No abstract

Insect olfactory receptor (Or) genes are large, rapidly evolving gene families of considerable interest for evolutionary studies. They determine the responses of sensory neurons which mediate critical behaviours and ecological adaptations. We investigated the evolution across the genus Drosophila of a subfamily of Or genes largely responsible for the perception of ecologically relevant aliphatic esters; products of yeast fermentation and fruits. Odour responses were recorded from eight classes of olfactory receptor neurons known to express this Or subfamily in D. melanogaster and from homologous sensilla in seven other species. Despite the fact that these species have diverged over an estimated 40 million years, we find that odour specificity is largely maintained in seven of the eight species. In contrast, we observe extensive changes in most neurons of the outgroup species D. virilis, and in two neurons across the entire genus. Some neurons show small shifts in specificity, whilst some dramatic changes correlate with gene duplication or loss. An olfactory receptor neuron response similarity tree did not match an Or sequence similarity tree, but by aligning Or proteins of likely functional equivalence we identify residues that may be relevant for odour specificity. This will inform future structure-function studies of Drosophila Ors.

The cuticular melanization phenotype of black flies is rescued by h-alanine, but h-alanine production, by aspartate decarboxylation, was reported to be normal in assays of black mutants, and although black/Dgad2 is expressed in the lamina, the first optic ganglion, no electroretinogram (ERG) or other visual defect has been demonstrated in black flies. The purpose of this study was to investigate the black gene, and protein, in black 1 mutants of Drosophila melanogaster in order to resolve the apparent paradox of the black phenotype. Using black 1 mutant flies we show that (1) aspartate decarboxylase activity is significantly reduced in adults and at puparium formation, consistent with defects in cuticular and non-cuticular processes, (2) that the black 1 mutation is a frameshift, and black 1 flies are nulls for the black/ DGAD2 protein, and (3) that behavioural experiments using Buridan's paradigm, demonstrate that black responds abnormally to visual cues. No ERG, or target recognition defects can be demonstrated suggesting a problem with higher order visual functions in black mutants. D