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General Information
Symbol
Dmel\Akt1UAS.Tag:HA
Species
D. melanogaster
Name
FlyBase ID
FBal0124420
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
UAS-dAkt1, UAS-Akt, UAS-AKT1
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
Carried in construct
Cytology
Nature of the lesion
Statement
Reference

UASt regulatory sequences drive expression of Akt1 tagged with Tag:HA.

Allele components
Product class / Tool use(s)
Encoded product / tool
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 )
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
Statement
Reference

No retinal phenotypes are seen when Akt1Scer\UAS.T:Ivir\HA1 is expressed under the control of Scer\GAL4GMR.PU.

The salivary glands of animals expressing Akt1Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4fkh.PH are greatly increased in area compared to controls at 13.5 hours after puparium formation. At 24 hours APF, animals expressing Akt1Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4fkh.PH still contain salivary gland tissue, in contrast to wild-type animals, where the salivary glands have completely degraded by this stage. The salivary glands in the mutant animals are always present at 24 hours APF, but are partly degraded. The induction of autophagy that is seen in wild-type salivary glands at 13.5 hours APF is not seen in animals expressing Akt1Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4fkh.PH.

DNA fragmentation is detected by TUNEL in salivary glands of animals expressing Akt1Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4fkh.PH at 13.5 hours after puparium formation, as occurs in control salivary glands at this stage.

Expression of Akt1Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4GMR.PU causes enlarged eyes, due to an increase in size of the ommatidia.

When Akt1Scer\UAS.T:Ivir\HA1 is driven by Scer\GAL4GMR.PF mutants have slightly enlarged eyes, and a mild disruption of the regular external lattice.

Akt1Scer\UAS.T:Ivir\HA1; Scer\GAL4GMR.PF flies exhibit a 150% increase in ommatidia size. Wing margin bristles in somatic clones of Akt1Scer\UAS.T:Ivir\HA1; Scer\GAL4Act5C.PI flies exhibit an average size increase of 186%.

When Akt1Scer\UAS.T:Ivir\HA1 is driven by Scer\GAL4GMR.PF, a larger bulging eye with enlarged ommatidia is seen. In addition to this change in size, the ommatidia array become irregular, eye bristles are enlarged with a frequent loss of number.

Expression of Akt1Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4GMR.PF results in an enlarged eye. Expression of Akt1Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4dpp.blk1 results in enlargement of the region encompassed by wing veins 3 and 4, the anterior crossvein and the wing margin.

Expression of Akt1Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4GMR.PF results in enlarged and bulging eyes which have a mild disruption of the regular, external lattice. The increase in eye size is due to an increase in size but not the number of ommatidia. Photoreceptor cell differentiation is normal. The pattern of apoptosis is normal in eye imaginal discs expressing Akt1Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4GMR.PF. Expression of Akt1Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL471B results in a marked enlargement of the wing imaginal disc. The surface of the adult wing blade is expanded in these animals (there is a 29% increase in wing surface area compared to wild type) and there is an increase in vein thickness. The proximo-distal alignment of hairs on the wing blade is often mildly disrupted. The number of cells in the wing is not different from wild type. The proportion of cells in G1, S and G2 phase in wing discs expressing Akt1Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL471B is indistinguishable from wild type. Expression of Akt1Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4dpp.blk1 along the anteroposterior boundary of the wing imaginal disc results in an enlargement of the corresponding region of the adult wing. Expression of Akt1Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4en-e16E results in a marked expansion of the posterior compartment of the wing disc, while the anterior compartment is unaffected. The size of the cells in the posterior compartment of the wing disc is increased compared to wild type, while the number of cells is unaltered. No differences in cell proliferation are seen between anterior and posterior compartment cells in wing discs expressing Akt1Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4en-e16E. Cells in the ZNC (zone of non-proliferating cells) are still in G1 arrest (as occurs in wild type). Clones of cells expressing Akt1Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4Act5C.PP in the wing imaginal disc are larger than control clones due to an increase in cell size but not cell number.

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

Akt1UAS.Tag:HA/Scer\GAL4GMR.PF is a non-suppressor of eye phenotype of Ras85DKP

Other
Additional Comments
Genetic Interactions
Statement
Reference

The severity of the eye defects caused by expression of foxoScer\UAS.cKb under the control of Scer\GAL4GMR.PF is suppressed by co-expression of Akt1Scer\UAS.T:Ivir\HA1.

Expression of Akt1Scer\UAS.T:Ivir\HA1 enhances the rough eye phenotype seen when Dcp-1Scer\UAS.cKa (insertion line P{UAS-Dcp-1.K}19-2) is expressed under the control of Scer\GAL4GMR.PF.

The eye phenotype in Ras85DKP mutant flies is not suppressed by ectopic expression of Akt1Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4GMR.PF.

Homozygosity for either rictorΔ24 or rictorΔ42 dramatically suppresses the enlarged eye (and enlarged ommatidium) phenotype caused by expression of Akt1Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4GMR.PU.

Overexpression of Akt1Scer\UAS.T:Ivir\HA1 (under the control of Scer\GAL4Act5C.PI) using the FLP/FRT system in brain somatic clones mutant for scrib1 and wtsx1 does not cause metastatic behaviour despite accelerated tumour growth.

Coexpression of Akt1Scer\UAS.T:Ivir\HA1 with DJ-1αdsRNA.Scer\UAS, under the control of Scer\GAL4GMR.PF suppresses the DJ-1αdsRNA.Scer\UAS-induced eye phenotype.

Expression of Akt1Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4Act5C.PI in clones in the eye disc which are homozygous for scrib1 increases the amount of mutant tissue compared to scrib1 single mutant clones, but the double mutant clones do not show metastatic behaviour. Expression of Akt1Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4Act5C.PI in scrib1 wtsx1 double mutant clones in the eye disc increases tumour size but does not result in metastatic behaviour.

The increase in ommatidial size seen in Akt1Scer\UAS.T:Ivir\HA1; Scer\GAL4GMR.PF flies is: unaffected by gigScer\UAS.T:Zzzz\FLAG, Tsc1Scer\UAS.T:Hsap\MYC or gigT437A.T1054A.Scer\UAS.T:Zzzz\FLAG alone; partially suppressed by gigScer\UAS.T:Zzzz\FLAG with Tsc1Scer\UAS.T:Hsap\MYC, or by gigS924A.Scer\UAS.T:Zzzz\FLAG or gigT1518A.Scer\UAS.T:Zzzz\FLAG alone; and fully suppressed by gigS924A.T1518A.Scer\UAS.T:Zzzz\FLAG alone, and by gigΔAkt-P.Scer\UAS.T:Zzzz\FLAG with or without Tsc1Scer\UAS.T:Hsap\MYC. In all these cases of full suppression, ommatidial size is actually reduced slightly compared to wild-type. The increase in wing margin bristle size seen in Akt1Scer\UAS.T:Ivir\HA1; Scer\GAL4Act5C.PI somatic clones is not suppressed by gigScer\UAS.T:Zzzz\FLAG, partially suppressed by gigScer\UAS.T:Zzzz\FLAG with Tsc1Scer\UAS.T:Hsap\MYC, and completely suppressed by gigΔAkt-P.Scer\UAS.T:Zzzz\FLAG alone, or by gigΔAkt-P.Scer\UAS.T:Zzzz\FLAG with Tsc1Scer\UAS.T:Hsap\MYC. In the latter case, the resulting bristles are significantly smaller than wild-type.

When Pk61CEP837 and Akt1Scer\UAS.T:Ivir\HA1 are coexpressed under the control of Scer\GAL4GMR.PF, the eyes display a severely crumpled morphology. The eye bristles are enlarged even more severely, and the boundaries of all ommatidia and photoreceptor cells disappear.

The enlarged eye phenotype caused by expression of Akt1Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4GMR.PF is partially suppressed by co-expression of ThorScer\UAS.cMa.

Xenogenetic Interactions
Statement
Reference

Expression of Akt1Scer\UAS.T:Ivir\HA1 suppresses the retinal phenotype seen when Hsap\HTT128Q.1-336.Scer\UAS is expressed under the control of Scer\GAL4GMR.PU.

Expression of Akt1Scer\UAS.T:Ivir\HA1 enhances the external eye and retinal phenotypes seen when Hsap\ATXN182Q.Scer\UAS is expressed under the control of Scer\GAL4GMR.PU.

Animals expressing Akt1Scer\UAS.T:Ivir\HA1 and Hsap\ATX182Q.Scer\UAS (under the control of Scer\GAL4GMR.PF) have a much stronger eye phenotype than seen in either Akt1Scer\UAS.T:Ivir\HA1 or Hsap\ATX182Q.Scer\UAS on their own. Profoundly disorganised ommatidia and numerous necrotic spots are seen, as well a severely disorganised retina with missing or malformed rhabdomeres.

Complementation and Rescue Data
Comments
Images (0)
Mutant
Wild-type
Stocks (0)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (2)
Reported As
Symbol Synonym
Akt1Scer\UAS.T:Ivir\HA1
Akt1UAS.Tag:HA
Name Synonyms
Secondary FlyBase IDs
    References (18)