir-1 mutant. Overexpression of unc-116 in AWC causes a 2AWC OFF phenotype, the same as the tir-1 overexpression phenotype. Like UNC-104, UNC-116 plays a non-cell-autonomous role in the AWC ON cell to promote AWC OFF cell subtype by regulating the dynamic trafficking of TIR-1 along the AWC axon. UNC-116 is strikingly colocalized with UNC-104, while both are generally adjacent to TIR-1. Taken together, these results suggest a model in which UNC-116/kinesin-1 and UNC-104/kinesin-3 may work cooperatively to transport some unknown presynaptic factor(s) in the future AWC ON cell that trans-synaptically regulates the dynamic trafficking of the TIR-1/SARM1 signaling complex to postsynaptic regions of the AWC axons in promoting the AWC OFF subtype.
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