Characterization of a behevior in Caenorhabditis elegans ADAR mutants

Adenosine deaminases that act on RNA (ADARs) are RNA editing enzymes that convert adenosine (A) to inosine (I) and are highly expressed in the nervous system. Homozygous deletion of the Drosphila ADAR results in flies with behavioral defects such as paralysis, uncoordination, tremors as well as brain lesions. In C. elegans, adr-1 is expressed widely in the nervous system and deletion of ADARs results in abnormal chemotaxis. In mammals, absence of editing by ADAR2 at the Q/R site of the glutamate receptor leads to early-onset seizures and postnatal lethality. RNA editing of serotonin receptors results in isoforms with reduced constitutive activity. Since these receptors function in learning and memory and have been shown to be involved in movement, we considered the possibility that worms lacking ADARs have defects in these skills. Using an established thermotaxis assay, we show that C. elegans adr-2 mutants, in contrast to wild type animals, are cryophilic and have defects in finding the temperature of cultivation. However, they retain the ability to track isothermally at a given temperature. Preliminary results also indicate defective thermotaxis behavior in adr-1 and RNAi mutants. Our study suggests that ADARs may have a regulatory role in learning and experience-dependent behavior.