FB2026_01 , released March 12, 2026
FB2026_01 , released March 12, 2026
Allele: Dmel\Shc111-40
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General Information
Symbol
Dmel\Shc111-40
Species
D. melanogaster
Name
FlyBase ID
FBal0105105
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
dshc111-40
Key Links
Genomic Maps

Nature of the Allele
Progenitor genotype
Cytology
Description

Nucleotide substitution: C?T. Amino acid replacement: R152Y.

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

C9427655T

Reported nucleotide change:

C?T

Amino acid change:

R151W | Shc-PA

Reported amino acid change:

R151Y

Comment:

The mutation was reported as CGG to TGG, which is R to W, rather than R to Y as reported.

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

Mutant border cell clusters (induced as clones) migrate posteriorly, but do not migrate dorsally.

Embryos that lack maternal Shc function (derived from females carrying homozygous germ line clones) have weak terminal defects. Embryos that lack both maternal and zygotic Shc function (derived from females carrying homozygous germ line clones mated to mutant males) have a weak flb-like phenotype. Homozygous adults have rough eyes.

When mutant somatic clones are made in the border cells no effect is seen.

Embryos derived from homozygous female germ-line clones display terminal defects. Most embryos fail to hatch and show a reduction of posterior Filzkorper and the 8th abdominal segment as well as mild defects in the anterior head skeleton. Malpighian tubules are always absent. Embryos lacking both maternal and zygotic Shc function show defects in germband retraction and a variable reduction of ventral denticle belts not seen in paternally rescued embryos. 70% of homozygotes die during the late pupal stage. Females that survive to adulthood do not lay eggs.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Suppressor of
Statement
Reference

Shc111-40/Shc[+] is a suppressor of visible | semidominant phenotype of EgfrE3

NOT Suppressor of
Statement
Reference

Shc111-40 is a non-suppressor of visible phenotype of sevS11.Tag:MYC

Other
Statement
Reference
Phenotype Manifest In
NOT Enhancer of
Statement
Reference

Shc111-40 is a non-enhancer of phenotype of Ras85DV12.sev

Shc111-40 is a non-enhancer of phenotype of rlSem

Shc111-40 is a non-enhancer of phenotype of Raf::tor12D.hs.sev

Suppressor of
Statement
Reference
NOT Suppressor of
Statement
Reference

Shc111-40 is a non-suppressor of phenotype of Ras85DV12.sev

Shc111-40 is a non-suppressor of phenotype of Raf::tor12D.hs.sev

Shc111-40 is a non-suppressor of phenotype of rlSem

Shc111-40 is a non-suppressor of eye phenotype of sevS11.Tag:MYC

Shc111-40 is a non-suppressor of ommatidium phenotype of sevS11.Tag:MYC

Other
Additional Comments
Genetic Interactions
Statement
Reference

Border cells clusters that are mutant for Shc111-40 and also expressing PvrDN.Scer\UAS under the control of Scer\GAL4slbo.2.6 show severely impaired posterior migration.

Heterozygous females carrying tor13D produce embryos that produce very little cuticle. This phenotype is weakly suppressed if the females are carrying one copy of Shc111-40; the embryos develop more cuticle and show posterior structures such as Filzkorper and Tuft structures. The phenotype is completely suppressed if the tor13D/+ females also carry homozygous Shc111-40 germline clones; embryos look normal and can hatch. The eye and wing phenotypes caused by EgfrE3 are dominantly suppressed by Shc111-40. The EgfrE3 phenotype is completely suppressed if the flies are also homozygous for Shc111-40 and the viability of these flies is restored. Expression of btl::EgfrScer\UAS.T:λ\cI-DD under the control of Scer\GAL4CY2 results in the formation of ectopic wing vein material at multiple sites on the wing. This phenotype is completely suppressed if the flies are also homozygous for Shc111-40. Females expressing btl::EgfrScer\UAS.T:λ\cI-DD under the control of Scer\GAL4CY2 produce strongly dorsalised eggs with no dorsal appendages. This phenotype is partially suppressed if the females are also homozygous for Shc111-40; dorsal appendage material is produced around the anterior circumference of the egg.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Comments
Images (0)
Mutant
Wild-type
Stocks (0)
Notes on Origin
Discoverer

Selected as: a mutation in which embryos derived from homozygous germ-line clones show patterning defects in the cuticle.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (4)
Reported As
Name Synonyms
Secondary FlyBase IDs
    References (6)