FB2026_01 , released March 12, 2026
FB2026_01 , released March 12, 2026
Allele: Dmel\Iswi1
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General Information
Symbol
Dmel\Iswi1
Species
D. melanogaster
Name
FlyBase ID
FBal0117726
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: Q953term.

Nucleotide substitution: C3182T.

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

C12640110T

Reported nucleotide change:

C3182T

Amino acid change:

Q953term | Iswi-PA; Q953term | Iswi-PB; Q953term | Iswi-PC

Reported amino acid change:

Q953term

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 ( 0 )
Disease
Evidence
References
Modifiers Based on Experimental Evidence ( 0 )
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

The fecundity of Iswi1/Iswi1 males is significantly reduced, and mature sperm cells appear to have enlarged nuclei and fail to fully compact their chromatin. Iswi1/Iswi1 females lay eggs but are completely sterile. Embryos from Iswi1/Iswi1 mothers do not survive beyond nuclear cycle 10, show increased accumulation at the pronuclear apposition stage, and exhibit significant increases in chromatin and mitotic defects, including the male pronucleus remaining abnormally condensed, mis-segregation of chromosomes at anaphase, chromatin bridges in telophase, chromatin exclusion in nuclear cycle 2, asynchronous zygotic divisions, and aneuploidy or haploidy at zygotic divisions.

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.

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

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

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.

Iswi1 mutants have a high incidence of melanotic tumours and an increased number of larval hemocytes.

99 % of clones of Iswi1 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 Iswi1 homozygous female germ-line stem cells is around 40% of wild-type, but these mutant cells show no significant increase in apoptosis.

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.

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. 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
Suppressed by
NOT suppressed by
Statement
Reference

Iswi1 has neoplasia phenotype, non-suppressible by Df(2R)ED3921

Suppressor of
Statement
Reference
Other
Phenotype Manifest In
Suppressed by
NOT suppressed by
Statement
Reference
Enhancer of
Statement
Reference
Suppressor of
Statement
Reference
Other
Additional Comments
Genetic Interactions
Statement
Reference

Double heterozygous stuxnet2;Iswi1 females display tergite boundary defects that are not observed in stuxnet2 single heterozygote females.

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 Iswi1.

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.

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.

Flies homozygous for dikar5 and heterozygous for Iswi1 are phenotypically normal - no genetic interaction is seen.

Df(2R)ED3921 fails to suppress the melanotic tumour and increased larval hemocyte number of Iswi1 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 Iswi1 (76%).

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.

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 Iswi1.

Complementation and Rescue Data
Not rescued by
Comments

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

Loss of Iswi1 homozygous clones from their stem cell niche is suppressed by IswiT:Ivir\HA1.

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