bru-3, Dm Bru-3
Gene model reviewed during 5.55
Gene model reviewed during 5.46
Stop-codon suppression (UAA) postulated; FBrf0243886.
Gene model reviewed during 6.32
The merge of bru-3 and CG34243 resulted in the loss of the CDS previously associated with CG34243.
Gene model reviewed during 5.44
Low-frequency RNA-Seq exon junction(s) not annotated.
Gene model reviewed during 5.56
gene_with_stop_codon_read_through ; SO:0000697
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\bru3 using the Feature Mapper tool.
Comment: reported as dorsal/lateral sensory complexes
GBrowse - Visual display of RNA-Seq signalsView Dmel\bru3 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.
Annotations CG12478 and CG34243 merged as CG43744 in release 5.44 of the genome annotation.
"gfr" mutant alleles do not behave as simple loss-of-function mutations: they are lethal in trans to each other, yet completely viable and without obvious phenotypes in trans to all available deficiencies and lethal lesions mapping to the 70A-70B chromosomal region (to which the "gfr" complementation group maps). Evidence suggests that "gfr" alleles behave as gain-of-function lesions and that overexpression of "bru-3" is central to the "gfr" mutant phenotype.