detached, det, DLP2, Dp186, Dystrophin Dp186
Annotated transcripts do not represent all possible combinations of alternative exons and/or alternative promoters.
Low-frequency RNA-Seq exon junction(s) not annotated.
Gene model reviewed during 5.47
Annotated transcripts do not represent all supported alternative splices within 5' UTR.
None of the polypeptides share 100% sequence identity.
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\Dys using the Feature Mapper tool.
Isoform-specific expression patterns are observed. Probes specific to Dys transcripts coding for the 116 kDa protein isoform detect expression in the embryonic and larval body wall musculature, while probes specific to transcripts coding for the 205 kDa protein isoform do not detect expression in these tissues. The 116-specific isoform is also observed at the midline of the embryonic and larval ventral nerve cords. The 205-specific isoform is observed in the pericardial cells of the embryonic dorsal vessel. Both isoforms are expessed in the embryonic ventral nerve cord and in the larval brain.
Dys protein is also expressed in three symmetric clusters on the lateral sides of the neuropil in thoracic segements of the larval ventral nerve cord. An antibody specific to the N-terminal of the 186 kDa isoform (Dys-PB) is immunoreactive in the brain and ventral nerve cord, but not in the eye discs.
GBrowse - Visual display of RNA-Seq signalsView Dmel\Dys 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: Dys det
The sole overt morphological defect associated with null det mutations is the variable loss of the posterior crossvein.
Absence of the large Dys isoforms in the post-synaptic muscle cell leads to elevated evoked neurotransmitter release from the presynaptic apparatus.
Short-term synaptic facilitation of evoked transmitter release is decreased in the mutants, suggesting that the absence of Dys results in increased probability of release.
One of 42 Drosophila genes identified as being most likely to reveal molecular and cellular mechanisms of nervous system development or plasticity relevant to human Mental Retardation disorders.
dsRNA made from templates generated with primers directed against this gene tested in RNAi screen for effects on Kc167 and S2R+ cell morphology.
Nichols-Skoog, 27th Nov. 1935.