Psychiatry related information on cac

• We conclude that cac causes only a limited array of well-defined defects: longer and louder tone pulses in the song and depressed locomotor activity [1].

High impact information on cac

• To indicate its similarity to this subfamily of vertebrate isoforms, we name this protein Dmca1A, for Drosophila melanogaster calcium channel alpha1 subunit, type A. Northern blot analysis detected a single 10 [2].
• Dmca1A maps to a chromosomal region implicated in, and is the likely candidate for, the gene involved in the generation of behavioral, physiological, and lethal phenotypes of the cacophony, nightblind-A, and lethal(1)L13 mutants [2].
• In a screen for behavioral mutants that disrupt synaptic transmission, an allele of the N-type calcium channel locus (Dmca1A) was identified that caused synaptic undergrowth [3].
• However, the amount of estimated gene flow among the Sobral siblings is about seven times higher than the previously estimated for period, another lovesong gene, perhaps indicating that introgression might be affecting cacophony more than period [4].
• Genetic analysis of a synaptic calcium channel in Drosophila: intragenic modifiers of a temperature-sensitive paralytic mutant of cacophony [5].

Biological context of cac

• To further examine the functions and interactions of cac-encoded calcium channels, a genetic screen was performed to isolate new mutations that modify the cac(TS2) paralytic phenotype [5].
• The cacH18 mutant exhibits defects in visual physiology (including complete unresponsiveness to light in certain genetic combinations) and visually mediated behaviors; this mutant (originally nbAH18) has a stop codon in an alternative exon (within the cac ORF), which is differentially expressed in the eye [6].
• Possible implications of these findings are discussed in the context of structure-function studies of synaptic calcium channels, as well as alternative splicing and mRNA editing of the cac transcript [7].
• This mutant has allowed synaptic electrophysiology after acute perturbation of a specific calcium-channel gene product, demonstrating that cac encodes a primary calcium channel functioning in neurotransmitter release [7].
• Here we report the molecular lesion in cac(TS2), a missense mutation within a calcium-dependent regulatory domain of the alpha1 subunit, as well as phenotypic rescue of temperature-sensitive and lethal cac mutations by transgenic expression of a wild-type cac cDNA [7].

Other interactions of cac

• Electrophysiological studies in this mutant, designated cac(TS2), indicated cac encodes a primary calcium channel alpha1 subunit functioning in neurotransmitter release [5].
• However, the most recently isolated cac mutant was identified as an enhancer of a comatose mutation's effects on general locomotion [8].
• Owing to cacophony being originally identified as a "behavioral gene," the possible significance of Dmca1A RNA editing for influencing the relevant neuro-functional phenotypes is discussed [9].
• This shows that the song gene(s) may be located inside a large X-chromosomal inversion in D. littoralis (as previously suggested), but that it may also be located on an area between this inversion and the centromere, close to nonA and Dmca1A [10].

Analytical, diagnostic and therapeutic context of cac

• We have shown by RT-PCR that the Drosophila L-type calcium channel alpha1-subunit genes Dmca1D and Dmca1A (nbA) are both expressed in tubules [11].
• Using degenerate-primers PCR we isolated and sequenced fragments from the sand fly Lutzomyia longipalpis homologous to two behavioural genes in Drosophila, cacophony and period [12].

References