3C2;h28
3C2;20B
3C1-3C2;20A
3C1-3C2;h28
l(1)2Ea << bk1 << w << CR << bk2
Breakpoint reported to map between R5 cordinates X:2661012 and X:2662278 .
Breakpoint(s) molecularly mapped
Left (3C1-2) breakpoint at -24.5 kb in the restriction map of the w locus (0 point at site of the copia insertion in wa); right (20F) breakpoint near 5' end of a Type I mobile element (Tartof et al., 1984). Left breakpoint less than 3kb distal to the w-a copia insertion (Pirrotta et al., 1983).
The X heterochromatin in Dp(1;f)1173 appears to suppress the eye colour variegation phenotype of In(1)wm4.
The X heterochromatin in Dp(1;f)1187 appears to suppress the eye colour variegation phenotype of In(1)wm4.
The X heterochromatin in Dp(1;f)1205 appears to suppress the eye colour variegation phenotype of In(1)wm4.
The X heterochromatin in Dp(1;f)1346 appears to suppress the eye colour variegation phenotype of In(1)wm4.
The autosomal heterochromatin in Dp(2;f)e51 appears to suppress the eye colour variegation phenotype of In(1)wm4.
The autosomal heterochromatin in Dp(2;f)e58 appears to suppress the eye colour variegation phenotype of In(1)wm4.
The autosomal heterochromatin in Dp(2;f)e97 appears to suppress the eye colour variegation phenotype of In(1)wm4.
The position effect variegation (PEV) at the w locus seen in the In(1)wm4 chromosome is suppressed if males are also carrying one of Df(Y)bb-465, Df(Y)bb-76, Df(Y)l-481, Df(Y)l-498, Df(Y)l-510 or Df(Y)l-473.
Df(3L)Aprt-21 dominantly enhances the position effect variegation of the w gene caused by In(1)wm4.
The position effect variegation of w seen in In(1)wm4 is suppressed by one copy of Df(3R)crb-F89-4.
Variegation is not affected by Df(2R)pk-sple-51/+, Df(2R)nap2/+, Df(2R)sple-D2/+, Df(2R)sple-D1/+, Df(2R)pk30/+ or Df(2R)pk30/Df(2R)pk30/+.
Position effect variegation (PEV) at the w locus caused by In(1)wm4 is dominantly enhanced by Dp(2;2)Mdh and suppressed by Df(2R)en-A or Df(2R)en-SFX31.
The position effect variegation at the w locus caused by In(1)wm4 is suppressed by Df(3R)Ace-HD1.
The position effect variegation of w caused by In(1)wm4 is enhanced by Df(2L)cl-h1 and Df(2L)cl-h4. This phenotype is suppressed by Hel25E+t4.5; the level of variegation seen in In(1)wm4 ; Df(2L)cl-h4/Hel25E+t4.5 flies is the same as seen in In(1)wm4/+ flies.
A notable enhancement of position effect variegation in observed in the presence of B chromosomes, small, heterochromatic chromosomes that are transmitted in a non-Mendelian manner.
Tn10\tetRey.3.5.T:Hsim\VP16-mediated expression of Hsap\HMGA1MATH20.tetO in In(1)wm4 flies results in significant derepression of the w gene and a general loss of the variegating phenotype. Tetracycline treatment inhibits Hsap\HMGA1MATH20.tetO-induced suppression of PEV. Tn10\tetRey.3.5.T:Hsim\VP16-mediated expression of Hsap\HMGA1MATH11.tetO in In(1)wm4 flies results in no significant derepression of the w gene, no loss of the variegating phenotype.
The position effect variegation at the w locus caused by In(1)wm4 is enhanced by Su(var)3-7+t6.5.
Variegated eye phenotype is enhanced in the presence of mod(mdg4)ul, mod(mdg4)u2 and mod(mdg4)B2, eyes appear yellow with orange spots. In the presence of su(Hw)MC the phenotype is no longer enhanced and the eye phenotype returns to wild type. These results indicate that the variegating phenotype is caused by the su(Hw) protein.
z+ In(1)wm4 flies reared at 25oC have dark red/brown mottled eyes. z1 In(1)wm4 males and females have fewer red/brown patches on a lighter background, paired copies of In(1)wm4 are not repressed to z eye colour (lemon yellow). Repression of In(1)wm4 by z1 cannot be restored by Su(var)205. zv77h In(1)wm4 females and males have almost bleached white eye colour with a few scattered red facets, Su(var)205 only moderately suppresses PEV.
Carnitine compounds (L-Carnitine, L-Acetylcarnitine and L-Propionylcarnitine) show a significant suppression on w variegation. Butyrate gives a weaker suppression. In males the suppression effect of the compounds was seen at all concentrations, but in females the effect is weak and is only seen with high concentrations.
Eyes have a "sectored" phenotype - ommatidia are either fully pigmented or not pigmented at all.
Enhances the expression of PgdA in larvae and adults.
Males and homozygous females are viable and fertile.
Muller, 1929.
The presence of a variegating chromosome and a modifier chromosome in the same parental genome can alter the amount the amount of variegation formed in the progeny. The genomic imprinting is not determined by the parental origin of the variegating chromosome but is instead determined by the genetic background the variegating chromosome is subjected to during gametogenesis.
w transvection is eliminated by PEV.
X ray-induced revertants of In(1)wm4 may or may not carry a segment of flanking heterochromatin: variegation is not controlled from immediately adjacent heterochromatic sequences at the euchromatin/ heterochromatin border but from a site more internal to the heterochromatin domain.
A strongly variegating line has been designated In(1)wm4h.
Distal inversion breakpoint is ~20kb from the 3' end of the w locus, the proximal inversion breakpoint is within centric heterochromatin distal to bb. Heterochromatic breakpoint is flanked by a Type I mobile element (FBrf0040503).
Proximal breakpoint defines the distal boundary of the bb locus.
Proximal breakpoint is approximate. The distal breakpoint is to the left of w and the proximal breakpoint is to the left of bb.
Limits of break 1 from polytene analysis (FBrf0018623) Limits of break 2 from polytene analysis (FBrf0040503)