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General Information
Symbol
Dmel\Akt1
Species
D. melanogaster
Name
FlyBase ID
FBal0051404
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
Akt11, dPKB1, Aktq, dAkt1, Dakt1q, PKB1, q, Akt1q
Key Links
Mutagen
    Nature of the Allele
    Mutagen
    Mutations Mapped to the Genome
     
    Type
    Location
    Additional Notes
    References
    Nucleotide change:

    T16102298A

    Amino acid change:

    F327I | Akt1-PA; F327I | Akt1-PB; M1T | Akt1-PC; F327I | Akt1-PD; F327I | Akt1-PE

    Reported amino acid change:

    F327I

    Comment:

    Site of nucleotide substitution in mutant inferred by FlyBase based on reported amino acid change.

    Associated Sequence Data
    DNA sequence
    Protein sequence
     
     
    Progenitor genotype
    Cytology
    Nature of the lesion
    Statement
    Reference

    Amino acid replacement: F327I. Mutation is in a core residue in subdomain VII of the kinase catalytic domain, forming the DFG motif.

    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 ( 1 )
    Disease
    Evidence
    References
    Modifiers Based on Experimental Evidence ( 1 )
    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

    Akt11 mutant larval brains show abnormal accumulations of POSH protein.

    Akt11/Akt13 mutant adult flies have a reduced body weight compared to heterozygous controls. Wing area is also reduced compared to controls.

    Lipid content is increased in Akt11/Akt13 mutant flies compared to controls. Carbohydrate content is similar to controls.

    Akt11/Akt13 mutant flies exhibit defective electroretinogram (ERG) readings.

    Cholinesterase activity is significantly reduced in Akt11/Akt13 mutant flies compared to controls.

    8% of Akt13/Akt11 mutant wings show small ectopic vein-like patches. No ectopic wing vein is seen in either heterozygote.

    Eye size is reduced in an Akt11 heterozygous background.

    Homozygous clones in the eye show severe undergrowth and the eye is severely reduced compared to wild type.

    Long term synaptic depression at larval neuromuscular junctions is strongly impaired in Akt104226/Akt11 third instar larvae. This effect is seen when LTD is tested using 0.2 or 0.4 mM Ca2+ saline or when high frequency stimulation (40Hz) is used.

    No effect is seen on long term synaptic depression at larval neuromuscular junctions in Akt11/+ animals.

    When Akt11/Akt11; Akt1hs.PS animals are raised at 25'C with daily heat-shocks and then switched to 18'C for 24-36 hours following the last heat shock and prior to harvesting as late third instar larvae, long term synaptic depression (LTD) at neuro-muscular junctions is severely disrupted. However LTD is normal if the heat shock regime is continued to the time of testing.

    Head capsule reduced - pinhead phenotype.

    Ommatidial size in Akt11/Akt13 flies is reduced to 0.65 of wild-type.

    Homozygous mutant clones in the eye have smaller cells and are rarely recovered in adults.

    Akt11 germ-line clones lead to 100% maternal effect embryonic lethality with embryonic extensive cell death. Akt11 homozygotes die as larvae, and appear to be phenotypically identical to Akt11/Df(3R)sbd45 animals. Stage 16 Akt11/Df(3R)sbd45 embryos have only very mild tracheal branching defects.

    Homozygous clones in the eye contain ommatidia which are smaller than normal.

    Akt11 mutants lacking both maternal and zygotic Akt1 function exhibit ectopic and widespread apoptosis.

    Homozygous Akt11 mutant larvae, pupae and adults are significantly smaller in size than Akt11/+ heterozygous animals.

    Cells of somatic clones of Akt11 mutant cells in the wing are smaller in size than their Akt11/+ neighbours. Flow cytometry of dissociated Akt11 mutant wing imaginal cells confirms that the mutant cells are smaller than similarly treated wild-type cells.

    Eyes composed of somatic clones of Akt11 mutant cells are smaller in size as compared to wild-type eyes.

    Rhabdomeres are reduced in size in homozygous clones in the eye. In mosaic ommatidia, both small and normal sized rhabdomeres can be present. Homozygous clones are rare and small and are only obtained when they are induced during the third larval instar stage.

    Embryos derived from germline clones lack portions of cuticle at the end of embryogenesis. In the absence of zygotic Akt1 embryos show almost complete loss of cuticle, embryos with some zygotic activity exhibit loss of cuticular head and dorsal structures. Heat induced expression of Akt1, maternally and zygotically, allows the reappearance of most cuticle structures. AO staining of embryos derived from germline clones shows extensive apoptosis. By stage 8 TUNEL signal reveals extensive DNA fragmentation.

    Semi-viable. Homozygotes are fertile and hemizygotes are lethal.

    External Data
    Interactions
    Show genetic interaction network for Enhancers & Suppressors
    Phenotypic Class
    Suppressed by
    Statement
    Reference
    Enhancer of
    Statement
    Reference
    NOT Enhancer of
    Statement
    Reference

    Akt1[+]/Akt1 is a non-enhancer of abnormal size | adult stage phenotype of sl9

    Suppressor of
    Statement
    Reference

    Akt1[+]/Akt1 is a suppressor | partially of flightless phenotype of Pten3/Pten5

    Akt1 is a suppressor of increased cell growth | nutrition conditional phenotype of Pten117

    Akt1 is a suppressor of increased cell growth phenotype of Pten117

    Akt1[+]/Akt1 is a suppressor of abnormal size | adult stage phenotype of sl2

    Akt1[+]/Akt1 is a suppressor of visible phenotype of Pdk1A467V.UAS, Scer\GAL4ap-md544

    NOT Suppressor of
    Statement
    Reference

    Akt1 is a non-suppressor of lethal | recessive | larval stage phenotype of Ptenunspecified

    Akt1 is a non-suppressor of visible | somatic clone phenotype of Tsc1Q600X

    Other
    Phenotype Manifest In
    Suppressed by
    Statement
    Reference
    Enhancer of
    Statement
    Reference
    NOT Enhancer of
    Statement
    Reference

    Akt1[+]/Akt1 is a non-enhancer of wing vein | ectopic phenotype of sl2

    Akt1[+]/Akt1 is a non-enhancer of wing blade phenotype of sl9

    Suppressor of
    Statement
    Reference

    Akt1 is a suppressor of eye | nutrition conditional phenotype of Pten117

    Akt1 is a suppressor of eye phenotype of Pten117

    Akt1[+]/Akt1 is a suppressor of wing blade phenotype of sl2

    Akt1[+]/Akt1 is a suppressor of eye phenotype of POSHUAS.cSa, Scer\GAL4GMR.PF, egrUAS.cMa

    Akt1/Akt3 is a suppressor of eye phenotype of Ptendj189/Pten117

    Akt1/Akt3 is a suppressor of rhabdomere phenotype of Ptendj189/Pten117

    Akt1[+]/Akt1 is a suppressor of wing phenotype of Pdk1A467V.UAS, Scer\GAL4ap-md544

    NOT Suppressor of
    Statement
    Reference

    Akt1 is a non-suppressor of eye phenotype of wdbIP

    Akt1 is a non-suppressor of ommatidium | somatic clone phenotype of Tsc1Q600X

    Other
    Additional Comments
    Genetic Interactions
    Statement
    Reference

    An Akt11 mutant background completely suppresses the Pten117 overgrowth phenotype, under normal as well as under starvation conditions.

    One copy of Akt11 suppresses the reduction in wing blade area seen in homozygous sl2 males, resulting in wings that are larger than wild type.

    One copy of Akt11 does not enhance the reduction in wing blade area seen in homozygous sl9 males.

    One copy of Akt11 does not enhance the ectopic wing vein phenotype seen in sl2 homozygotes.

    One copy of Akt11 partially suppresses the percentage of sl2 mutant ommatidia that contain extra R7 photoreceptors.

    Eye size in POSHScer\UAS.cSa egrScer\UAS.cMa (Scer\GAL4GMR.PF overexpression mutants is reduced in an Akt11 heterozygous background.

    77% of Pten3/Df(2L)flp170B animals survive to adulthood in the presence of Akt11/+.

    Akt11, wdbIP double mutant eye clones fail to differentiate ommatidia.

    The presence of an Akt11 mutant background considerably reduces the tumour load in scrib1 mutant clones expressing Ras85DV12.Scer\UAS (under the control of Scer\GAL4Act5C.PI) using the FLP/FRT system but does not impair metastatic behaviour.

    foxo25 Akt11 double homozygotes show considerable lethality; most animals die before the pupal stage, with most of the remaining animals dying as pupae and only a few escapers eclosing as adults. 71% of pupae still contain intact salivary glands at 20 hours after puparium formation (this is approximately 6 hours after the glands are normally destroyed in wild-type animals).

    The rhabdomere defects seen in Pten117/Ptendj189 mutant fly eyes are rescued in a Akt11/Akt13 mutant background. In these animals photoreceptor cell morphology is close to wild-type and eyes display a low frequency of deformed rhabdomeres.

    The nurse cells of Ptendj189/Pten117; Akt13/Akt11 viable females show normal lipid storage, while clones of Pten alleles show formation of large lipid droplets.

    Akt1;foxo double mutants develop into small pharate adults, most of which fail to eclose.

    The large size and disorganisation of ommatidia in Scer\GAL4GMR.PF/+; RhebEP50.084/+ flies is unaffected by Akt11/Akt13.

    The enlarged eye and ommatidia phenotype caused by expression of Pi3K92EScer\UAS.T:Hsap\MYC under the control of Scer\GAL4GMR.PF is completely suppressed in a Akt11/Akt13 background.

    Ptenunspecified flies rescued by the combination Akt11/Akt13 are wild-type in size. Ptenunspecified ; Akt11/Akt13 flies have essentially normal ommatidia and rhabdomeres in the eye and the wings show normal venation.

    Tsc129, Akt11 double mutant clones in the eye, show a similar size increase as seen in Tsc129 mutant clones alone.

    Akt11/+ is embryonic semi-lethal in combination Df(2L)Pi3K21B-A/+. By the end of embryogenesis these animals show severe loss of cuticle.

    Clones in the eye doubly mutant for Akt11 and Tsc1Q600X show the Tsc1Q600X single mutant phenotype of enlarged ommatidia.

    DNA fragmentation phenotype is not suppressed by loss of rpr, grim and W (Df(3L)H99).

    Xenogenetic Interactions
    Statement
    Reference

    The eye degeneration phenotype characteristic for adult flies expressing Hsap\CHMP2BIntron5.UAS under the control of Scer\GAL4GMR.PU is strongly enhanced by combination with Akt104226.

    Apoptosis seen in embryos derived from germline clones is effectively blocked by BacA\p35hs.PS. Scer\GAL4arm.PS-mediated expression of Btau\AKT1Scer\UAS.cSa also rescues lethality at a low efficiency.

    Complementation and Rescue Data
    Images (0)
    Mutant
    Wild-type
    Stocks (0)
    Notes on Origin
    Discoverer
    External Crossreferences and Linkouts ( 0 )
    Synonyms and Secondary IDs (19)
    References (43)