CapG, dcap-g, l(2)49Ff, vr9, l(2)vr9
Gene model reviewed during 5.49
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\Cap-G using the Feature Mapper tool.
GBrowse - Visual display of RNA-Seq signalsView Dmel\Cap-G 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: Cap-G CG17054
Immunoprecipitation and complex formation studies provide evidence that Cap-G does not associate with condensin II-specific subunits, while it can be readily detected in complexes with condensin I-specific proteins in vitro and in vivo.
Cap-G has a role in disassembly of the synaptonemal complex and proper retention of the chromosomes in a metaphase I-arrested state during female meiosis.
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.
Chromosome condensation appears largely unaffected in mutant embryos, while massive defects in sister chromatid segregation occur during mitosis.
Cap-G is required during mitosis for chromosome condensation during prophase and prometaphase.
Cap-G mutants show defects in chromosome condensation during prophase and prometaphase, but this defect is resolved by metaphase. Defects in sister chromatid separation are also seen in Cap-G mutants.
dsRNA directed against this gene causes defects in cytokinesis when tested in an RNAi screen in S2 cells.
Mutants are embryonic lethal and show defects in chromosome segregation in mitosis. There are no obvious defects in condensation at prophase and metaphase, but chromosome structure is affected, as evidenced by the failure of chromosome arms to separate fully at anaphase. Chromatid separation at the centromere is unaffected, and localization and delocalization of the mei-S332 centromeric cohesion protein is also normal.