EGL‐4/PKG regulates the role of an interneuron in a chemotaxis circuit of <i>C. elegans</i> through mediating integration of sensory signals

<jats:title>Abstract</jats:title><jats:p>Interneurons, innervated by multiple sensory neurons, need to integrate information from these sensory neurons and respond to sensory stimuli adequately. Mechanisms how sensory information is integrated to form responses of interneurons are not fully understood. In <jats:italic>Caenorhabditis</jats:italic> <jats:italic>elegans</jats:italic>, loss‐of‐function mutations of <jats:italic>egl‐4</jats:italic>, which encodes a cGMP‐dependent protein kinase (PKG), cause a defect in chemotaxis to odorants. Our genetic and imaging analyses revealed that the response property of AIY interneuron to an odorant is reversed in the <jats:italic>egl‐4</jats:italic> mutant, while the responses of two upstream olfactory neurons, AWA and AWC, are largely unchanged. Cell‐ ablation experiments show that AIY in the <jats:italic>egl‐4</jats:italic> mutant functions to suppress chemotaxis. Furthermore, the reversal of AIY response occurs only in the presence of sensory signals from both AWA and AWC. These results suggest that sensory signals are inadequately integrated in the <jats:italic>egl‐4</jats:italic> mutant. We also show that <jats:italic>egl‐4</jats:italic> expression in AWA and another sensory neuron prevents the reversed AIY response and restores chemotaxis in the <jats:italic>egl‐4</jats:italic> mutants. We propose that EGL‐4/PKG, by suppressing aberrant integration of signals from olfactory neurons, converts the response property of an interneuron to olfactory stimuli and maintains the role of the interneuron in the circuit to execute chemotactic behavior.</jats:p>