Disease relevance of rut

• The ventral ganglion, antennal lobes, and median bundle are likely the CNS structures sufficient for rutabaga AC- dependent spatial learning [1].
• Selection of mutations that suppress dunce sterility has led to the isolation of two rutabaga alleles [2].

Psychiatry related information on rut

• This is in contrast to the mutations dunce , rutabaga , and amnesiac , which primarily affect short-term memory [3].
• A conceptual model of operant conditioning and the levels at which rutabaga and white influence conditioning is proposed [4].

High impact information on rut

• Loss of calcium/calmodulin responsiveness in adenylate cyclase of rutabaga, a Drosophila learning mutant [5].
• The rutabaga adenylyl cyclase, an enzyme that is ubiquitously expressed in the Drosophila brain and that mediates synaptic plasticity, is needed exclusively in the Kenyon cells of the mushroom bodies for a component of olfactory short-term memory [6].
• NF1 appears to regulate the rutabaga-encoded adenylyl cyclase rather than the Ras-Raf pathway [7].
• These mutants, dunce and rutabaga, are defective in different steps of the cyclic adenosine 3',5'-monophosphate (cAMP) cascade [8].
• In both dunce and rutabaga larvae, voltage-clamp analysis of neuromuscular transmission revealed impaired synaptic facilitation and post-tetanic potentiation as well as abnormal responses to direct application of dibutyryl cAMP [8].

Biological context of rut

• Involvement of the cAMP cascade in Drosophila learning and memory is suggested by the aberrant behavioral phenotypes of the mutants dunce (cAMP phosphodiesterase) and rutabaga (adenylyl cyclase) [9].
• Using pan-neural and restricted CNS expression with the GAL4 binary transcription activation system, we have rescued the memory defect of the rutabaga mutant in a fast robust spatial learning paradigm [1].
• Pharmacogenetic rescue in time and space of the rutabaga memory impairment by using Gene-Switch [10].
• Seven lines were isolated with P element insertions in the cytogenetic vicinity of the learning and memory gene, rutabaga, from an enhancer detector screen designed to mark genes preferentially expressed in mushroom bodies [11].
• Drosophila memory mutants dunce (dnc) and rutabaga (rut) are known to have altered intracellular cAMP levels, nerve terminal growth, and plasticity of synaptic transmission [12].

Anatomical context of rut

• Previous studies show that activity-induced facilitation and potentiation are disrupted at larval neuromuscular junctions in the memory mutants dunce (dnc) and rutabaga (rut) of Drosophila [13].
• Induction of the rutabaga cDNA in the mushroom bodies only during adulthood, or during adulthood along with the larval and pupal developmental stages, corrects the olfactory memory impairment found in rutabaga mutants [10].
• Mutant alleles of rutabaga act in the germ line cells to partially suppress the developmental defects caused by dunce mutations [14].

Associations of rut with chemical compounds

• The rutabaga and dunce genes, encode two enzymes of the cyclic adenosine monophosphate transduction pathway in Drosophila, adenylyl cyclase and cyclic adenosine monophosphate phosphodiesterase, respectively [15].
• Postsynaptic expression of an adenylate cyclase encoded by rutabaga (rut), is sufficient to strengthen synaptic transmission at these identified central synapses [16].
• Serotonin reduces potassium current in rutabaga and wild-type Drosophila neurons [17].

Other interactions of rut

• Altered outward K(+) currents in Drosophila larval neurons of memory mutants rutabaga and amnesiac [18].
• DAC39E catalytic activity is inhibited by micromolar concentrations of calcium; therefore, DAC39E is oppositely regulated by calcium compared to the only other tmAC shown to be expressed in the Drosophila CNS, Rutabaga AC [19].
• In contrast to the learning mutants dunce and rutabaga, which are defective in the cAMP cascade, inhibition of CaM kinase in ala transformants caused increased sprouting at larval neuromuscular junctions near the nerve entry point, rather than altering the higher order branch segments [20].
• In Drosophila, Kenyon cells are the dominant site of expression of the dunce, DC0, and rutabaga gene products, enzymes in the cAMP cascade whose absence leads to specific defects in olfactory learning [21].
• Our results show that mutations altering each of four K+ channel subunits (Sh, slo, eag, and Hk) have distinct effects on habituation at least as strong as those of dunce and rutabaga, memory mutants with defective cAMP metabolism () [22].

Analytical, diagnostic and therapeutic context of rut

• Molecular cloning revealed that the P elements were inserted in the putative promoter of the rutabaga gene [11].
• RNA in situ hybridization and immunohistochemistry demonstrated that the expression of the rutabaga gene, which encodes a Ca2+/calmodulin-responsive adenylyl cyclase, is markedly elevated in the mushroom bodies of normal flies and that the insertion elements compromised its expression in the new rutabaga mutants [11].

References