Gene model reviewed during 5.39
Gene model reviewed during 5.52
2.6 (northern blot)
736 (aa); 97 (kD observed); 81 (kD predicted)
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\barr using the Feature Mapper tool.
GBrowse - Visual display of RNA-Seq signalsView Dmel\barr 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.
RNAi screen using dsRNA made from templates generated with primers directed against this gene results in defects in chromosome condensation and chromosome misalignment on the metaphase spindle when assayed in S2 cells. This phenotype can be observed when the screen is performed with or without Cdc27 dsRNA.
Inactivation of barr using RNA-mediated interference in S2 cells results in extensive defects in chromosome condensation and disrupts chromatid segregation.
Mutations in barr cause a failure of chromosomes to segregate correctly at anaphase, resulting in massive anaphase bridging. barr is not necessary for cell cycle progression out of mitosis. barr encodes a novel, conserved protein that localises throughout chromosomes during mitosis. barr protein associates with Top2 protein and affects its activity, this suggests barr protein functions in chromatid decatenation during the metaphase-anaphase transition.
Weak alleles of barr cause sterile adults with rough eyes and few bristles that die 3-4 days after eclosion. Embryos exhibit loss of some external sensory and multidendritic neurons in the dorsal cluster and most of the chordotonal neurons in the lateral cluster. Severe alleles cause substantial loss of neurons, fasciculation defects and disruptions in the CNS longitudinal tracts.