C. elegans GPCR kinase GRK-1 maintains behavioral persistence in a dynamic thermal environment.

How do animals maintain behavioral states as sensory inputs vary with movement and location? Here, we uncover a neuronal mechanism that allows the nematode Caenorhabditis elegans to move isothermally on a temperature gradient for several minutes at temperatures associated with its food experience. We find that prolonged isothermal tracking along the preferred temperature requires GRK-1, the C. elegans homolog of human GPCR kinase GRK5. Loss of grk-1 reduces isothermal tracking durations, and these defects can be rescued by simultaneous grk-1 expression in RIM and AVA interneurons. Furthermore, silencing RIM and AVA restores the short isothermal tracking defects in the absence of grk-1, while leaving wild-type isothermal tracking unchanged. These data suggest that wild-type RIM and AVA are in a suppressed neuronal state during isothermal tracking. Also, imposing a normally suppressed neuronal state in RIM and AVA during isothermal tracking can functionally compensate for the loss of grk-1. Together, our findings reveal a previously unknown molecule-to-circuit function of GRK-1/GRK5 in RIM and AVA interneurons that maintains a minute-scale behavioral state on a temperature gradient.