Contains two defective P-elements in tandem.
Tandem insertion of two small P-elements.
Insertion of two inverted P-elements.
Insertion of P-element.
Insertion of a 2 kb P element.
Bristle phenotype is suppressed by su(s)71, and partly suppressed by su(s)sn-w:R.
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. Gnarled macrochaetae and kinky microchaetae.
The presence of P\T66 causes a drastic reduction in destabilisation of snw to sne or sn(+). This repression is not increased by P\T66D1.hs, but it is increased by P\T66C2.hs.
Can mutate during a dysgenic cross to either wild type phenotype or a more extreme (sne) bristle phenotype depending on which one of the P-elements excises.
Phenotype is unaffected by mod(mdg4)ul.
The viability of Mnn1e200 mutants (Df(2L)Mnn1e200 mutants in which milt function is rescued by expression of the milt+22 transgene) is not affected by a snw background.
P{Icarus} destabilises the mutation snw in germ line cells at a maximal rate even without heat shock. P{Icarus} does not destabilise snw in somatic cells.
snw is hypermutable in the M cytotype, mutating either to a more extreme allele (sne), or reverting to wild type. This mutation rate can exceed 50%, with the two derivatives being generated at approximately equal rates. This hypermutability is probably due to the presence of two P-element insertions in snw.
Some somatic reversion of this allele is seen. The rate of somatic reversion is 0.06%. The movements of the P-elements in these somatic reversions occur early in development, and require a trans-acting maternal effect component (P\TMo). Somatic reversion occurs preferentially in attached-X stocks.
Unstable in the M cytotype in the presence of a transposase, mutating either to sne (a more extreme allele) or to sn+ (apparent wild-type).