Abstract
Genetic connections between learning and rhythmicity were suggested to have been established in a previous study, in part because the duskyAndante (dyAnd) mutation in Drosophila disrupted both behaviors. dyAnd, isolated as a slow-clock variant, was reported to cause an approximately fourfold decrement in courtship-suppression conditioning. These effects have been reexamined; the experiments were buttressed by testing the effects of several recently isolated mutations at the dusky locus, along with the original And Allele that had been induced there. The reexamination was also prompted by anatomical concerns, certain of which have recently focused on dy-induced decrements in cell size, but only in terms of wing morphology. Another anatomical issue involves the discovery of a neuronal pathway that seems to connect circadian pacemaker cells to a structure in the Drosophila brain that is involved in learning. In observer-blind experiments, however, it was found that neither pacemaker-slowing (Andante-like) dy mutations nor others that cause no rhythm defects produced subnormal conditioned courtship. Moreover, in the adult brain of a slow-clock dyAnd mutant, no axonal pathway defects were readily discernible and putative pacemaker neurons appeared to be normal in size.