FlyBase Allele Report: Dmel\Akt[1]

General Information

Symbol

Dmel\Akt¹

Species

D. melanogaster

Name

FlyBase ID

FBal0051404

Feature type

allele

Associated gene

Dmel\Akt

Associated Insertion(s)

Carried in Construct

Also Known As

Akt1¹, Akt^q, dPKB¹, dAkt¹, Dakt1q, PKB¹, q, Akt1^q

Key Links

Genomic Maps

JBrowse

Allele class

loss of function allele

Mutagen

Nature of the Allele

Allele class

loss of function allele

(Jin et al., 2001, Staveley et al., 1998)

Mutagen

Progenitor genotype

Cytology

Description

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

(Staveley et al., 1998)

Mutations Mapped to the Genome

Curation Data

Type

Location

Additional Notes

References

point_mutation

3R:16,102,298..16,102,298 [+]

Nucleotide change:

T16102298A

Amino acid change:

Reported amino acid change:

F327I

Comment:

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

(Stocker et al., 2002)

Variant Molecular Consequences

Associated Sequence Data

DDBJ / EMBL / GenBank

DNA sequence

Protein sequence

UniProtKB/Swiss-Prot

UniProtKB/TrEMBL

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

model of type 2 diabetes mellitus

CEA with Akt³

(Murillo-Maldonado et al., 2011)

Modifiers Based on Experimental Evidence ( 1 )

Disease

Interaction

References

ameliorates carcinoma

modeled by Ras85D^V12.UAS, scrib¹

(Igaki et al., 2006)

Comments on Models/Modifiers Based on Experimental Evidence ( 0 )

Disease-implicated variant(s)

Phenotypic Data

Phenotypic Class

abnormal body size (with Akt⁰⁴²²⁶)

(Vereshchagina et al., 2008)

abnormal body size | embryonic stage | recessive

(Scanga et al., 2000)

abnormal body size | pupal stage | recessive

(Scanga et al., 2000)

abnormal body size | recessive

(Scanga et al., 2000)

abnormal cell death | embryonic stage | maternal effect | recessive

(Scanga et al., 2000)

abnormal cell size | recessive | somatic clone

(Scanga et al., 2000)

abnormal neurophysiology | adult stage (with Akt³)

(Murillo-Maldonado et al., 2011)

abnormal neurophysiology | third instar larval stage, with Akt^hs.PS

(Guo and Zhong, 2006)

abnormal neurophysiology | third instar larval stage (with Akt⁰⁴²²⁶)

(Guo and Zhong, 2006)

decreased body size | adult stage (with Akt³)

(Murillo-Maldonado et al., 2011)

decreased cell size | somatic clone

(Gao and Pan, 2001)

increased cell death | germline clone

(Staveley et al., 1998)

lethal | embryonic stage | germline clone | maternal effect

(Jin et al., 2001)

lethal | larval stage

(Jin et al., 2001)

lethal | recessive

(Guo and Zhong, 2006, Heitzler et al., 1996)

lethal - all die before end of larval stage

(Junger et al., 2003)

lethal - all die during embryonic stage | maternal effect | recessive

(Staveley et al., 1998)

some die during embryonic stage | recessive | maternal effect | recessive

(Staveley et al., 1998)

some die during larval stage

(Junger et al., 2003)

viable (with Akt³)

(Murillo-Maldonado et al., 2011)

visible | adult stage (with Akt³)

(Murillo-Maldonado et al., 2011)

visible | recessive

(Scanga et al., 2000)

visible | recessive | somatic clone

(Potter et al., 2001, Scanga et al., 2000)

visible | somatic clone

(Hietakangas and Cohen, 2007, Junger et al., 2003)

Phenotype Manifest In

adult head capsule | somatic clone

(Junger et al., 2003)

embryo

(Scanga et al., 2000)

embryonic/first instar larval cuticle | germline clone | maternal effect

(Staveley et al., 1998)

eye

(Tsuda et al., 2010)

eye | somatic clone

(Hietakangas and Cohen, 2007, Scanga et al., 2000)

larval brain | third instar larval stage

(West et al., 2018)

neuromuscular junction | third instar larval stage, with Akt^hs.PS

(Guo and Zhong, 2006)

neuromuscular junction | third instar larval stage (with Akt⁰⁴²²⁶)

(Guo and Zhong, 2006)

ommatidium (with Akt³)

(Stocker et al., 2003)

ommatidium | somatic clone

(Potter et al., 2001)

rhabdomere | somatic clone

(Verdu et al., 1999)

tracheal branch primordium

(Jin et al., 2001)

tracheal branch primordium (with Df(3R)sbd45)

(Jin et al., 2001)

wing (with Akt³)

(Murillo-Maldonado et al., 2011)

wing hair | somatic clone

(Scanga et al., 2000)

wing vein | ectopic (with Akt³)

(Murillo-Maldonado et al., 2011)

Detailed Description

Statement

Reference

Akt1¹ mutant larval brains show abnormal accumulations of POSH protein.

(West et al., 2018)

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.

(Murillo-Maldonado et al., 2011)

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

(Murillo-Maldonado et al., 2011)

Eye size is reduced in an Akt1¹ heterozygous background.

(Tsuda et al., 2010)

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

(Hietakangas and Cohen, 2007)

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; Akt1^hs.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.

(Guo and Zhong, 2006)

Head capsule reduced - pinhead phenotype.

(Junger et al., 2003)

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

(Stocker et al., 2003)

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

(Gao and Pan, 2001)

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.

(Jin et al., 2001)

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

(Potter et al., 2001)

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.

(Scanga et al., 2000)

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.

(Verdu et al., 1999)

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.

(Staveley et al., 1998)

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

(Heitzler et al., 1996)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Suppressed by

Statement

Reference

Akt¹/Akt⁰⁴²²⁶ has abnormal body size phenotype, suppressible by wdb[+]/wdb^IP

(Vereshchagina et al., 2008)

Akt¹ has lethal | larval stage phenotype, suppressible by foxo²⁵/foxo²¹

(Junger et al., 2003)

Akt¹ has visible | somatic clone phenotype, suppressible by foxo²⁵

(Junger et al., 2003)

Akt¹ has decreased cell size | somatic clone phenotype, suppressible by Tsc1²⁹

(Gao and Pan, 2001)

Akt¹ has increased cell death | germline clone phenotype, suppressible by BacA\p35^hs.PS

(Staveley et al., 1998)

Akt¹ has lethal phenotype, suppressible by Scer\GAL4^arm.PS/Btau\AKT1^UAS.cSa

(Staveley et al., 1998)

Enhancer of

Statement

Reference

Akt¹ is an enhancer of visible | adult stage phenotype of Hsap\CHMP2B^Intron5.UAS, Scer\GAL4^GMR.PU

(West et al., 2018)

NOT Enhancer of

Statement

Reference

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

(Murillo-Maldonado et al., 2011)

Akt¹ is a non-enhancer of abnormal size | adult stage | somatic clone phenotype of Tsc1^Q600X

(Potter et al., 2001)

Suppressor of

Statement

Reference

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

(Mensah et al., 2015)

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

(Nowak et al., 2013)

Akt¹ is a suppressor of increased cell growth rate phenotype of Pten¹¹⁷

(Nowak et al., 2013)

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

(Murillo-Maldonado et al., 2011)

Akt1[+]/Akt¹ is a suppressor of increased cell number | adult stage phenotype of sl²

(Murillo-Maldonado et al., 2011)

Akt1[+]/Akt¹ is a suppressor | partially of lethal | late third instar larval stage phenotype of Df(2L)flp170B/Pten³

(Vereshchagina et al., 2008)

Akt¹ is a suppressor of neoplasia | somatic clone phenotype of Ras85D^V12.UAS, scrib¹

(Igaki et al., 2006)

Akt¹ is a suppressor of neoplasia | somatic clone phenotype of Ras85D^V12.UAS, Scer\GAL4^Act5C.PI, scrib¹

(Igaki et al., 2006)

Akt¹/Akt³ is a suppressor of visible phenotype of Pi3K92E^UAS.Tag:MYC, Scer\GAL4^GMR.PF

(Radimerski et al., 2002)

Akt¹/Akt³ is a suppressor of lethal | recessive | larval stage phenotype of Pten^unspecified

(Stocker et al., 2002)

Akt1[+]/Akt¹ is a suppressor of visible phenotype of Pdk1^A467V.UAS, Scer\GAL4^ap-md544

(Rintelen et al., 2001)

NOT Suppressor of

Statement

Reference

Akt¹ is a non-suppressor of lethal | recessive | larval stage phenotype of Pten^unspecified

(Stocker et al., 2002)

Akt¹ is a non-suppressor of visible | somatic clone phenotype of Tsc1^Q600X

(Potter et al., 2001)

Other

Statement

Reference

Akt¹, foxo²⁵ has lethal phenotype

(Liu and Lehmann, 2006)

Akt¹/Akt³, Hsap\FOXO3^UAS.cFa, Scer\GAL4^GMR.PF has visible phenotype

(Junger et al., 2003)

Akt¹/Akt³, Pten¹¹⁷ has viable phenotype

(Lee et al., 2003)

Akt¹, Df(2L)Pi3K21B-A/+ has partially lethal - majority die phenotype

(Jin et al., 2001)

Phenotype Manifest In

Suppressed by

Statement

Reference

Akt¹ has adult head capsule | somatic clone phenotype, suppressible by foxo²⁵

(Junger et al., 2003)

Enhancer of

Statement

Reference

Akt¹ is an enhancer of eye phenotype of Hsap\CHMP2B^Intron5.UAS, Scer\GAL4^GMR.PU

(West et al., 2018)

NOT Enhancer of

Statement

Reference

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

(Murillo-Maldonado et al., 2011)

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

(Murillo-Maldonado et al., 2011)

Suppressor of

Statement

Reference

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

(Nowak et al., 2013)

Akt¹ is a suppressor of eye phenotype of Pten¹¹⁷

(Nowak et al., 2013)

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

(Murillo-Maldonado et al., 2011)

Akt1[+]/Akt¹ is a suppressor of photoreceptor cell R7 | adult stage phenotype of sl²

(Murillo-Maldonado et al., 2011)

Akt1[+]/Akt¹ is a suppressor of eye phenotype of POSH^UAS.cSa, Scer\GAL4^GMR.PF, egr^UAS.cMa

(Tsuda et al., 2010)

Akt¹/Akt³ is a suppressor of eye phenotype of Pten^dj189/Pten¹¹⁷

(Pinal et al., 2006)

Akt¹/Akt³ is a suppressor of rhabdomere phenotype of Pten^dj189/Pten¹¹⁷

(Pinal et al., 2006)

Akt¹/Akt³ is a suppressor of eye phenotype of Pi3K92E^UAS.Tag:MYC, Scer\GAL4^GMR.PF

(Radimerski et al., 2002)

Akt¹/Akt³ is a suppressor of ommatidium phenotype of Pi3K92E^UAS.Tag:MYC, Scer\GAL4^GMR.PF

(Radimerski et al., 2002)

Akt¹ is a suppressor | partially of tracheal primordium | ectopic phenotype of Scer\GAL4^arm.PS, trh^{S665D.UAS.Tag:FLAG}

(Jin et al., 2001)

Akt¹ is a suppressor of tracheal primordium | ectopic phenotype of Scer\GAL4^arm.PS, trh^UAS.Tag:FLAG

(Jin et al., 2001)

Akt1[+]/Akt¹ is a suppressor of wing phenotype of Pdk1^A467V.UAS, Scer\GAL4^ap-md544

(Rintelen et al., 2001)

NOT Suppressor of

Statement

Reference

Akt¹ is a non-suppressor of eye phenotype of wdb^IP

(Vereshchagina et al., 2008)

Akt¹/Akt³ is a non-suppressor of ommatidium phenotype of Rheb^EP50.084, Scer\GAL4^GMR.PF

(Stocker et al., 2003)

Akt¹ is a non-suppressor of ommatidium | somatic clone phenotype of Tsc1^Q600X

(Potter et al., 2001)

Other

Statement

Reference

Akt¹, foxo²⁵ has embryonic/larval salivary gland phenotype

(Liu and Lehmann, 2006)

Akt¹/Akt³, Pten^dj189/Pten¹¹⁷ has lipid particle & nurse cell phenotype

(Vereshchagina and Wilson, 2006)

Akt¹/Akt³, Hsap\FOXO3^UAS.cFa, Scer\GAL4^GMR.PF has eye phenotype

(Junger et al., 2003)

Akt¹, Df(2L)Pi3K21B-A/+ has embryonic/first instar larval cuticle phenotype

(Jin et al., 2001)

Additional Comments

Genetic Interactions

Statement

Reference

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

(Nowak et al., 2013)

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.

(Murillo-Maldonado et al., 2011)

Eye size in POSH^Scer\UAS.cSa egr^Scer\UAS.cMa (Scer\GAL4^GMR.PF overexpression mutants is reduced in an Akt1¹ heterozygous background.

(Tsuda et al., 2010)

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

Akt1¹, wdb^IP double mutant eye clones fail to differentiate ommatidia.

(Vereshchagina et al., 2008)

The presence of an Akt1¹ mutant background considerably reduces the tumour load in scrib¹ 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.

(Igaki et al., 2006)

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).

(Liu and Lehmann, 2006)

The rhabdomere defects seen in Pten¹¹⁷/Pten^dj189 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.

(Pinal et al., 2006)

The nurse cells of Pten^dj189/Pten¹¹⁷; Akt1³/Akt1¹ viable females show normal lipid storage, while clones of Pten alleles show formation of large lipid droplets.

(Vereshchagina and Wilson, 2006)

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

(Junger et al., 2003)

The large size and disorganisation of ommatidia in Scer\GAL4^GMR.PF/+; Rheb^EP50.084/+ flies is unaffected by Akt1¹/Akt1³.

(Stocker et al., 2003)

The enlarged eye and ommatidia phenotype caused by expression of Pi3K92E^{Scer\UAS.T:Hsap\MYC} under the control of Scer\GAL4^GMR.PF is completely suppressed in a Akt1¹/Akt1³ background.

(Radimerski et al., 2002)

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

(Stocker et al., 2002)

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

(Gao and Pan, 2001)

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

(Jin et al., 2001)

Clones in the eye doubly mutant for Akt1¹ and Tsc1^Q600X show the Tsc1^Q600X single mutant phenotype of enlarged ommatidia.

(Potter et al., 2001)

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

(Staveley et al., 1998)

Xenogenetic Interactions

Statement

Reference

The eye degeneration phenotype characteristic for adult flies expressing Hsap\CHMP2B^Intron5.UAS under the control of Scer\GAL4^GMR.PU is strongly enhanced by combination with Akt1⁰⁴²²⁶.

(West et al., 2018)

Apoptosis seen in embryos derived from germline clones is effectively blocked by BacA\p35^hs.PS. Scer\GAL4^arm.PS-mediated expression of Btau\AKT1^Scer\UAS.cSa also rescues lethality at a low efficiency.

(Staveley et al., 1998)

Complementation and Rescue Data

Rescued by

Akt¹ is rescued by Akt^tub.PH

(Hietakangas and Cohen, 2007)

Akt¹ is rescued by Akt^S505A.tub

(Hietakangas and Cohen, 2007)

Akt¹ is rescued by Akt^hs.PS

(Guo and Zhong, 2006)

Akt¹ is rescued by Akt^hs.PS

(Scanga et al., 2000)

Akt¹ is rescued by Scer\GAL4^arm.PS/Akt^UAS.cSa

(Staveley et al., 1998)

Akt¹ is rescued by Akt^hs.PS

(Staveley et al., 1998)

Not rescued by

Akt¹ is not rescued by Akt^R45A.tub

(Hietakangas and Cohen, 2007)

Akt¹ is not rescued by Akt^T342A.tub

(Hietakangas and Cohen, 2007)

Comments

Scer\GAL4^arm.PS-mediated expression of Akt1^Scer\UAS.cSa rescues lethality.

(Staveley et al., 1998)

Images (0)

Mutant

Wild-type

Stocks (0)

Notes on Origin

Discoverer

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (19)

Reported As

Symbol Synonym

AKT¹

(Hwang et al., 2019, West et al., 2018)

AKT^q

(Hietakangas and Cohen, 2007)

Akt1 1

(Park et al., 2014)

Akt1¹

(Santabárbara-Ruiz et al., 2019, Rives-Quinto et al., 2017, Lanet et al., 2013, Tsuda et al., 2010, Vereshchagina et al., 2008, Pinal et al., 2006)

Akt1^q

(Amoyel et al., 2016, Mensah et al., 2015)

Akt¹

(Zheng and Sehgal, 2010, Koike-Kumagai et al., 2009, Vereshchagina and Wilson, 2006)

Akt^kd

(Kang et al., 2018)

Akt^q

(Gao and Pan, 2001, Jin et al., 2001)

Dakt1q

(Radimerski et al., 2002, Scanga et al., 2000, Staveley et al., 1998)

Daktq1

(Kohanski, 2002)

PKB¹

(Nowak et al., 2013, Murillo-Maldonado et al., 2011, Murillo-Maldonado et al., 2011, Stocker et al., 2003)

akt1

(Funakoshi et al., 2018)

akt¹

(Bardet et al., 2013, Guo and Zhong, 2006, Igaki et al., 2006, Igaki et al., 2006)

akt^89Bq1

(Potter et al., 2001)

akt^q

(Parker and Struhl, 2015, Kockel et al., 2010)

dAkt¹

(Lee et al., 2003, Stocker et al., 2002, Rintelen et al., 2001)

dPKB¹

(Liu and Lehmann, 2006, Junger et al., 2003, Oldham and Hafen, 2003, Radimerski et al., 2002, Radimerski et al., 2002)

l(3)89Bq

(Verdu et al., 1999)

(Scanga et al., 2000, Staveley et al., 1998)

Name Synonyms

Secondary FlyBase IDs

References (44)

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