Point mutation in the splicing site leading to deletion of the domain important for its localisation in the nucleus and association with heterochromatin in salivary glands.
Nucleotide substitution: G?A. Mutation at the first nucleotide position of intron 4. Mutation leads to exon skipping.
Nucleotide substitution: G?A. Mutation at the first nucleotide of the last intron.
G8210352A
G?A
Mutation in the first nucleotide of intron 4. The mutation leads to exon skipping.
neuroblast & larval brain
Neuroblasts in the brain of Su(var)2051/Su(var)2055 or Su(var)2054/Su(var)2051 larvae show a high frequency of abnormal metaphase configurations, including telomere-telomere fusions.
Homozygous embryos are found to be mostly devoid of intact nuclei. Any remaining nuclei have defects in chromosome segregation and abnormal morphology (chromatin bridges, chromosome lagging during anaphase and under- or over-condensed nuclei). Mitotic synchrony is lost in a high proportion of embryos and defective nuclei are seen beneath the normal plane of nuclei, they appear to be falling into the interior of the embryo.
Dominant suppression of heterochromatic position effect.
homozygous lethal triplo-enhancer homozygous lethal
Su(var)2051 is an enhancer of visible | dominant phenotype of N55e11, RpL15[+]/RpL1572
Su(var)205[+], E(Pc)[+], Su(var)2051, E(Pc)unspecified is an enhancer of abnormal eye color phenotype of lt1/lt11
Su(var)208[+], Su(var)208unspecified, Su(var)205[+], Su(var)2051 is an enhancer of abnormal eye color phenotype of lt1/lt11
Su(var)2051/E(Pc)unspecified is an enhancer of abnormal eye color | recessive phenotype of lt11
Su(var)208unspecified/Su(var)2051 is an enhancer of abnormal eye color | recessive phenotype of lt11
Su(var)2-1v9, Su(var)2051, lt1/lt11 has partially lethal phenotype
Su(var)2051, Su(var)208unspecified, lt1/lt11 has partially lethal phenotype
Su(var)2051 is an enhancer of wing margin | posterior | female phenotype of In(3L)C90/+, RpL153
Su(var)2051 is an enhancer of wing margin phenotype of N55e11, RpL15[+]/RpL1572
Su(var)2051 is an enhancer of wing margin | posterior phenotype of In(3L)C90/+, RpL1572
Su(var)205[+], E(Pc)[+], Su(var)2051, E(Pc)unspecified is an enhancer of pigment cell phenotype of lt1/lt11
Su(var)208[+], Su(var)208unspecified, Su(var)205[+], Su(var)2051 is an enhancer of pigment cell phenotype of lt1/lt11
Su(var)2051/E(Pc)unspecified is an enhancer of pigment cell phenotype of lt11
Su(var)208unspecified/Su(var)2051 is an enhancer of pigment cell phenotype of lt11
13% of RpL1572/In(3L)C90 males and 60% of RpL1572/In(3L)C90 females have a mutant posterior wing margin phenotype. The penetrance of this phenotype is increased to 100% if the flies are also carrying Su(var)2051/+. 13% of RpL153/In(3L)C90 females have a mutant posterior wing margin phenotype. The penetrance of this phenotype is increased to 81% if the females are also carrying Su(var)2051/+. RpL1572/+ slightly enhances the weak wing margin phenotype of N55e11/+. The effect of RpL1572 on N55e11 is further enhanced if the flies also carry Su(var)2051.
Eye pigmentation in lt11/lt1 flies is reduced if the flies are also carrying E(Pc)unspecified/Su(var)2051 or Su(var)208unspecified/Su(var)2051. lt11/lt1; Su(var)2-1v9/Su(var)2051 flies have reduced viability. Viability is partially restored in XO males. lt11/lt1; Su(var)208unspecified/Su(var)2051 flies have reduced viability. Viability is restored in XO males.
Su(var)2051 is rescued by Su(var)205hs.PE
The presence of Su(var)2051 suppresses position effect variegation (PEV) of lines with insertions in centromeric regions or in the fourth chromosome. Insertions near the telomeres 2L, 2R or 3R show no suppression.