Open Close
General Information
Symbol
Dmel\mblE27
Species
D. melanogaster
Name
FlyBase ID
FBal0082451
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Key Links
Allele class
Nature of the Allele
Allele class
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Cytology
Nature of the lesion
Statement
Reference

Imprecise excision removing exons 1 and 2.

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 ( 1 )
 

FlyBase curator comment: Interactions with Dg[086] and/or Dg[323] were detected in a Dg[086]/+ or Dg[323]/+ background which exhibits no obvious changes in muscle morphology. Nonetheless, these interactions have been captured as 'modifier' ('exacerbates') annotations here to best capture the experimental finding and the authors' intention.

Disease-implicated variant(s)
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
Statement
Reference

Flies homozygous for mblE27 are not viable.

mblE27/+ mutant flies exhibit temperature-induced mobility defects.

mblE27 flies expressing mblC.Scer\UAS.T:Avic\GFP-EGFP under the control of Scer\GAL4da.G32 do not undergo larval molting and die as first instar larvae up to three days after hatching.

mblE27 flies expressing mblC.Scer\UAS under the control of Scer\GAL4da.G32 do not undergo larval molting and die as first instar larvae up to three days after hatching.

mblchst/mblE27 females show reduced sexual receptivity compared to controls.

mblE27/+ mutant flies do not exhibit any obvious indirect flight muscle defects.

mblk07103/mblE27 escapers have wing blisters, wing venation defects or unexpanded wings.

Mutants die as stage 17 embryos or during hatching and show no obvious defects in the formation of somatic and visceral muscles. At the end of embryogenesis embryos are severely paralysed, only twitching movements can be observed and their abdominal segments are strongly contracted. syt staining reveals the neuromuscular junctions can assemble normally. The extracellular tendon matrix (TM) is severely reduced, the muscles are forced to compete for epidermal surface at the segment border. At the ultrastructural level the thick and thin filaments are less ordered and dense in muscles, I-bands are absent, Z-bands are absent and instead only spindle-like concentrations of dark thin fibers can be seen.

Mutant clones in the eye exhibit phenotypic defects in many mutant ommatidia, the rhabdomeres of up to 4 outer photoreceptors have a smaller diameter resembling the rhabdomeres of receptor cell R7. All photoreceptors are abnormally differentiated and have malformed rhabdomeres that frequently do not extend into basal regions of the retina.

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

mbl Dys double heterozygous flies (mblE27/Df(3R)Exel6184) exhibit indirect flight muscle degeneration.

mblE27 DgO86 double heterozygous flies exhibit indirect flight muscle degeneration.

One copy of mblE27 enhances the indirect flight muscle degeneration seen when DysdsRNA.NH2.Scer\UAS is expressed under the control of Scer\GAL4Act.PU.

One copy of mblE27 enhances the indirect flight muscle degeneration seen when DgdsRNA.Scer\UAS is expressed under the control of Scer\GAL4tub.PU.

mblE27 Dg323 double heterozygous flies exhibit indirect flight muscle degeneration.

Combination of Df(3R)Exel6184 in heterozygous state with a single copy of mblE27 results in a significantly increased frequency of lamina plexus defects in the third instar larval brain, whereas the rhabdomere length in the adult eye remains unaffected in the double heterozygotes.

Combination of DgO86 in heterozygous state with a single copy of mblE27 does not significantly affect the frequency of lamina plexus defects in the third instar larvae but results in a significantly reduced rhabdomere length in the adults.

One copy of mblE27 strongly suppresses the detached posterior crossvein phenotype seen when DysdsRNA.NH2.Scer\UAS is expressed under the control of Scer\GAL4Act.PU. The indirect flight muscle degeneration phenotype is enhanced.

One copy of mblE27 strongly suppresses the detached posterior crossvein phenotype seen when DysdsRNA.C.Scer\UAS is expressed under the control of Scer\GAL4tub.PU but produces extra wing vein material.

One copy of mblE27 suppresses the posterior crossvein phenotype seen when DgdsRNA.Scer\UAS is expressed under the control of Scer\GAL4tub.PU.

Xenogenetic Interactions
Statement
Reference

Expression of Zzzz\CAG99.Scer\UAS.T:Hsap\MYC,T:Zzzz\FLAG in the presence of heterozygous mblE27 using Scer\GAL4da.G32 leads to no significant change in tergite-phenotype proportion compared with expression of Zzzz\CAG99.Scer\UAS.T:Hsap\MYC,T:Zzzz\FLAG alone.

Statistical analysis reveals a significant decrease in the proportion of flies expressing Zzzz\CAGrCUG.99.Scer\UAS.T:Hsap\MYC,T:Zzzz\FLAG using Scer\GAL4da.G32 that show any phenotype in the presence of heterozygous mblE27 compared with flies expressing Zzzz\CAGrCUG.99.Scer\UAS.T:Hsap\MYC,T:Zzzz\FLAG alone. However, no change is observed when comparing the proportion within the strongest two categories only, perhaps indicating that only those with the weakest phenotype are suppressed.

The eye defects caused by expression of Zzzz\CTGi480.Scer\UAS.cGa under the control of Scer\GAL4sev.PU are not significantly modified by mblE27/+, but are enhanced by mblk07103/mblE27.

One copy of mblE27 partially suppresses the shortened lifespan seen when Hsap\ATXN3tr.Q78.Scer\UAS.T:Ivir\HA1 is expressed in the developing eye under the control of Scer\GAL4elav-C155.

The embryonic lethality of mblE16/mblE27 animals is partially rescued by expression of Hsap\MBNLScer\UAS.cGCa under the control of Scer\GAL4da.G32; 78.9% of the embryos hatch.

The embryonic lethality of mblE16/mblE27 animals is only slightly rescued by expression of Hsap\MBNLScer\UAS.cGCa under the control of Scer\GAL4Mef2.PR; 18.0% of the embryos hatch.

78.14% of mblE16/mblE27 embryos expressing Hsap\MBNLScer\UAS.cGCa under the control of Scer\GAL4da.G32 hatch into larvae (in contrast to 0% of mblE16/mblE27 embryos) and the hypercontracted abdomen phenotype is greatly reduced.

Complementation and Rescue Data
Images (0)
Mutant
Wild-type
Stocks (1)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (3)
References (19)