FlyBase Allele Report: Dmel\Pi3K92E[A]

General Information

Symbol

Dmel\Pi3K92E^A

Species

D. melanogaster

Name

FlyBase ID

FBal0100417

Feature type

allele

Associated gene

Dmel\Pi3K92E

Associated Insertion(s)

Carried in Construct

Also Known As

Dp110^A, Dp110A

Key Links

Genomic Maps

JBrowse

Allele class

Mutagen

P-element activity

Nature of the Allele

Allele class

Mutagen

P-element activity

(Weinkove et al., 1999)

Progenitor genotype

P{lacW}H^D179

(Weinkove et al., 1999)

Caused by aberration

Df(3R)Pi3K92E^A

Cytology

Description

Deletion removes 9.3kb from nucleotide 26 in the H 5' UTR, though the H transcription unit and up to nucleotide 2296 in the Pi3K92E cDNA (coordinates of FBrf0091111). The predicted remnant of Pi3K92E would be amino acids 1-668 plus RCAV, followed by a stop, though this remnant is either unstable or not expressed.

(Weinkove et al., 1999)

Mutations Mapped to the Genome

Curation Data

Type

Location

Additional Notes

References

deletion

3R:20,621,949..20,631,257 [-]

Comment:

9.3 kb deletion resulting from the imprecise excision of P{lacW}H^D179. Extends from nucleotide 26 of H 5'UTR (GB:M95192 coordinates used) to base 2296 of the Pi3K92E cDNA (GB:Y09070 coordinates used). Position of deletion on reference sequence inferred by FlyBase curator.

(Weinkove et al., 1999)

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 Pi3K92E^2H1

(Murillo-Maldonado et al., 2011)

CEA with Pi3K92E^5W3

(Murillo-Maldonado et al., 2011)

model of glucose metabolism disease

CEA with Pi3K92E^5W3

(Álvarez-Rendón and Riesgo-Escovar, 2020)

Modifiers Based on Experimental Evidence ( 0 )

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

Follicle cell organisation is not disrupted by homozygous clones in the follicle cells.

(Claret et al., 2014)

11% of embryos fail to reach dorsal closure. Of those that reach dorsal closure, 19% fail to complete the process, with a further 11% closing but showing puckering at the dorsal seam. Embryos that reach the latter stages of dorsal closure consisting show a change in the shape of the dorsal hole, having an elongated flattened shape compared to the wild-type eye shape. The number of filopodia at the leading edge is significantly reduced in mutant embryos.

(Pickering et al., 2013)

Pi3K92E^2H1/Pi3K92E^A mutant adult flies have a reduced body weight compared to heterozygous controls.

Lipid and carbohydrate content are increased in Pi3K92E^2H1/Pi3K92E^A mutant flies compared to controls.

Pi3K92E^2H1/Pi3K92E^A mutant flies exhibit normal electroretinogram (ERG) readings.

Cholinesterase activity is not significantly reduced in Pi3K92E^2H1/Pi3K92E^A mutant flies compared to controls.

Pi3K92E^A/Pi3K92E^5W3 mutant adult flies have a reduced body weight compared to heterozygous controls.

Lipid and carbohydrate content are increased in Pi3K92E^A/Pi3K92E^5W3 mutant flies compared to controls.

Pi3K92E^A/Pi3K92E^5W3 mutant flies exhibit defective electroretinogram (ERG) readings.

Cholinesterase activity is not significantly reduced in Pi3K92E^A/Pi3K92E^5W3 mutant flies compared to controls.

(Murillo-Maldonado et al., 2011)

Flies with the genotype "Df(3R)Pi3K92E^A, P{HBS}/Df(3R)Pi3K92E^A", which are effectively heterozygous for H but null for Pi3K92E, do not eclose.

(Orme et al., 2006)

Pi3K92E^A exhibits a high-diapause phenotype, where the proportion of individuals in diapause is higher than in wild-type flies.

(Williams et al., 2006)

Pi3K92E^A mutants show no defects in opsin regulation.

(Mikeladze-Dvali et al., 2005)

Homozygous clones in the eye have very small ommatidia with rotation defects.

(Bateman and McNeill, 2004)

Autophagy induced in fat body even under non-starvation conditions.

(Scott et al., 2004)

The Pi3K92E^A/Pi3K92E^2H1 combination results in proportionally smaller than normal flies.

(Halfar et al., 2001)

Df(3R)Pi3K92E^A/Df(3R)Pi3K92E-B, P{HBS} mutants (null for Pi3K92E) stop growing early in the third larval instar. Though they continue to move and feed for approximately 20 days they never get any bigger. Larvae are transparent, lack imaginal discs and have reduced fat body. Nervous system, trachea and gut appear normal. Mutant clones in the eye reveal that Pi3K92E is autonomously required for adult cells to reach their normal size.

(Weinkove et al., 1999)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

NOT Suppressor of

Statement

Reference

Pi3K92E^2H1/Pi3K92E^A is a non-suppressor of visible phenotype of Ras85D^{G12V.Y40C.UAS}, Scer\GAL4^GMR.PF

(Halfar et al., 2001)

Phenotype Manifest In

NOT Suppressor of

Statement

Reference

Pi3K92E^2H1/Pi3K92E^A is a non-suppressor of ommatidium phenotype of Ras85D^{G12V.Y40C.UAS}, Scer\GAL4^GMR.PF

(Halfar et al., 2001)

Additional Comments

Genetic Interactions

Statement

Reference

The rough eye phenotype caused by expression of Ras85D^{G12V.Y40C.Scer\UAS} under the control of Scer\GAL4^GMR.PF is not suppressed by Pi3K92E^A/Pi3K92E^2H1.

(Halfar et al., 2001)

Xenogenetic Interactions

Statement

Reference

Complementation and Rescue Data

Rescued by

Pi3K92E^A is rescued by Pi3K92E^Tag:MYC

(Orme et al., 2006)

Pi3K92E^A is rescued by Pi3K92E^{t.RBD.Tag:MYC}

(Orme et al., 2006)

Pi3K92E^A is rescued by Pi3K92E^+t14.7

(Williams et al., 2006)

Pi3K92E^A is rescued by Pi3K92E^+t14.7

(Weinkove et al., 1999)

Partially rescued by

Pi3K92E^A is partially rescued by Pi3K92E^{t.RBD.Tag:MYC}

(Orme et al., 2006)

Comments

Expression of Pi3K92E^+t14.7 rescues the Pi3K92E^A high-diapause phenotype.

(Williams et al., 2006)

Images (0)

Mutant

Wild-type

Stocks (3)

Bloomington

25900

w^*; Df(3R)Pi3K92E^A, H^A Pi3K92E^A, P{HBS}3/TM6B, Tb¹

25917

w¹¹¹⁸; P{H^+tLa}2; Df(3R)Pi3K92E^A, P{Myc-Dp110}1, Pi3K92E^A H^A

25906

w¹¹¹⁸; P{H^+tLa}2; Df(3R)Pi3K92E^A, H^A Pi3K92E^A, P{Myc-Dp110^RBD}1

Notes on Origin

Discoverer

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (6)

Reported As

Symbol Synonym

Dp110^A

(Álvarez-Rendón and Riesgo-Escovar, 2020, Amoyel et al., 2016, Avet-Rochex et al., 2014, Murillo-Maldonado et al., 2011, Orme et al., 2006, Williams et al., 2006, Coelho et al., 2005, Bateman and McNeill, 2004, Radimerski et al., 2002, Clancy et al., 2001, Halfar et al., 2001, Weinkove et al., 1999)

Dp110A

(Mikeladze-Dvali et al., 2005, Gaengel and Mlodzik, 2003)

PI3K92E^A

(Luo et al., 2020, Pickering et al., 2013)

Pi3K92E^A

dp110^A

(Claret et al., 2014, Claret et al., 2014, Chell and Brand, 2010)

p110^A

(Scott et al., 2004, Scott et al., 2004)

Name Synonyms

Secondary FlyBase IDs

References (21)

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