Insects rely on olfaction for virtually all aspects of their existence, thus this chemosensory system has evolved into an exceptionally discriminative network capable of perceiving thousands of odours. In the model organism Drosophila melanogaster, detection of volatile cues is achieved by three families of receptor proteins, the odorant receptor (OR), gustatory receptor (GR), and ionotropic-like receptor (IRs) families, which are expressed in specific functional classes of olfactory receptor neurons (ORNs). Odorant ligands binding to these proteins initiate signal transduction, however, the underlying mechanisms of olfactory signalling are not well defined. In a search for new olfactory genes, we undertook a large scale EMS-induced mutant screen using electrophysiology to test for olfactory defects. We found a mutant with a pronounced reduction in the responses of ORNs expressing ORs, whilst GR- and IR- expressing ORNs were unaffected. Deficiency mapping and whole genome re-sequencing identified the causative gene, dATP8B. RNAi analyses showed that OR-expressing neurons require dATP8B for olfactory function. Immunohistochemistry analyses indicate that dATP8B localises to the site of signal transduction in the dendritic membrane of OR-expressing ORNs. OR localisation and dendritic morphology appear normal in the dATP8B mutant. As dATP8B encodes a P4-type ATPase, a family of proteins thought to be essential for maintaining the natural asymmetry of phospholipids in bilayered membranes, our findings suggest a requirement of phospholipid asymmetry for OR signalling.