Low-frequency RNA-Seq exon junction(s) not annotated.
Annotated transcripts do not represent all supported alternative splices within 5' UTR.
Gene model reviewed during 5.47
Annotated transcripts do not represent all possible combinations of alternative exons and/or alternative promoters.
4.0 (northern blot)
None of the polypeptides share 100% sequence identity.
1058 (aa); 114 (kD predicted)
Interacts with wash. Interacts with spir.
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\capu using the Feature Mapper tool.
capu transcripts are detected as early as germarium stage 2 in the ovary. They are present in nurse cells in stage S1-S13 egg chambers. They are also detected in the oocyte nucleus from stage S4 to S9 and weakly in follicle cells from stage S4 to S11. On northern blots, capu transcripts are detected throughout embryogenesis, are absent in 1st and 2nd instars, and reappear in third instar larvae. They are also found in ovaries, in ovarectomized females, and in males.
GBrowse - Visual display of RNA-Seq signalsView Dmel\capu 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.
dsRNA made from templates generated with primers directed against this gene tested in RNAi screen for effects on Kc167 and S2R+ cell morphology.
dsRNA made from templates generated with primers directed against this gene is tested in an RNAi screen for effects on actin-based lamella formation.
The chic mutant phenotype resembles that caused by disrupting the actin cytoskeleton with cytochalasin D, and that of capu and spir. Mutants in chic resemble those in capu in that they fail to localize stau protein and osk mRNA to the posterior pole of the developing oocyte.
Analysis of capu mutant oocytes suggests that the microtubule cytoskeleton is misregulated resulting in premature microtubule bundling at the cortex of the oocyte and premature microtubule-dependent cytoplasmic streaming within the oocyte. Induction of premature microtubule based streaming in wild type embryos does not sweep away all previously localised molecular determinants, in support of the suggestion that the premature streaming alone cannot explain all of the patterning defects.
The posterior signal can be active at the anterior independent of capu function.
capu is required specifically for the localization, not the synthesis, of the posterior signal.
Mutations in maternal dorsal class gene capu do not interact with RpII140wimp.