FB2026_01 , released March 12, 2026
FB2026_01 , released March 12, 2026
Allele: Dmel\AktGD1361
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General Information
Symbol
Dmel\AktGD1361
Species
D. melanogaster
Name
FlyBase ID
FBal0198698
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
UAS-Akt-RNAi, UAS-AktRNAi
Key Links
Genomic Maps

Transgenic product class
Nature of the Allele
Transgenic product class
Progenitor genotype
Carried in construct
Cytology
Description

UASt regulatory sequences drive expression of an inverted repeat.

Allele components
Component
Use(s)
Encoded product / tool
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

Knockdown of Akt1 through the expression of Akt1GD1361, under the control of Scer\GAL4ppl.PP, leads to small cell size and an ectopic lipid storage phenotype in the salivary gland.

The dendrites of ddaC neurons of larvae expressing Akt1GD1361 under the control of Scer\GAL4ppk.PG show reduced regeneration (after dendrite severing at 48 hours after egg laying) compared to wild-type controls.

Expression of Akt1GD1361 using Scer\GAL4nub-AC-62 results in abnormally small wings in which cell size and cell number are decreased.

Compared with controls, the age-related dysplasia of the intestinal epithelium is strongly reduced in flies expressing Akt1GD1361 under the control of Scer\GAL4esg-NP5130 and Scer\GAL80ts.αTub84B.

Expression of Akt1GD1361 under the control of Scer\GAL4esg-NP5130 and Scer\GAL80ts.αTub84B results in significant lifespan shortening compared with controls.

Compared with controls, female flies expressing Akt1GD1361 under the control of Scer\GAL4bun-GSG5961 show a moderate, but significant, reduction in intestinal cell proliferation at old age. These flies are significantly longer lived when exposed to RU486 than isogenic siblings exposed to mock treatment.

Depending on the insertion line used, expression under the control of Scer\GAL4Mef2.PR can result in early larval lethality or undefined lethality.

Expression under the control of Scer\GAL4Mef2.PR results in grossly normal larval body wall muscles.

Expression under the control of Scer\GAL4Mef2.PR results in sarcomeres with irregular aggregates of Z-lines in the larval body wall muscles.

Knocking down Akt1 expression via Scer\GAL4ppk.PG-driven expression of Akt1GD1361 in class IV neurons causes a significant reduction in dendrite growth and dendrite coverage of larval hemisegments.

Expression of Akt1GD1361 under the control of Scer\GAL4Bx-MS1096 leads to crinkled wings.

External Data
Bristle Screen Database (Knoblich Lab) - A database for RNAi phenotypes in bristle and notum development
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhanced by
NOT Enhanced by
Enhancer of
NOT Enhancer of
Suppressor of
NOT Suppressor of
Phenotype Manifest In
Additional Comments
Genetic Interactions
Statement
Reference

Co-expression of hppyScer\UAS.cMa and Akt1GD1361 using Scer\GAL4nub-AC-62 results in a strong synergistic phenotype of reduced wing size and reduced cell size and number.

Expression of Akt1GD1361 suppresses the increase in circulating lamellocytes seen when ND75GD6309 is expressed under the control of Scer\GAL4Dot.PK.

Knockdown of Akt1 in Ras85DV12.Scer\UAS-dlg1GD4689 cells, through expression of Akt1GD1361, causes a complete suppression of neoplastic growth and even causes a near-complete absence of mutant eye cells. Only small structures, which contain few cells, remain.

The Scer\GAL4ppk.PG-driven Akt1GD1361-phenotype is epistatic to the dendrite overgrowth seen in Df(3L)banΔ1 mutants. In addition, reducing Akt1 expression by Scer\GAL4ppk.PG-driven Akt1GD1361 blocks the exuberant dendrite invasion activity of Df(3L)banΔ1 mutants.

Expression of Akt1GD1361 strongly suppresses the glial neoplasia seen in third instar larvae when btl::EgfrScer\UAS.T:λ\cI-DD and Pi3K92EScer\UAS.T:Hsap\MYC,T:Hsap\CAAX are co-expressed under the control of Scer\GAL4repo.PU.

Depletion of Akt1 through expression of Akt1GD1361 in TORCScer\UAS.cWa-expressing developing eyes (both lines under the control of Scer\GAL4GMR.PF) enhances the TORC-mediated rough eye phenotype.

Xenogenetic Interactions
Statement
Reference

Expression of Akt1GD1361 strongly suppresses the hemocyte overproliferation seen in third instar larvae when Hsap\RUNX1::Hsap\RUNX1T1Scer\UAS.cSa is expressed under the control of Scer\GAL4Hml.Δ.

Complementation and Rescue Data
Comments
Images (0)
Mutant
Wild-type
Stocks (1)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 1 )
Linkouts
Bristle Screen Database (Knoblich Lab) - A database for RNAi phenotypes in bristle and notum development
Synonyms and Secondary IDs (2)
Reported As
Symbol Synonym
Akt1GD1361
AktGD1361
Name Synonyms
Secondary FlyBase IDs
    References (25)