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 "sn^f", "sn^m", "sn^s" and "sn^ext", 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 "sn^A" and "sn^B", "sn^A" alleles mutating to normal and back to the original phenotype only and "sn^B" 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.

In(1)T2. y^mos w^Y1 sn^mY1 strain suppresses y gene mutability and activates sn gene mutability.

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 w^a 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.

The effects of varying degrees of P-element activity and X irradiation on sn^w mutability are assessed. Analysis of the combined effects of P-element activity, X irradiation and either excision or post-replication DNA repair on sterility and fecundity is performed.

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.

Mutations in sn induced by P-M hybrid dysgenesis have been analysed to determine why sn is a hotspot for mutation during P-M hybrid dysgenesis.

Mutant alleles are useful as markers in clonal analysis.

Locus divided into three recombinationally different sites from distal to proximal: (sn³ and sn^36a) (sn² and sn⁴) (sn¹, sn⁵ and sn^50k) (Ives and Noyes, 1951; Hexter, 1955a; Hexter, 1955b). Of these, sn³ and sn^36a 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).