casy-1 encodes a type I transmembrane protein with two extracellular cadherin domains and an LG/LNS domain that is the sole C. elegans calsyntenin/alcadein ortholog; genetic studies indicate that in C. elegans casy-1 activity is required, in parallel to the insulin-like signaling pathway, for several types of learning, including salt chemotaxis learning, temperature learning, olfactory adaptation, and integration of two sensory stimuli; large-scale RNAi experiments also suggest that casy-1 plays a role in embryonic development; casy-1 expression in adult animals is able to rescue salt chemotaxis learning defects, indicating that CASY-1 function in mature animals is sufficient to effect proper chemotactic behavior; in addition, CASY-1 expression in the ASER neuron, but not other neurons, rescues salt chemotaxis learning defects, indicating the CASY-1 can act solely in this chemosensory neuron for normal salt chemotaxis learning; a casy-1::GFP promoter fusion is expressed throughout the nervous system, including the head amphid sensory neurons, with additional expression seen in the intestine and gonadal sheath cells; a CASY-1::GFP protein fusion localizes to the plasma membrane and intracellular membranes of neuronal cell bodies, with specific N-terminal fusions indicative of CASY-1 ectodomain release into the extracellular space; domain-specific rescue experiments indicate that the secreted, proteolytically processed CASY-1 extracellular domain is sufficient to rescue salt chemotaxis learning defects.
Predicted to enable several functions, including X11-like protein binding activity; amyloid-beta binding activity; and kinesin binding activity. Involved in several processes, including GABAergic synaptic transmission; olfactory learning; and positive regulation of synaptic vesicle transport. Located in several cellular components, including extracellular region; neuromuscular junction; and neuronal cell body membrane. Expressed in neurons. Is an ortholog of human CLSTN2 (calsyntenin 2) and CLSTN3 (calsyntenin 3).
Map position created from combination of previous interpolated map position (based on known location of sequence) and allele information. Therefore this is not a genetic map position based on recombination frequencies or genetic experiments. This was done on advice of the CGC.