A polymorphic inframe deletion in the ODR-10 extracellular loop 2 abolishes diacetyl sensing.

Abstract

The C. elegans wild strain DL226 carries a 30 bp inframe deletion in the odr-10 gene coding for the diacetyl olfactory receptor. DL226 animals are defective for attraction to diacetyl but not to pyrrole, an unrelated odorant also sensed by AWA neurons. Using genome editing in the N2 background, we show that this inframe deletion is causal for the defect in diacetyl sensing. The deletion specifically removes the predicted ligand-binding extracellular loop 2 (ECL2).