Abstract
Nociception, the ability to detect noxious stimuli, allows organisms to detect potentially harmful environmental factors. Members of the transient receptor potential (TRP) ion channel family have been implicated in chemical nociception in all animals studied. TRPA1 is used by both mammals and insects to detect reactive electrophiles and Painless, another member of the TRPA subfamily, has been implicated in reactive electrophile detection. We used two behavioral feeding paradigms, the Proboscis Extension Response (PER) assay and the Capillary Feeding (CAFE) assay, to screen for genes involved in reactive electrophile detection in Drosophila. Using RNAi lines targeting genes isolated in a noxious heat screen, we found nine candidate genes involved specifically in reactive electrophile detection. RNAi knockdown of one gene, Rpn5, rendered flies defective in avoiding both reactive electrophiles and bitter compounds. This as well as other candidate genes supported the potential role of the proteolysis pathway in chemical nociception. We also used our feeding assays to examine potential interactions between TRPA1and Painless because of their shared involvement in reactive electrophile detection. We found no evidence of genetic or physical interaction between the two channels and discovered that previous PER sensory phenotypes seen in Painless mutants may be attributed to an increase in hunger.