Mutant males and homozygous females impaired in
several types of learning and memory; associative conditioning
defective in tests using either reward (Tempel et al., 1983)
or aversive unconditioned stimuli (e.g. Dudai, 1983, Proc.
Nat. Acad. Sci. USA 80: 5445-48; Dudai, Svi, and Segel, 1984,
J. Comp. Physiol. 155: 569-76; Livingstone et al.), including
tests of "classical" (e.g. Tully and Quinn, 1985) and
"operant" conditioning (Mariath, 1985); able to learn in associative conditioning tests involving visual cues, but at subnormal levels (Folkers, 1982, J. Insect. Physiol. 28: 535-39), and memory appears to be normal. Learning scores subnormal when measured immediately after certain types of training;
then either scores decay rapidly with time (Tempel et al.,
1983; Tully and Quinn, 1985) or there is no indication of
memory (Mariath). Although defective in some aspects of
learning, heterozygous females behave essentially normally in
shock/odor tests (Dudai et al., 1983). Courtship also defective; unlike wild-type males, rut males court inseminated and
virgin females with equal vigor; they may be unable to distinguish them (Gailey et al.). In tests of non-associative conditioning, rut shows aberrant habituation and sensitization to
sugar stimuli (Duerr and Quinn); rut males subnormal in learning to avoid courtship of immature males; and homozygous or
hemizygous rut females defective in "priming" of mating
behavior by prestimulations with artificial courtship songs;
effects of such acoustical prestimulations decay more rapidly
than normal (Kyriacou and Hall). In either the homozygous or
heterozygous condition rut acts as a partial suppressor of the
sterility of homozygous dnc females inversely related to
degree of rescue, suggesting both a maternal and a zygotic
role of rut (Bellen, Gregory, Olsson, and Kiger, 1987, Dev.
Biol. 121: 432-44; Bellen and Kiger, 1988, Roux's Arch. Dev.
Biol. 197: 258-68). Double mutant females mated to Canton-S
males lay many eggs, but most of the eggs fail to hatch.
Biochemically, rut influences adenylate cyclase activity
(Dudai et al., Livingstone et al.); it seems to abolish a
calcium or calmodulin stimulated component of adenylate
cyclase activity (Livingstone, Dudai, and Zvi, 1984, Neurosci.
Lett. 47: 119-24), while leaving intact a component of
activity stimulated by guanyl nucleotides, fluoride, or
monoamines, suggesting that rut may directly affect the catalytic subunit of the adenylate cyclase complex (Livingstone et
al., Dudai et al., 1984); consistent with this hypothesis is
the observation that cyclase activity in rut is lower than
normal, even in the presence of forskolin (Dudai et al., 1984;
Dudai, Sher, Segal, and Yovell, 1985, J. Neurogenet. 2: 365-80). rut primarily affects total cyclase activity in the
adult abdomen, with progressively milder effects on thoracic
and head cyclase (Livingstone et al., Dudai and Svi, 1985, J.
Neurochem. 45: 355-64); reduction of abdominal adenylate
cyclase activity of rut1>rut2>rut3 (Bellen et al.); the majority of adenylate cyclase activity in wild type is in a particulate fraction, and rut lacks up to 35% of total particulate
activity (Dudai and Zvi, 1985). That rut may in fact encode a
component of the fly's adenylate cyclase catalytic subunit is
suggested by altered Km of enzyme activity in mutant flies
(e.g. Dudai et al., 1983, 1985) and by the fact that hypoploidy of rut+ in females leads to approximately half normal
levels of that cyclase activity specifically affected by the
rut mutations (Livingstone et al.), and hyperploidy for the
normal allele leads to increased activity (Livingstone). The
biochemical results suggest that rut1 could be a null mutation.