FB2026_01 , released March 12, 2026
FB2026_01 , released March 12, 2026
Allele: Dmel\lncRNA:HsrωEP93D
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General Information
Symbol
Dmel\lncRNA:HsrωEP93D
Species
D. melanogaster
Name
FlyBase ID
FBal0194560
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
EP93D
Key Links
Allele class
Nature of the Allele
Allele class
Associated Insertion(s)
Cytology
Description

Insertion at -130bp position in the Hsrω promoter.

Carries a P{EP} insertion at the same site as the P{PZ} insertion in Hsrω05241, from which it was generated by P-transposon swapping.

Allele components
Component
Use(s)
Mutations Mapped to the Genome
Curation Data
Type
Location
Additional Notes
References
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 ( 1 )
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
 
Disease-implicated variant(s)
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
Statement
Reference

Expression of HsrωEP93D under the control of Scer\GAL4GMR.PS results in rough eye phenotype in adult flies.

The synaptic morphology at lncRNA:HsrωEP93D larval muscle 6/7 NMJs is comparable to controls.

Expression of a single copy of lncRNA:HsrωEP93D under the control of Scer\GAL4dpp.blk1 causes a mild disruption of photoreceptor cells; expression of two copies causes high mortality during development and severe disruption of photoreceptors.

Expression of a single copy of lncRNA:HsrωEP93D under the control of Scer\GAL4elav-C155 has no effect on lifespan.

Expression of a single copy of lncRNA:HsrωEP93D under the control of Scer\GAL4ptc-559.1 causes extra or missing scutellar bristles; expression of two copies additionally causes the notum to be deformed.

Expression of a single copy of lncRNA:HsrωEP93D under the control of Scer\GAL4C805 causes partial lethality during the P-stage and an increase in the proportion of female adults; expression of two copies causes greater lethality, with most dying as fully differentiated pharates, and wing blistering.

Expression of lncRNA:HsrωEP93D under the control of Scer\GAL4c825 does not result in sex comb defects.

Expression of lncRNA:HsrωEP93D under the control of Scer\GAL4Act5C.PI causes a majority of animals to die before adult stage, with higher mortality in lncRNA:HsrωEP93D homozygotes than heterozygotes; surviving adults are fertile, but the gender ratio is skewed in favor of females. Expression of lncRNA:HsrωEP93D under the control of Scer\GAL4Act5C.PI also results in fewer, larger omega speckles in the nucleus.

Eyes of HsrωEP93D homozygous flies show disorganisation of ommatidial units.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhanced by
Suppressed by
Enhancer of
NOT Enhancer of
Suppressor of
NOT Suppressor of
Statement
Reference
Other
Phenotype Manifest In
Enhanced by
Suppressed by
Enhancer of
Statement
Reference
NOT Enhancer of
NOT Suppressor of
Additional Comments
Genetic Interactions
Statement
Reference

The eye morphology defects (rough appearance with fused ommatidia) characteristic for flies expressing either cazVDRC.cUa or HsrωEP93D individually are further enhanced when the two transgenes are co-expressed.

Expression of HsrωEP93D under the control of Scer\GAL4Act5C.PI enhances the polytene chromosome condensation defects of Iswiunspecified mutants.

Coexpression of one copy of HsrωEP93D in the Scer\GAL4GMR.PF, nejF2161A.Scer\UAS.T:SV5\V5 background exaggerates the eye damage.

Co-expression of HsrωEP93D in the Scer\GAL4GMR.PF, nejdsRNA.Scer\UAS.cKa background enhances eye degeneration with the loss of ommatidial integrity extending to most of the eye.

Co-expression of HsrωEP93D enhances the eye damage seen in Scer\GAL4GMR.PF, nejΔNZK.Scer\UAS flies.

Xenogenetic Interactions
Statement
Reference

The rough eye phenotype seen in the absence of any responder transgene in animals carrying two copies of Scer\GAL4GMR.PU is enhanced by the addition of lncRNA:HsrωEP93D/lncRNA:HsrωEP93D.

Expression of HsrωEP93D in the Scer\GAL4GMR.PF, Zzzz\CAG127Q.Scer\UAS.T:Ivir\HA1, Df(3R)Hrb87F/+ background significantly enhances the appearence of black lesions on the eye surface, although it has no effect on mortality.

Expression of nejF2161A.Scer\UAS.T:SV5\V5 in the Scer\GAL4GMR.PF, Zzzz\CAG127Q.Scer\UAS.T:Ivir\HA1 background results in 23% lethality at the pupal stage. Surviving flies show a reduction in eye size and a greater disruption in ommatidial arrays. Additional co-expression of HsrωEP93D results in a greater reduction in eye size, near complete loss of ommatidial arrays and bristles and the appearence of black lesions on the eye surface. Co-expression of HsrωEP93D does not enhance pupal death.

Expression of two copies of HsrωEP93D enhances the rough eye, photoreceptor degeneration, and increased apoptosis phenotypes seen in Scer\GAL4GMR.PF/Scer\GAL4GMR.PF flies.

Co-expression of HsrωEP93D leads to a slight enhancement of the eye phenotype in Scer\GAL4GMR.PF,thdsRNA.Scer\UAS.cLa flies. Co-expression of HsrωEP93D suppresses the pupal lethality of Scer\GAL4GMR.PF,thdsRNA.Scer\UAS.cLa flies.

Coexpression of HsrωEP93D enhances the Scer\GAL4GMR.PF, egrScer\UAS.cIa eye phenotype, leading to severe head malformations and the formation of black lesions on the eye, though pupal lethality is not increased.

Coexpression of HsrωEP93D enhances the Scer\GAL4GMR.PF, Tak1Scer\UAS.cTa eye phenotype, though pupal lethality is not increased.

Co-expression of HsrωEP93D significantly enhances the Zzzz\CAG127Q.Scer\UAS.T:Ivir\HA1, Scer\GAL4GMR.PF eye phenotype, leading to extensive black lesions on the eye surface.

Co-expression of a single copy of P{Sym-UAS-Hsrω} eliminates the enhancing effect of HsrωEP93D expression on the Zzzz\CAG127Q.Scer\UAS.T:Ivir\HA1, Scer\GAL4GMR.PF eye phenotype, and also substantially reverses the eye degeneration primarily induced by Zzzz\CAG127Q.Scer\UAS.T:Ivir\HA1.

The neurodegeneration phenotype caused by expression of Zzzz\CAG127Q.Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4GMR.PF is enhanced by co-expression of HsrωEP93D under the control of Scer\GAL4GMR.PF; extensive black necrotic lesions are seen in the eye.

Complementation and Rescue Data
Comments
Images (0)
Mutant
Wild-type
Stocks (1)
Notes on Origin
Discoverer

FlyBase curator comment: the HsrωEP93D allele was generated from Hsrω05241, which has since been shown (see FBrf0205520) to carry a second site mutation (ms(3)2121) on the chromosome. Thus the HsrωEP93D chromosome may also carry this second site mutation.

Separable from: A secondary mutation causing recessive male sterility.

The P{PZ} transposon of P{PZ}Hsrω05241 was swapped with an unspecified P{EP} transposon present in the robo gene to create P{EP}HsrωEP93D.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (3)
Reported As
Name Synonyms
Secondary FlyBase IDs
    References (9)