Genetic connections between learning and rhythmicity were suggested to
have been established in a previous study, in part because the dusky(
Andante) (dy(And)) mutation in Drosophila disrupted both behaviors. dy
(And), isolated as a slow-clock variant, was reported to cause an appr
oximately fourfold decrement in courtship-suppression conditioning. Th
ese effects have been reexamined; the experiments were buttressed by t
esting 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 involve
s the discovery of a neuronal pathway that seems to connect circadian
pacemaker cells to a structure in the Drosophila brain that is involve
d in learning. In observer-blind experiments, however, it was found th
at neither pacemaker-slowing (Andante-like) dy mutations nor others th
at cause no rhythm defects produced subnormal conditioned courtship. M
oreover, in the adult brain of a slow-clock dy(And) mutant, no axonal
pathway defects were readily discernible and putative pacemaker neuron
s appeared to be normal in size.