Bic-C, BG:DS00913.2 , l(2)br34, br34
Gene model reviewed during 5.52
Annotated transcripts do not represent all supported alternative splices within 5' UTR.
Gene model reviewed during 5.54
4.2, 4.0, 3.5, 2.7 (northern blot)
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\BicC using the Feature Mapper tool.
BicC protein is first detected in the oocyte at stage 3 but remains faint until stage 5 when the levels increase substantially. In stages 4-6, BicC protein is present throughout the ooctye cytoplasm but is enriched at the posterior pole. In stages 7 to 9, it is abundant in the oocyte cytoplasm. In addition, it is enriched at the anterior of the oocyte and around the cortex. From stage 10 on, BicC protein is present at high levels in nurse cells.
GBrowse - Visual display of RNA-Seq signalsView Dmel\BicC 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: BicC CG4824
One or more of the processed
transcripts for these genes contain two non-overlapping open reading frames (ORFs). The non-overlapping
BicC produces a localised RNA, which encodes a putative RNA binding protein containing KH domains. The spatial and temporal characteristics of BicC expression and the nature of the BicC protein indicate a function for it in the localisation of specific RNAs during oogenesis.
BicC is required for the correct targeting of the migrating anterior follicle cells and for specifying anterior position.
Mutations at the BicC locus cause defects in midoogenesis.
10 additional alleles are discussed but are not named.
A maternal-effect semi-lethal; the majority of embryos produced by BicC/+ mothers given rise to normal larvae a minority fail to hatch and vary in phenotype. Double-abdomen embryos have a normal posterior end and the anterior end replaced by mirror image series of posterior segments, e.g. A8-A4|A4-A8 to A8-A6|A6-A8; they need not have the same number of segments on either side of the reversal of polarity, the duplicated portion having fewer segments; generally more segments seen ventrally than dorsally. Less severely affected embryos may be headless, or with reduced mouth parts, or even normal appearing but failing to hatch. The incidence and severity of abnormal embryos vary with genetic background and temperature, the incidence being highest at 25oC and decreasing at lower and higher temperatures. The majority of the embryos produced by BicC/BicD trans heterozygotes are abnormal. Homozygotes are abnormal. Homozygous BicC females sterile, germ-cell differentiation blocked at the beginning of vitellogenesis. Follicle cells do not invade between oocyte and nurse cells; they do synthesize a chorion which remains open ended like a chalice or a cup; such eggs never fertilized.