Acts as an actin bundling protein (PubMed:1723709, PubMed:19729655). May have a role in the asymmetric organization and/or movement of cytoplasmic components (PubMed:1723709). It has a role in somatic cells during the formation of adult bristles and hairs, and in the female germline during oogenesis (PubMed:1723709, PubMed:19729655).

(UniProt, Q24524)

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, J. Morph. 122: 367-80 (fig.)]. 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, Z. Indukt. Abstamm. Vererbungsl. 28: 1-22 (fig.)]. Sterility autonomous in transplants (sn1; Clancy and Beadle, 1937, Biol. Bull. 72: 47-56; Perrimon and Gans, 1983, Dev. Biol. 100: 365-73). Heterozygotes between female-sterile and fertile alleles are fertile, between female sterile alleles are sterile.

Macrochaetae gnarled in a fairly extreme manner. Microchaetae wild type. sn36a is only allele to cause pronounced reduction in replication of oocyte nurse cell DNA [King and Burnett, 1957, Growth 21: 263-80 (fig.)]. Also causes more extreme retardation of vitellogenesis than other female-sterile sn alleles (Bender). sn36a sn4 homozygote has nearly normal bristles and is sterile. RK1.

A strong allele of sn recovered from a natural population. Associated with simultaneous mutation to club wing, clw, a defect in wing expansion with low penetrance. sn49 is unstable, producing an array of derivatives that are in turn stable or unstable. and the expression of clw differs among them. It mutates to sn+ and back at a rate of approximately 10-3; a rare moderate singed derivative exhibits an approximately ten-fold elevation in mutation frequency, mutating either back to the strong allele or to an unstable normal allele; a single extreme singed derivative of a normal derivative of the moderate allele produces strong-singed and non-singed derivatives, which can in turn revert to the extreme allele and in the case of the strong derivative to non singed (Yurchenko, Zakharov, and Golubovsky, 1984, Mol. Gen. Genet. 194: 279-85).

Moderate sn phenotype. Prototype type B mutable allele; mutation rate 0.1 to 1.2%. Produces both extreme singed and normal-appearing derivatives as well as an array of intermediate phenotypes. In addition strongly reversible alleles (25-50 x more mutable than parental allele) are produced. This allele also associated with increased rate of mutation to fw.

Extreme sn phenotype. Prototype type A mutable allele; mutates to an unstable sn+, which mutates back to extreme alleles; no intermediate alleles recovered.

An allele of sn that is mutable in dysgenic but not in non-dysgenic genotypes. Mutation takes place in two directions; one is to apparent stable reversions and the other to a more extreme phenotype, snex, which is in turn unstable.

Weak singed phenotype, probably class 2. Highly mutable in dysgenic genotypes; 40% to 60% of offspring are either normal (sn(+)) or extreme singed (sne) in phenotype. These derivatives are in turn mutable, but at much lower levels. Completely stable in non-dysgenic genotypes.