profilin, sand, chi, stranded
Gene model reviewed during 5.40
Annotated transcripts do not represent all supported alternative splices within 5' UTR.
Low-frequency RNA-Seq exon junction(s) not annotated.
Gene model reviewed during 5.44
1.2, 1.0 (northern blot)
Occurs in many kinds of cells as a complex with monomeric actin in a 1:1 ratio.
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\chic using the Feature Mapper tool.
GBrowse - Visual display of RNA-Seq signalsView Dmel\chic in GBrowse 2
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.
Identified in an RNAi screen for host factors that alter infection of SL2 cells by M.fortuitum.
dsRNA directed against this gene causes defects in cytokinesis when tested in an RNAi screen in S2 cells.
dsRNA made from templates generated with primers directed against this gene is tested in an RNAi screen for effects on actin-based lamella formation.
chic regulates actin filament formation throughout the cell cortex in the follicular epithelium.
Mutations in chic disrupt cytokinesis during male meiosis, preventing the formation of both the central spindle and the contractile ring.
Identification: Enhancer trap screen designed to discover genes involved in the cellular aspects of defense mechanisms, as well as in melanotic tumor formation processes linked to blood cell dysregulation.
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.
Phenotypic analysis of chic male-sterile alleles reveals defects in meiotic cytokinesis and suggests that proper actin assembly is necessary for centrosome separation and migration.
Induced expression of chic proteins causes aberrant cell shapes reflecting defects in cytokinesis and/or cel shape maintenance.
Proliferation defect locus.
Identification: Screen for mutations affecting neuromuscular connectivity, using an antibody to Fas2.
The network of cytoplasmic actin filaments in each nurse cell is missing in chic egg chambers: this does not account for the chic phenotype. Cytoplasm transport is disrupted as nuclei are not properly held in position during chic nurse cell regression and when flow starts the nuclei are pushed into the ring canals thus blocking the pathway to the oocyte.
There are at least 10 P element insertions at chic with effects on both male and female fertility and bristle formation. Female sterile mutation caused by loss of ovary specific transcript. P insert in first exon.
Promotes actin assembly.