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Identification of Kinesin-1 Cargos Using Fluorescence Microscopy
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Kinesin-1 trans-synaptically regulates synaptic localization of SARM1 for asymmetric neuron diversification
Anaam Khalid1, Peter Sahyouni1, Jun Yang1
1Department of Biological Sciences, University of Illinois at Chicago.
Biorxiv : the Preprint Server for Biology
|January 16, 2026
Summary
The kinesin-1 motor UNC-116, like kinesin-3 UNC-104, promotes AWC OFF subtype specification in C. elegans. Both kinesins cooperate in AWC ON cells to regulate TIR-1 trafficking, ensuring correct neuronal development.
Area of Science:
- Neuroscience
- Cell Biology
- Developmental Biology
Background:
- The Caenorhabditis elegans AWC olfactory neuron pair differentiates into AWC OFF and AWC ON subtypes.
- TIR-1/SARM1 adaptor protein complex is crucial for cell-autonomous AWC OFF specification via axonal transport.
- UNC-104/kinesin-3 motor protein plays a non-cell-autonomous role in AWC ON to promote AWC OFF subtype.
Purpose of the Study:
- To investigate the role of unc-116/kinesin-1 in AWC subtype differentiation.
- To elucidate the relationship between UNC-116, UNC-104, and TIR-1 trafficking in AWC development.
Main Methods:
- Genetic analysis of unc-116 mutants and overexpression in C. elegans.
- Analysis of AWC subtype differentiation phenotypes (AWC OFF and AWC ON).
- Microscopy to observe colocalization of UNC-116, UNC-104, and TIR-1.
Main Results:
- unc-116 mutants enhance the AWC ON phenotype of hypomorphic tir-1 mutants, similar to unc-104 mutants.
- Overexpression of unc-116 in AWC leads to an AWC OFF phenotype, mirroring tir-1 overexpression.
- UNC-116, like UNC-104, acts non-cell-autonomously in AWC ON to regulate TIR-1 trafficking and promote AWC OFF.
Conclusions:
- UNC-116/kinesin-1 cooperates with UNC-104/kinesin-3 in AWC ON cells.
- These kinesins likely transport presynaptic factors that regulate TIR-1/SARM1 complex trafficking.
- This cooperative mechanism ensures proper AWC OFF subtype specification through trans-synaptic regulation.
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