fascin, fs(1)K418, fs(1)M45
fascin homolog - crosslinks actin filaments - the gnarled, kinky bristle phenotype is due to the lack of Actin filament bundles in both large and small bristles - regulates nuclear actin during oogenesis - required for blood cell migration during embryogenesis
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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 5.50
3.6, 3.3, 3.0 (northern blot)
512 (aa); 57 (kD observed)
512 (aa); 57 (kD predicted)
Bacterially expressed sn protein is able to bundle F-actin in vitro.
Interacts with Rab35, with stronger binding to the Rab35-GTP form compared to the Rab35-GDP form.
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\sn using the Feature Mapper tool.
Comment: reported as procephalic ectoderm primordium
Comment: reported as procephalic ectoderm primordium
Comment: reported as procephalic ectoderm primordium
Comment: reported as procephalic ectoderm primordium
Comment: reported as procephalic ectoderm primordium
Comment: reported as procephalic ectoderm primordium
Comment: reported as dorsal vessel specific anlage
Comment: reported as plasmatocytes anlage
Comment: reported as visceral branch specific anlage
sn transcript is expressed in the head (procephalic) mesoderm starting at embryonic stage 8, becoming prominent at stages 9-10. sn transcript is expressed in circulating hemocytes throughout embryogenesis, in the CNS from stage 11, and in epidermal cells forming apical extensions from stage 14-16. sn is not detected in crystal cells.
sn is enriched in border follicle cells relative to follicle cells.
sn protein is localized to the nuclei of nurse cells from oogenesis stage 10B-12; and to the nuclear periphery of nurse cells at oogenesis stage 13.
The sn protein is found in the cytoplasm of nurse cells and the cytoplasm of the developing bristles of the pupa.
sn protein is upregulated in border cells relative to follicle cells.
sn protein expression is enriched in border follicle cells relative to other cells in the egg chamber throughout migration.
sn protein is expressed during oogenesis, and during pupal bristle formation. In stage 9 egg chambers, sn protein is present in border cells and posterior follicle cells. In early stage 10, centripetal follicle cells express sn protein. Although sn protein is present in the nurse cell cytoplasm from early oogenesis, the amounts of the protein increase dramatically early in stage 10. By late stage 10, when the actin filament bundles form, the nurse cell cytoplasm contains high amounts of sn protein, and the high levels persist through stage 11. sn protein is also expressed during bristle formation. In pupae, the cytoplasm of extending bristles and tormogen cells express sn protein.
GBrowse - Visual display of RNA-Seq signals
View Dmel\sn in GBrowse 21-22
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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.
monoclonal
Source for identity of: sn CG1536
Source for merge of: sn CG15331
Annotations CG1536 and CG15331 merged as CG32858 in release 3 of the genome annotation.
Bender has classified sn alleles into four classes: class 1 = female sterile with gnarled macrochaetae and kinky microchaetae; class 2 = female fertile with kinky macrochaetae only; class 3 = female fertile with gnarled macrochaetae and kinky microchaetae; class 4 = female sterile with gnarled macrochaetae only. To these Golubovsky and Kozlovskaya (1978) have added class 5 = kinky microchaetae only. Derivative alleles have sometimes been designated generically as "snf", "snm", "sns" and "snext", for faint, moderate, strong and extreme phenotypes; these symbols do not specify particular alleles (e.g., Zakharov and Golubovsky, 1984). Unstable alleles also classed as "snA" and "snB", "snA" alleles mutating to normal and back to the original phenotype only and "snB" alleles mutating to an array of intermediate states as well as to normal.
sn is an important determinant of class III neuron dendrite morphology, and is necessary for the formation of the characteristic spiked protrusions which are the terminal branchlets of this neuron class.
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.
Definitive denticle belt phenotypes (abnormal hairs and/or bristles) are foreshadowed by abnormal organisation of the actin cytoskeleton in embryonic epidermal cells.
One of a class of genes with TATA-less promoters that have a subset of the conserved DPE sequence.
Single amino acid mutations in the fascin encoded by sn disrupt actin bundling function.
sn is required for actin filament bundle formation in the cytoplasm of nurse cells during oogenesis and for organised actin filament bundle formation in the cellular extension that forms a bristle.
Mutant sn nurse cells lack actin halo and transport of cytoplasm is blocked.
Superunstable mutations generated in crosses of π2 strain to a wa strain or its derivatives. Each superunstable mutation gives rise to a large family of new super-unstable mutations with a wide range of phenotypic expression. Mutations with the same phenotype often differ in the specificity of their potential for further mutation. Each superunstable mutation is associated with a specific, "paired", reversible mutation. Active transposase encoded by P elements is necessary to maintain superinstability. X transposable element is also implicated in the mutability system.
Site selected mutagenesis and isolation of sn mutations.
Four independently obtained families of super-unstable mutations at the sn locus have been studied.
Alleles show P cytotype-dependent sterility and aberrant oocyte morphology in a P cytotype genetic background.
Mutant alleles are useful as markers in clonal analysis.
Locus divided into three recombinationally different sites from distal to proximal: (sn3 and sn36a) (sn2 and sn4) (sn1, sn5 and sn50k) (Ives and Noyes, 1951; Hexter, 1955a; Hexter, 1955b). Of these, sn3 and sn36a show lesions between -0.9 and 0.0 kb, whereas sn2 has a lesion between 8.0 and 10.5. The others show no detectable molecular lesions and are presumed to be point mutations within the coding region between 11.1 and 13.8 kb.
Macrochaetae deformed, from short and gnarled to wavy, depending on allele. Similarly, microchaetae may be straight or wavy. Electron-microscope examination of developing bristle shaft shows flattened fiber bundles around periphery, which occupy but 5% of cross-sectional profile, compared to wild type, which have fiber bundles that are circular in cross-section and occupy 20% of cross-sectional area (Overton, 1967). Females homozygous for the most extreme alleles are completely sterile; vitellogenesis defective. Eggs laid by sn1 homozygotes are normal in number, but are short, blunt and wrinkled with small blunt dorsal appendages (Mohr, 1922. Sterility autonomous in transplants (sn1; Clancy and Beadle, 1937; Perrimon and Gans, 1983). Heterozygotes between female-sterile and fertile alleles are fertile, between female sterile alleles are sterile. The sn locus seems to be a very favorable site for P-element insertion; a number of alleles have been isolated from natural populations in the USSR or are derivatives thereof. These alleles are highly mutable, generating innumerable derivative mutable normal-appearing and extreme singed alleles; some have been shown to carry P-element sequences at sn (Golubovsky, Ivanov, and Green, 1977; Green, 1977). Also some display slight increases in the rate of nondisjunction from Basc (Golubovsky, 1983).