Dmca1A, nbA, l(1)L13, 13, cacaphony
Gene model reviewed during 6.25
Triple stop-codon suppression (UAG, UGA, UAG) postulated; FBrf0234051, FlyBase analysis.
Gene model reviewed during 5.56
Gene model reviewed during 5.41
Gene model reviewed during 5.39
Gene model reviewed during 5.45
Annotated transcripts do not represent all possible combinations of alternative exons and/or alternative promoters
Low-frequency RNA-Seq exon junction(s) not annotated.
1851 (aa); 212 (kD predicted)
Putative phenylalkylamine binding site predicted.
Each of the four internal repeats contains five hydrophobic transmembrane segments (S1, S2, S3, S5, S6) and one positively charged transmembrane segment (S4). S4 segments probably represent the voltage-sensor and are characterized by a series of positively charged amino acids at every third position.
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\cac using the Feature Mapper tool.
GBrowse - Visual display of RNA-Seq signalsView Dmel\cac 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.
Source for identity of: cac CG1522
Source for merge of: cac CG15928
Annotations CG1522 and CG15928 merged as CG43368 in release 5.36 of the genome annotation.
"E(TS2)22" has not been separated from "cacTS2" in meiotic mapping experiments examining more than 1000 recombinant chromosomes. It is either an intragenic mutation in "cac" or is within a closely linked gene.
Annotation CG15928 restored in release 5.15 of the genome annotation.
Hypomorphic mutations in cac result in defects at the mature larval neuromuscular junction; there is a decrease in both synaptic terminal branching and varicosity number. This reduced synapse proliferation is not due to increased synapse retraction. These mutants do not show defects in neuromuscular junction morphology at the late embryonic stage.
Annotation CG15928 eliminated in release 3 of the genome annotation, October 2002.
The cac gene product, an α1-subunit of the L-type calcium channel, plays a role in epithelial fluid transport, in a distinct calcium entry mechanism mediated by CAP2b, cGMP and thapsigargin.
The cac Ca channels mediate multiple, separable biological functions. These correlate in part with transcript diversity generated by alternative splicing.
Mutants exhibit defective courtship song.
Light-on and light-off transient spikes of electroretinogram are reduced in amplitude, and possibly absent in mutants. The prolonged depolarization after potential (PDA) is also abnormal.
cac mutants show complex complementation patterns and interactions. Courtship song is polycyclic in cac mutants, yet courtship hums and wing beats are normal suggesting a specific role of 'cac' in the neural program underlying a feature of wing vibrations. In 'slow phototaxis/Y-tube' tests (using ordinary white fluorescent light), mutant adults were extremely subnormal and in fact preferred the dark-arm of the Y.
Mutants show weak orientation to spots in Y-maze test.
Light-on and light-off transient spikes of electroretinogram are reduced in amplitude, and possibly absent in mutants.
Mutants require higher than normal light-intensity thresholds for optomotor or phototactic responses. More specifically, high-acuity optomotor responses (ability to respond to relatively narrow moving stripes) are relatively normal, but high-sensitivity flies (ability to respond to moving stimuli in dim light conditions) are impaired, hence, a 'night-blind' phenotype.