AC, Rut-AC, adenylyl cyclase
membrane-bound Ca2+/calmodulin-activated adenylyl cyclase - a crucial memory pathway protein - responsible for synthesis of cAMP - plays a key role in regulating behavioral, neuroanatomical, and electrophysiological plasticity
Gene model reviewed during 5.50
Annotated transcripts do not represent all possible combinations of alternative exons and/or alternative promoters.
Annotated transcripts do not represent all supported alternative splices within 5' UTR.
Gene model reviewed during 5.46
Low-frequency RNA-Seq exon junction(s) not annotated.
Gene model reviewed during 5.52
Multiphase exon postulated: exon reading frame differs in alternative transcripts; overlap >20aa.
9.5, 7.5 (northern blot)
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\rut using the Feature Mapper tool.
rut transcripts are expressed at high levels in the mushroom body perikarya and at lower levels in most cells of the central brain, the optic lobes, the subesophageal ganglion and the thoracic/abdominal ganglia.
rut protein is strongly expressed in the mushroom body alpha', beta', alpha, beta and gamma lobes, and spur, and weakly expressed in the mushroom body calyx.
rut protein is strongly expressed in the neuropil of the mushroom bodies along the stalk and in the α, β, and γ lobes, suggesting that it is transported into the axonal projections of the mushroom body neurons. It is expressed at lower levels in the mushroom body calyx and in the neuropil of the central brain, the optic lobes, the subesophageal ganglion, and the thoracic/abdominal ganglia.
GBrowse - Visual display of RNA-Seq signalsView Dmel\rut in GBrowse 2
Please Note FlyBase no longer curates genomic clone accessions so this list may not be complete
Please Note This section lists cDNAs and ESTs that fall within the genomic extent of the gene model, which may include cDNAs and ESTs of genes within introns, or of overlapping genes. Please see GBrowse for alignment of the cDNAs and ESTs to the gene model.
For each fully sequenced cDNA the DGRC maintains various forms of the cDNA (e.g tagged or untagged) in several different host vectors for subsequent cloning and expression in Drosophila and Drosophila cell lines.
RNAi generated by PCR using primers directed to this gene causes a cell growth and viability phenotype when assayed in Kc167 and S2R+ cells.
rut expression in the mushroom bodies of adult flies is both necessary and sufficient to correct the olfactory memory defect in rut flies - ruling out a requirement for rut expression during development of the mushroom bodies.
The acute role for the rut-encoded type I adenyl cyclase is consistent with rut functioning as a molecular coincidence detector for the convergence of simultaneous signals (e.g. those from a conditioned and an unconditioned stimulus) on a neuron.
rut is required exclusively in the Kenyon cells of the mushroom bodies for a component of olfactory short-term memory.
Subsets of dnc and rut neurons display abnormal spontaneous spikes and altered firing patterns in 'giant' neuron cultures. Abnormal spike activity and reduced K+ current remain in dnc rut double mutants suggesting that the opposite effects on cAMP metabolism by dnc and rut do not counterbalance the mutual functional defects. The aberrant spontaneous activity and altered frequency coding in different stimulus paradigms may present problems in the stability and reliability of neural circuits for information processing during certain behavioural tasks, raising the possibility of modulation in neuronal excitability as a cellular mechanisms underlying learning and memory.
Mutations of rut affect habituation of the electrically stimulated giant fibre response.
Phenotypic analysis reveals control of growth cone mobility requires optimal cAMP levels within an operational range.
Injection of Acp70A into mutant virgin females elicits a small response in behaviour.
rut gene product is preferentially expressed in the mushroom bodies. Cell specific ablation of the mushroom bodies, by hydroxyurea, demonstrates they mediate associative odour learning in flies.
The rutabaga gene was cloned from a Ecol\lacZ enhancer trap-induced rut allele: wild type rut expression is elevated in mushroom bodies, suggesting that mushroom bodies are the principal sites mediating olfactory learning and memory.
The open reading frame is homologous to a major portion of the mammalian adenylyl cyclases. Nucleotide sequence analysis of the open reading frame predicts the encoded protein is 2249 amino acids in length. The amino terminal half appears to share the same overall structure and hydropathy profile as the previously isolated mammalian adenylyl cyclases (Feinstein, 1991, in press, Gao, 1991, in press).
rut plays a secondary role in the maternal regulation of embryonic cAMP content.
rut mutant analysis suggests that the cAMP cascade plays a role in the shaping neuronal connectivity. The sensory neuron innervating the antero-notopleural bristle has an abnormally large number of side branches and varicosities in a defined segment of the axon. Ultrastructure studies suggest that the varicosities are potential synaptic sites.
rut mutants are defective in a step of the cAMP cascade: they show impaired synaptic facilitation and post-tetanic potentiation as well as abnormal responses to direct application of dibutyryl cAMP. Results suggest that the cAMP cascade plays a role in synaptic facilitation and potentiation and indicate that synaptic plasticity is altered in memory mutants.
Mutations in rut affect the sensory fatigue due to anteronotopleural bristle deflection, not sensory adaptation.
Mutant analysis provides evidence for the participation of a G0-like protein in learning and memory.
Mutations in rut significantly reduce the females song memory after prestimulation with courtship hums. This suggests a simple sensitization process may be involved with the female pulse song memory (Kyriacou and Hall, Nature 308: 62).
Mutant males and homozygous females impaired in several types of learning and memory; associative conditioning defective in tests using either reward (Tempel, Bonini, Dawson and Quinn, 1983) or aversive unconditioned stimuli (e.g. Dudai, 1983; Dudai, Svi and Segel, 1984; Livingstone, Sziber and Quinn, 1984), 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) 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, Bonini, Dawson and Quinn, 1983; Tully and Quinn, 1985) or there is no indication of memory (Mariath, 1985). Although defective in some aspects of learning, heterozygous females behave essentially normally in shock/odor tests (Dudai, Uzzan and Zvi, 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, Jackson and Siegel, 1984). In tests of non-associative conditioning, rut shows aberrant habituation and sensitization to sugar stimuli (Duerr and Quinn, 1982); 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, 1984). 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, 1984; Bellen and Kiger, 1988). 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, Svi and Segel, 1984; Livingstone, Dudai and Zvi, 1984); it seems to abolish a calcium or calmodulin stimulated component of adenylate cyclase activity (Livingstone, Dudai and Zvi, 1984), 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, Dudai and Zvi, 1984; Dudai, Svi and Segel, 1984); consistent with this hypothesis is the observation that cyclase activity in rut is lower than normal, even in the presence of forskolin (Dudai, Svi and Segel, 1984; Dudai, Sher, Segal and Yovell, 1985). rut primarily affects total cyclase activity in the adult abdomen, with progressively milder effects on thoracic and head cyclase (Livingstone, Dudai and Zvi, 1984; Dudai and Svi, 1985); 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, Uzzan and Zvi, 1983; Dudai, Sher, Segal and Yovell 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.