FB2024_03 , released June 25, 2024
Allele: Dmel\Iswi2
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General Information
Symbol
Dmel\Iswi2
Species
D. melanogaster
Name
FlyBase ID
FBal0117725
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Key Links
Genomic Maps

Nature of the Allele
Progenitor genotype
Cytology
Description

Amino acid replacement: W800term.

Nucleotide substitution: G2725A.

Mutations Mapped to the Genome
Curation Data
Type
Location
Additional Notes
References
Nucleotide change:

G12639533A

Reported nucleotide change:

G2725A

Amino acid change:

W800term | Iswi-PA; W800term | Iswi-PB; W800term | Iswi-PC

Reported amino acid change:

W800term

Variant Molecular Consequences
Associated Sequence Data
DNA sequence
Protein sequence
 
Expression Data
Reporter Expression
Additional Information
Statement
Reference
 
Marker for
Reflects expression of
Reporter construct used in assay
Human Disease Associations
Disease Ontology (DO) Annotations
Models Based on Experimental Evidence ( 1 )
Disease
Evidence
References
Modifiers Based on Experimental Evidence ( 1 )
Disease
Interaction
References
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
 
Disease-implicated variant(s)
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
Statement
Reference

Iswi2 homozygous third instar larvae show a decreased mitotic index in the brain lobes; C4da neurons show decreased dendrite complexity (decreased dendrite length and branch number); there are tilling defects between C4da neurons ddaC and v'ada.

Iswi1/Iswi2 transheterozygote males display defects in the morphology of the polytene chromosome X in larval salivary glands. The X chromosome is shorter and more compact compared to wild-type.

Flies containing eyes homozygous for Iswi2 (generated using the EGUF technique) have rough eyes of reduced size.

Polytene chromosomes of Iswi1/Iswi2 male larvae show condensation defects, particularly of the X chromosome.

Flies containing homozygous eyes in an otherwise heterozygous background (generated using the EGUF technique) have rough eyes which also show colour variegation and loss of cell identity (bristles grow in parts of the eye territory normally occupied by photoreceptors). Loss of ommatidia boundaries and orientation and reduced number of photoreceptors are seen.

Mutant imaginal disc cell populations show changes in cell cycle profiles compared to wild type, showing a significant decrease of the G[[1]] and G[[2]]/M peaks and an increase in the pre-G[[1]] peak.

Mutant larval brain neuroblast cell populations show changes in cell cycle profiles compared to wild type, with a small but reproducible increase in the G[[2]]/M peak and a shorter S phase than normal.

The male X polytene chromosome is decondensed in salivary glands of Iswi1/Iswi2 larvae, although the banding pattern is usually retained.

Expression of IswiK159R.Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4ey.PH in an otherwise wild-type background results in flies with rough and reduced eyes. The severity of the phenotype is increased when IswiK159R.Scer\UAS.T:Ivir\HA1 is expressed under the control of Scer\GAL4ey.PH in an Iswi2 background.

Iswi1/Iswi2 animals often survive until the early to mid pupal stages, and have slightly misshapen wing discs at the late third larval instar.

The X polytene chromosome is decondensed in male Iswi1/Iswi2 larvae but not in female Iswi1/Iswi2 larvae.

Mitotic chromosomes prepared from neuroblasts of Iswi1/Iswi2 third instar larvae are indistinguishable from wild type.

Animals expressing IswiK159R.Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4da.G32 and derived from Iswi2/+ females survive until late larval stages at 18[o]C but do not complete embryogenesis at 25[o]C. At 25[o]C, the embryos show defects in chromosome condensation and in the organisation of the mitotic spindle as early as nuclear cycle 12.

Iswi2 mutants have a high incidence of melanotic tumours and an increased number of larval hemocytes.

Iswi2/+ flies exhibit a wild-type number of dorsocentral bristles on the heminotum (2.0 per heminotum).

96 % of clones of Iswi2 homozygous female germ-line stem cells are lost from their stem cell niche by 17 days after induction, compared to only 35% of wild-type clones. The division rate of Iswi2 homozygous female germ-line stem cells is around 40% of wild-type, but these mutant cells show no significant increase in apoptosis. Iswi2 homozygous clone follicle stem cells exhibit only a slightly increased rate of loss from their stem cell niche in the ovary compared to wild-type.

The circulating hemocyte cell number in hemolymph isolated from Iswi1/Iswi2 mutants is increased considerably with respect to wild-type animals, having about 12500 per ul-1, compared to about 4500 in wild-type.

The X chromosome is grossly abnormal in salivary gland polytene chromosome preparations from homozygous male larvae, having a bloated appearance and an almost complete loss of the characteristic banding pattern.

All chromosomes appear normal in salivary gland polytene chromosome preparations from homozygous female larvae.

Heterozygotes are viable and phenotypically normal. Hemizygotes die during late larval or early pupal development and show no obvious homeotic transformations or other pattern defects. Homozygous clones can be observed in all body segments, although the size and frequency of clones in the genitalia, head and thoracic segments is reduced compared to controls. No homeotic transformations or other defects are seen in the clones. Germline clonal analysis indicates that loss of maternal Iswi+ function blocks oogenesis at an early stage; females carrying homozygous germline clones are not fertile. The structure of the polytene X chromosome of male Iswi1/Iswi2 larvae is much shorter and broader than normal. This alteration in structure of the X chromosome is highly penetrant and is never seen in female Iswi1/Iswi2 larvae. The polytene autosomes are often thinner than normal in both male and female mutant larvae. The structure of mitotic chromosomes of hemizygous larvae appears relatively normal.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhanced by
Statement
Reference

Iswi2 has visible | somatic clone phenotype, enhanceable by Acf1

Suppressed by
Statement
Reference

Iswi2 has visible | somatic clone phenotype, suppressible by wun[+]/wunPBacF48

NOT suppressed by
Suppressor of
Statement
Reference
Other
Phenotype Manifest In
Enhanced by
Statement
Reference

Iswi2 has eye | somatic clone phenotype, enhanceable by Acf1

Iswi2 has eye | somatic clone phenotype, enhanceable by E(bx)Nurf301-2

Suppressed by
Statement
Reference

Iswi2 has eye | somatic clone phenotype, suppressible by wun[+]/wunPBacF48

Iswi2 has X chromosome | male phenotype, suppressible by mle1

NOT suppressed by
Enhancer of
Statement
Reference
Suppressor of
Statement
Reference
Other
Additional Comments
Genetic Interactions
Statement
Reference

The formation of ectopic wing veins observed in adult flies expressing Marcal1Scer\UAS.cBa under the control of Scer\GAL4tub.PU is ameliorated by combination with a single copy of Iswi2.

One copy of Iswi2 does not enhance the loss of His2Av810 mutant germline stem cells (GSCs) in the testis. A similar proportion of testes contain His2Av810 mutant GSC clones as with His2Av810 alone.

Expression of HsrωdsRNA.Sym.Scer\UAS under the control of Scer\GAL4ey.PH suppresses the defects seen in homozygous Iswi2 eyes.

Expression of HsrωdsRNA.Sym.Scer\UAS under the control of Scer\GAL4ey.PH suppresses the X chromosome condensation defects seen in the polytene chromosomes of Iswi1/Iswi2 male larvae.

Acf11 and E(bx)Nurf301-2 each enhance the eye defects seen in flies in which the eyes are homozygous for Iswi2 in an otherwise heterozygous background (generated using the EGUF technique).

The defects seen in homozygous Iswi2 eyes (generated using the EGUF technique) are dominantly suppressed by wunPBacF48.

The defects seen in homozygous Iswi2 eyes (generated using the EGUF technique) are dominantly suppressed by ttkEP3314, mbf1EP3684 or effEP3627 expressed under the control of Scer\GAL4ey.PH.

caspPBacG75α and wunPBacF48 each suppress the shortening of the S phase, but not the G[[2]]/M increase which is seen in Iswi2 larval brain neuroblast cell populations.

caspPBacG75α and wunPBacF48 each suppress the pre-G1 defects seen in Iswi2 imaginal disc cell populations, restoring a cell cycle profile similar to wild type.

Expression of either effEP3627 or ttkEP3314 under the control of Scer\GAL4ey.PH weakly suppresses the pre-G[[1]] and G[[1]]-G[[2]]/M defects seen in Iswi2 eye disc cell populations.

Expression of mbf1EP3684 under the control of Scer\GAL4ey.PH strongly suppresses the pre-G[[1]] and G[[1]]-G[[2]]/M defects seen in Iswi2 eye disc cell populations.

Iswi1/Iswi2; Acf1[5]/+ animals have a significant developmental delay compared to Iswi1/Iswi2 single mutants, surviving to late third larval instar or early pupation.

Df(2R)ED3921 fails to suppress the melanotic tumour and increased larval hemocyte number of Iswi2 mutants.

The frequency of abnormal dorsal appendages in embryos derived from females carrying EcRB1-ΔC655.F645A.Scer\UAS under the control of Scer\GAL4slbo.2.6 (23%) is increased if the females are also heterozygous for Iswi2 (45%).

Iswi2/+ ; pnrD1/+ flies display on average 2.84 dorsocentral bristles per heminotum, so reducing the number observed in pnrD1/+ single mutants. Iswi2/+ ; pnrVX1/+ flies display on average 1.61 dorsocentral bristles per heminotum, so aggravating the pnrD1/+ single mutant phenotype (1.86 bristles/heminotum). Iswi2/+ ; ChiE/+ flies display on average 1.29 dorsocentral bristles per heminotum, so accentuating the pnrD1/+ single mutant phenotype (1.6 per heminotum).

When heterozygous Iswi1 or Iswi2 is combined with homozygous Acf11, animals exhibit a homeotic transformation in the abdomen of males. This phenotype is manifested as ectopic reduced pigmentation of the abdominal A5 tergites, consistent with an A4 to A5 transformation. The penetrance (in Acf11/Acf11, Iswi2/+ animals) is 26%. In addition mutant flies often display an aberrant, asymmetric segmentation of the lower abdomen.

mle1 completely suppresses the morphological defects of the X chromosome that are seen in salivary gland polytene chromosome preparations from Iswi2 males.

Expression of msl-2Hsp83.PK in a Iswi2 background (but not in a wild-type background) results in the X chromosome having a bloated morphology in salivary gland polytene chromosome preparations from female larvae. In approximately 30% of the salivary gland nuclei, the phenotype is so severe that the X chromosome is almost completely dispersed and detaches from the chromocenter.

Xenogenetic Interactions
Statement
Reference

The formation of ectopic wing veins observed in adult flies expressing Hsap\SMARCAL1Scer\UAS.cBa under the control of Scer\GAL4Bx-MS1096 is ameliorated by combination with a single copy of Iswi2.

Complementation and Rescue Data
Not rescued by
Comments

The eye defects seen in flies in which the eyes are homozygous for Iswi2 in an otherwise heterozygous background (generated using the EGUF technique) are fully rescued by Iswi+t12.

The eye defects seen in flies in which the eyes are homozygous for Iswi2 in an otherwise heterozygous background (generated using the EGUF technique) are not rescued by IswiK159R.T:Ivir\HA1.

Expression of IswiScer\UAS.T:Zzzz\TAP under the control of Scer\GAL4Act5C.PU rescues the lethality of Iswi1/Iswi2 animals.

Loss of Iswi2 homozygous clones from their stem cell niche is supressed by IswiT:Ivir\HA1.

Images (0)
Mutant
Wild-type
Stocks (0)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (3)
References (23)