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 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.
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.
HDAC115-1 enhances the variegation of w in In(1)wm4 flies and in 5-10% of the eyes patches of ommatidia show disorganisation characteristic of the rst mutation (enhancement of variegation allows the silencing to spread past the w locus to inactivate rst in a fraction of the cells).
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.
In(1)wm4 flies show position effect variegation at the w locus, at 23oC the phenotype varies from a sectored red and white eye to a red eye peppered with small flecks of red and brown pigmented ommatidia.
Eyes have a "sectored" phenotype - ommatidia are either fully pigmented or not pigmented at all.
Males and homozygous females are viable and fertile.
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.
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.