|Inserted element||P-element||Expression data|
|Affected gene(s)||sn||Viability / fertility|
|Causes allele(s)||snw||Stock availability||none publicly available|
|Chromosomal location||X ( 7D1-7D2 )||Sequence location|
|Member of Large Scale Dataset(s)|
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|Detailed Mapping Data|
(computed by FlyBase)
7D1-7D2 ( near gene of known cytology )
|Alleles and Phenotypes|
(Collins et al., 1983, Lindsley and Zimm, 1992, Simmons et al., 2002, Biryukova et al., 1999, Rio, 1990, Georgiev and Gerasimova, 1989, Brookfield and Lewis, 1989, Rasmusson et al., 1990, Simmons et al., 1990, Daniels et al., 1990, Ronsseray et al., 1996, Henderson and Glover, 1998, Roiha et al., 1988)
|Phenotype Manifest In|
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.
Repression potential of a P-element repressor protein in a singed sterility assay of snw/snX2 heterozygotes shows partial correspondence with gonadal dysgenic sterility in that strong repression of gonadal dysgenic sterility shows some effect in the singed sterility assay.
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.
used in assay
|Data on Genetic Line|
|Origin as a multiple insertion line|
|Progenitor(s) within the Genome|
|Related Aberration or Balancer|
|Stocks ( 0 )|
|Synonyms & Secondary IDs|
|Secondary FlyBase IDs|
|References ( 18 )|