Frameshift after ten amino acids.
Dinucleotide deletion of positions 339 and 340, predicted consequence of the frameshift is a nonsense peptide having only the first 10 amino acids.
Dinucleotide deletion of the last base of the 10th codon and the first base of the 11th codon. The predicted consequence of the frameshift is a peptide having only the first 10 amino acids of the authentic Su(var)205 protein.
Dinucleotide deletion of the last base of the 10th codon and the first base of the 11th codon causing a frameshift.
enhancer of variegation (with Su(var)205205), with ltunspecified
chromosome | larval stage (with Su(var)2054)
meiosis & nuclear chromosome | male
mitosis & nuclear chromosome (with Su(var)2054)
neuroblast & larval brain
neuroblast | larval stage (with Su(var)2054)
In Su(var)2054/Su(var)2055 homozygous larvae, neuroblasts exhibit telomeric fusions, particularly in autosomes.
Severe neuroblast loss is seen in the brains of Su(var)2054/Su(var)2055 mutant larvae. Many of the remaining neuroblasts exhibit necrosis markers, including aggregation of mitochondria and the presence of ubiquitin-conjugated protein aggregates.
Su(var)2055 dominantly suppresses position effect variegation of a variegating dp allele.
Su(var)2055 dominantly suppresses variegation of the w gene caused by In(1)wm4, T(2;3)V21-P{lacW}92E.x3 and P{RS3}panCB-5204-3.
Su(var)2055 does not dominantly suppress variegation of the w gene caused by P{RS5}5-HA-1902 and P{RS5}5-HA-1992.
Su(var)2055 suppresses variegation of the w gene caused by P{hsp26-pt-T}118E-10.
Su(var)2055 does not suppress variegation of the w gene caused by P{RS5}5-HA-1005.
One copy of Su(var)2055 strongly suppresses position effect variegation (PEV) at the w locus caused by In(1)wm4.
One copy of Su(var)2055 is unable to suppress the telomeric position effect (TPE) in stocks carrying a variegating P{hsp26-pt-T}39C-5 insertion at the telomere of the left arm of chromosome two.
A moderately sized pseudopuff is seen in the area of the 20F-3C eu-heterochromatin junction in the In(1)wm4h salivary gland polytene chromosome in the Su(var)20503/Su(var)2055 mutant background.
Polytene chromosomes of Su(var)2054/Su(var)2055 larvae partly lose the distinct pattern of band-interband regions, especially in the male X chromosome.
The X chromosome is bloated in polytene chromosome squashes from male Su(var)2054/Su(var)2055 third instar larvae.
The larval imaginal discs of Su(var)2055/Su(var)2052 mutants are similar to wild-type imaginal discs. Larval imaginal discs of Su(var)2054/Su(var)2055 mutants exhibit extensive apoptosis. Multiple telomere fusions are seen in metaphase neuroblasts of Su(var)2054/Su(var)2055 larvae.
Su(var)2054/Su(var)2055 larval mitotic chromosomes show telomeric fusions.
Heterozygotes show a suppression of the position effect variegation seen in In(1)wm4. This phenotype shows a cooperative effect with the enhancement of PEV caused by the loss of a Y chromosome, resulting in a variegated eye phenotype.
Neuroblasts in the brain of Su(var)2051/Su(var)2055, Su(var)20503/Su(var)2055 or Su(var)2054/Su(var)2055 larvae show a high frequency of abnormal metaphase configurations, including telomere-telomere fusions. Neuroblasts in the brain of Su(var)2052/Su(var)2055 larvae show normal metaphase configurations. The imaginal discs of Su(var)2054/Su(var)2055 larvae are reduced in size. Abnormal metaphase configurations showing telomeric fusions are seen in imaginal disc cells. Abnormal meiotic chromosomes are seen in the male germline.
Suppresses the position effect variegation at the w locus caused by In(1)wm4. This suppression is partly reduced if the flies are also carrying Su(var)3-7+t6.5.
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.
mod(mdg4)neo129 suppresses the strong dominant suppressor effect.
Su(var)2055/Su(var)2054 has abnormal neuroanatomy | larval stage phenotype, suppressible | partially by Scer\GAL4wor.PA/fzyUAS.cKa
Su(var)2055, SxlfP7B0 has partially lethal - majority die | dominant | maternal effect phenotype, suppressible by cav2248
Su(var)2055, SxlfP7B0 has partially lethal - majority die | dominant | maternal effect phenotype, suppressible by cav1
Su(var)2055/Su(var)2054 has lethal phenotype, non-suppressible by JIL-1z2
Su(var)2055/Su(var)205[+] is an enhancer of increased cell death phenotype of Hsap\MAPTR406W.UAS, Scer\GAL4elav.PU
Su(var)2055/Su(var)205[+] is an enhancer of abnormal locomotor behavior phenotype of Hsap\MAPTR406W.UAS, Scer\GAL4elav.PU
Su(var)2055/Su(var)205[+] is a suppressor | partially of partially lethal - majority live phenotype of ctA, lncRNA:flamA
Su(var)2055/Su(var)205[+] is a non-suppressor of lethal | recessive phenotype of JIL-1z2
Dp(1;3)FF184439/+, Su(var)2055 has abnormal eye color phenotype
Dp(1;2)FF026056/+, Su(var)2055 has abnormal eye color phenotype
Su(var)2055, peo1/peo[+] has abnormal mitotic cell cycle | larval stage phenotype
Su(var)2055, SxlfP7B0 has partially lethal - majority die | dominant | maternal effect phenotype
Su(var)2055, Sxlf1 has partially lethal - majority die | dominant | maternal effect phenotype
In(1)wm4h, LamCEX187, Su(var)2055/Su(var)205[+] has suppressor of variegation | dominant phenotype
In(1)wm4h, LamCEX296, Su(var)2055/Su(var)205[+] has suppressor of variegation | dominant phenotype
Su(var)2055/Su(var)2054 has neuroblast | larval stage phenotype, suppressible | partially by Scer\GAL4wor.PA/fzyUAS.cKa
Su(var)2055/Su(var)2054 has polytene chromosome phenotype, non-suppressible by JIL-1[+]/JIL-1z2
Su(var)2055/Su(var)205[+] is an enhancer of neuron phenotype of Hsap\MAPTR406W.UAS, Scer\GAL4elav.PU
Su(var)2055/Su(var)205[+] is a non-suppressor of polytene chromosome phenotype of JIL-1z2
Su(var)2055/Su(var)2054 is a non-suppressor of polytene chromosome phenotype of JIL-1z2
Su(var)2055 is a non-suppressor of phenotype of wSc2
Su(var)2055 is a non-suppressor of phenotype of wcre1
Su(var)2055, peo1/peo[+] has larval neuroblast phenotype
Su(var)2055, peo1/peo[+] has FlyBase_internalproperty type:chromosome:chromosome | larval stage phenotype
Su(var)2055, Dp(1;3)FF184439 and Su(var)2055, Dp(1;2)FF026056 double heterozygotes exhibit a significant decrease in eye pigmentation as compared to Su(var)2055 single heterozygotes.
Su(var)2055/+ partially suppresses the increased pharate stage mortality seen in flamA, ctA double homozygotes.
peo1, Su(var)2055 double heterozygosity leads to telomeric fusions in larval neuroblasts.
Expression of fzyScer\UAS.cKa under the control of Scer\GAL4wor.PA suppresses the neuroblast loss seen in Su(var)2054/Su(var)2055 mutant larval brains. However, these surviving neuroblasts display phenotypes indicative of mitotic catastrophe including multinucleation and enlargement of cell diameter.
In progeny from Su(var)2055 heterozygous females crossed to SxlfP7B0/Y males, female viability is dramatically reduced. The effect of Su(var)2055 is strictly maternal; no significant reduction in female viability is observed in the reciprocal cross.
In progeny from Su(var)2055 heterozygous females crossed to Sxlf1/Y males, female viability is dramatically reduced. The effect of Su(var)2055 is strictly maternal; no significant reduction in female viability is observed in the reciprocal cross.
The introduction of cav2248 into Su(var)2055 mothers when crossed to SxlfP7B0 males suppresses the Su(var)2055 maternal effect on female viability in the progeny.
The introduction of cav1 into Su(var)2055 mothers when crossed to SxlfP7B0 males suppresses the Su(var)2055 maternal effect on female viability in the progeny.
The defects in polytene chromosome morphology seen in Su(var)2054/Su(var)2055 larvae are not altered by one copy of JIL-1z2.
The defects in polytene chromosome morphology seen in JIL-1z2 homozygous larvae are not altered by one copy of Su(var)2054 or Su(var)2055.
The polytene chromosome morphology of Su(var)2054/Su(var)2055 ; JIL-1z2/JIL-1z2 double mutants resembles that of JIL-1z2/JIL-1z2 single mutants.
When P{P-Sal}89D is present, the w gene of the P{lacW}ciDplac insertion variegates, resulting (in a w- background) in an eye that is mostly white with a few patches of red ommatidia. This P-element-dependent silencing of P{lacW}ciDplac is dominantly suppressed by Su(var)2055.
Su(var)2055 Df(3R)Ace-HD1 double heterozygotes show an increase in crossing over between kni and pp. Su(var)2055 Su(var)3-96 double heterozygotes show an increase in crossing over between kni and pp.
Heterozygous Su(var)2055 enhances the Scer\GAL4elav.PU>Hsap\MAPTR406W.Scer\UAS induced neuronal apoptosis and locomotory defects.
Su(var)2055 is rescued by Su(var)205hs.PE
Su(var)2055/Su(var)2054 is partially rescued by Su(var)205Tag:BTS,Tag:proteinA
Su(var)2055/Su(var)2054 is partially rescued by Su(var)205hs.PE
Su(var)205T:Zzzz\BTS,T:Saur\A rescues the lethality of Su(var)2054/Su(var)2055 to 58%.
The abnormal metaphase configurations seen in the brains of Su(var)2054/Su(var)2055 larvae are partly rescued by expression of Su(var)205hs.PE, although a high frequency of chromosome aberrations are seen.
Lethality is rescued by expression of the heat shock activated Su(var)205 construct. Rescued adults behave lethargically, walk slowly and never fly, and die several days after eclosion. If heat shock is induced after 3-4 days adults are rescued but heat shock after 5-6 days adults exhibit mild to severe defects in eye and ocellar development.