Gene model reviewed during 5.49
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 5.53
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\GLS using the Feature Mapper tool.
GBrowse - Visual display of RNA-Seq signalsView Dmel\GLS 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: GLS CG42708
The "nemy" mutant was previously associated with the CG8772 annotation in FlyBase, based on information in GenBank accession AF417120. However, data from FBrf0207202 indicates that the nemy mutant phenotype is due to an effect on the neighbouring CG8776 annotation, and not due to an effect on CG8772. Thus, the CG8772 annotation has been split out into a separate gene report in FlyBase (and has been renamed CG42708 in release 5.26 of the genome annotation to avoid confusion) and the nemy mutant has instead been merged with the gene corresponding to the CG8776 annotation in FlyBase.
Identified as a gene with significant level of mRNA cycling as assessed by expression analysis using high density oligonucleotide arrays with probe generated from adult heads harvested over six time points over the course of a day. Showed no change of expression in Clk mutants in microarray experiments. Identified in S2/cycloheximide assay as a direct target of Clk mediated transcriptional regulation.