|Feature type||allele||Associated gene||Dmel\Akt1|
|Also Known As||dPKB1, Akt1, Aktq, dAkt1, Dakt1q, PKB1, q|
|Map ( GBrowse )|
|Allele class||loss of function allele|
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|Nature of the Allele|
|Mutations Mapped to the Genome|
|Associated Sequence Data|
|Nature of the lesion|
Amino acid replacement: F327I. Mutation is in a core residue in subdomain VII of the kinase catalytic domain, forming the DFG motif.
|Phenotype Manifest In|
8% of Akt1/Akt1 mutant wings show small ectopic vein-like patches. No ectopic wing vein is seen in either heterozygote.
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.
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.
Akt1 mutants lacking both maternal and zygotic Akt1 function exhibit ectopic and widespread apoptosis. Homozygous Akt1 mutant larvae, pupae and adults are significantly smaller in size than Akt1/+ heterozygous animals. Cells of somatic clones of Akt1 mutant cells in the wing are smaller in size than their Akt1/+ neighbours. Flow cytometry of dissociated Akt1 mutant wing imaginal cells confirms that the mutant cells are smaller than similarly treated wild-type cells. Eyes composed of somatic clones of Akt1 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.
|NOT Enhancer of|
Akt1[+]/Akt11 is a suppressor | partially of lethal | late third instar larval stage phenotype of Df(2L)flp170B/Pten3
Akt11/Akt13 is a suppressor of visible phenotype of Pi3K92EScer\UAS.T:Hsap\MYC, Scer\GAL4GMR.PF/Scer\GAL4GMR.PF
Akt11 is a suppressor of tumorigenic | somatic clone phenotype of Ras85DV12.Scer\UAS, Scer\GAL4Act5C.PI/Scer\GAL4Act5C.PI, scrib1
|NOT Suppressor of|
|Phenotype Manifest In|
|NOT Enhancer of|
Akt1[+]/Akt11 is a suppressor of eye phenotype of POSHScer\UAS.cSa, Scer\GAL4GMR.PF, egrScer\UAS.cMa
Akt11/Akt13 is a suppressor of eye phenotype of Pi3K92EScer\UAS.T:Hsap\MYC, Scer\GAL4GMR.PF/Scer\GAL4GMR.PF
Akt11/Akt13 is a suppressor of ommatidium phenotype of Pi3K92EScer\UAS.T:Hsap\MYC, Scer\GAL4GMR.PF/Scer\GAL4GMR.PF
Akt11 is a suppressor | partially of tracheal primordium | ectopic phenotype of Scer\GAL4arm.PS, trhS665D.Scer\UAS.T:Zzzz\FLAG
|NOT Suppressor of|
Akt11/Akt13 is a non-suppressor of ommatidium phenotype of RhebEP50.084, Scer\GAL4GMR.PF/Scer\GAL4GMR.PF
One copy of Akt1 suppresses the reduction in wing blade area seen in homozygous sl males, resulting in wings that are larger than wild type. One copy of Akt1 does not enhance the reduction in wing blade area seen in homozygous sl males. One copy of Akt1 does not enhance the ectopic wing vein phenotype seen in sl homozygotes. One copy of Akt1 partially suppresses the percentage of sl mutant ommatidia that contain extra R7 photoreceptors.
Eye size in POSH[Scer\UAS.cSa] egr[Scer\UAS.cMa] (Scer\GAL4[GMR.PF] overexpression mutants is reduced in an Akt1 heterozygous background.
77% of Pten/Df(2L)flp170B animals survive to adulthood in the presence of Akt1/+. Akt1, wdb[IP] double mutant eye clones fail to differentiate ommatidia.
The presence of an Akt1 mutant background considerably reduces the tumour load in scrib mutant clones expressing Ras85D[V12.Scer\UAS] (under the control of Scer\GAL4[Act5C.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 Pten/Pten[dj189] mutant fly eyes are rescued in a Akt1/Akt1 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.
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.
|Complementation & Rescue Data|
|Not rescued by|
|Stocks ( 0 )|
|Notes on Origin|
|External Crossreferences & Linkouts|
|Synonyms & Secondary IDs ( 14 )|
|Secondary FlyBase IDs|
|References ( 29 )|
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|Recent research papers ( 1 )|
|Recent reviews (0)|
|All reviews listed in FlyBase were published before 2011|