FlyBase Allele Report: Dmel\Exn[EY01953]

General Information

Symbol

Dmel\Exn^EY01953

Species

D. melanogaster

Name

FlyBase ID

FBal0148229

Feature type

allele

Associated gene

Dmel\Exn

Associated Insertion(s)

P{EPgy2}Exn^EY01953

Carried in Construct

Key Links

Genomic Maps

JBrowse

Allele class

Mutagen

P-element activity

Nature of the Allele

Allele class

Mutagen

P-element activity

(Gene Disruption Project members, 2001-)

Progenitor genotype

Associated Insertion(s)

P{EPgy2}Exn^EY01953

Cytology

Description

Allele components

Component

Use(s)

Inserted element

P{EPgy2}

misexpression element

Regulatory region(s)

UASp

binary expression system - regulatory region

Mutations Mapped to the Genome

Curation Data

Type

Location

Additional Notes

References

transposable_element_insertion_site

3L:16,991,017..16,991,017 [+]

(Frank et al., 2009, Gene Disruption Project members, 2001-)

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 ( 0 )

Disease

Evidence

References

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

abnormal immune response | larval stage

(Howell et al., 2012)

abnormal neurophysiology | recessive | third instar larval stage

(Frank et al., 2009)

Phenotype Manifest In

Detailed Description

Statement

Reference

Mutant larvae fail to encapsulate eggs when parasitised by the avirulent L. boulardi wasp strain G486 (no melanisation is seen). Plasmatocytes fully cover the egg, while lamellocytes partially cover it.

(Howell et al., 2012)

There is a small, but statistically significant, defect in presynaptic vesicle release at the neuromuscular junction (NMJ) in the Exn^EY01953 mutants compared to wild-type controls. Presynaptic release is decreased at each tested external calcium concentrations over a range of 0.2-0.5 mM. Quantal content measured at the NMJ is decreased in Exn^EY01953 mutant larvae.

The rapid induction of homeostatic signaling following philanthatoxin (PhTx) application at the NMJ is normal in homo- and heterozygotes of Exn^EY01953.

(Frank et al., 2009)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

NOT Enhancer of

Statement

Reference

Exn^EY01953/Exn[+] is a non-enhancer of abnormal neurophysiology | third instar larval stage | recessive phenotype of GluRIIA^SP16

(Frank et al., 2009)

Exn^EY01953/Exn[+] is a non-enhancer of abnormal neurophysiology | third instar larval stage | recessive phenotype of GluRIIA^SP16, Rho1^72O/Rho1[+]

(Frank et al., 2009)

Exn^EY01953/Exn[+] is a non-enhancer of abnormal neurophysiology | third instar larval stage | recessive phenotype of GluRIIA^SP16, Rho1[+]/Rho1^k02107b

(Frank et al., 2009)

Exn^EY01953/Exn[+] is a non-enhancer of abnormal neurophysiology | third instar larval stage | recessive phenotype of GluRIIA^SP16, Rac1^J11/Rac1[+]

(Frank et al., 2009)

Suppressor of

Statement

Reference

Exn^EY01953, Exn[+], Eph[+], Eph^x652 is a suppressor of abnormal neurophysiology | recessive | third instar larval stage phenotype of GluRIIA^SP16

(Frank et al., 2009)

NOT Suppressor of

Statement

Reference

Exn^EY01953/Exn[+] is a non-suppressor of abnormal neurophysiology | recessive | third instar larval stage phenotype of GluRIIA^SP16

(Frank et al., 2009)

Other

Statement

Reference

Cdc42[+]/Cdc42⁴, Exn^EY01953/Exn[+], GluRIIA^SP16 has abnormal neurophysiology | recessive | third instar larval stage phenotype

(Frank et al., 2009)

Exn^EY01953, GluRIIA^SP16 has abnormal neurophysiology | recessive | third instar larval stage phenotype

(Frank et al., 2009)

Exn^EY01953, GluRIIA^SP16, cac^S/cac[+] has abnormal neurophysiology | recessive | third instar larval stage phenotype

(Frank et al., 2009)

Exn^EY01953, GluRIIA^SP16, Scer\GAL4^elav-C155, cac^UAS.EGFP has abnormal neurophysiology | recessive | third instar larval stage phenotype

(Frank et al., 2009)

Cdc42[+]/Cdc42³, Exn^EY01953/Exn[+], GluRIIA^SP16 has abnormal neurophysiology | recessive | third instar larval stage phenotype

(Frank et al., 2009)

Phenotype Manifest In

NOT Enhancer of

Statement

Reference

Exn^EY01953/Exn[+] is a non-enhancer of embryonic/larval neuromuscular junction phenotype of GluRIIA^SP16

(Frank et al., 2009)

Exn^EY01953/Exn[+] is a non-enhancer of embryonic/larval neuromuscular junction phenotype of GluRIIA^SP16, Rho1^72O/Rho1[+]

(Frank et al., 2009)

Exn^EY01953/Exn[+] is a non-enhancer of embryonic/larval neuromuscular junction phenotype of GluRIIA^SP16, Rho1[+]/Rho1^k02107b

(Frank et al., 2009)

Exn^EY01953/Exn[+] is a non-enhancer of embryonic/larval neuromuscular junction phenotype of GluRIIA^SP16, Rac1^J11/Rac1[+]

(Frank et al., 2009)

Suppressor of

Statement

Reference

Exn^EY01953, Exn[+], Eph[+], Eph^x652 is a suppressor of embryonic/larval neuromuscular junction phenotype of GluRIIA^SP16

(Frank et al., 2009)

NOT Suppressor of

Statement

Reference

Exn^EY01953/Exn[+] is a non-suppressor of embryonic/larval neuromuscular junction phenotype of GluRIIA^SP16

(Frank et al., 2009)

Other

Statement

Reference

Exn^EY01953, GluRIIA^SP16 has NMJ bouton phenotype

(Frank et al., 2009)

Exn^EY01953, GluRIIA^SP16 has embryonic/larval neuromuscular junction phenotype

(Frank et al., 2009)

Exn^EY01953, GluRIIA^SP16, cac^S/cac[+] has embryonic/larval neuromuscular junction phenotype

(Frank et al., 2009)

Exn^EY01953, GluRIIA^SP16, Scer\GAL4^elav-C155, cac^UAS.EGFP has embryonic/larval neuromuscular junction phenotype

(Frank et al., 2009)

Cdc42[+]/Cdc42³, Exn^EY01953/Exn[+], GluRIIA^SP16 has embryonic/larval neuromuscular junction phenotype

(Frank et al., 2009)

Cdc42[+]/Cdc42⁴, Exn^EY01953/Exn[+], GluRIIA^SP16 has embryonic/larval neuromuscular junction phenotype

(Frank et al., 2009)

Additional Comments

Genetic Interactions

Statement

Reference

In GluRIIA^SP16; Exn^EY01953 double mutant third instar larvae, similarly to GluRIIA^SP16 single mutants, the spontaneous miniature release amplitude (mepsp) is decreased at the neuromuscular junctions. However, in contrast to GluRIIA^SP16 single mutants, GluRIIA^SP16; Exn^EY01953 double mutant neuromuscular junctions do not show a corresponding increase in quantal content.

GluRIIA^SP16 mutant larvae, also homozygous for an Exn^EY01953 allele, show a slight but significant increase in bouton number at the NMJ compared to GluRIIA^SP16 single mutants.

GluRIIA^SP16 mutant larvae, also homozygous for an Exn^EY01953 allele, show no difference in average active zone number per NMJ compared to GluRIIA^SP16 single mutants.

The recessive GluRIIA^SP16 single mutant NMJ synaptic homeostasis phenotype is not enhanced nor suppressed by a heterozygous Exn^EY01953/+ mutation.

The recessive GluRIIA^SP16 single mutant NMJ synaptic homeostatic response is completely suppressed in the presence of a heterozygous cac^S/+ mutation in combination with an Exn^EY01953/+ heterozygous genetic background.

Expression of cac^{Scer\UAS.T:Avic\GFP-EGFP} driven by Scer\GAL4^elav-C155 in a GluRIIA^SP16; Exn^EY01953 double mutant background restores the NMJ synaptic homeostatic response to a significant degree.

cac^S/+; ; Exn^EY01953/+ double heterozygotes show a severe disruption of the rapid induction of homeostatic signaling at the neuromuscular junction following philanthatoxin (PhTx) application.

The Exn^EY01953/+ heterozygous mutation does not enhance the Rho1^72O/+, GluRIIA^SP16 double mutant NMJ synaptic homeostasis phenotype.

The Exn^EY01953/+ heterozygous mutation does not enhance the Rho1^k02107b/+, GluRIIA^SP16 double mutant NMJ synaptic homeostasis phenotype.

The Exn^EY01953/+ heterozygous mutation does not enhance the Rac1^J11/+, GluRIIA^SP16 double mutant NMJ synaptic homeostasis phenotype.

Synaptic homeostasis is completely blocked in larvae that are double heterozygotes for Cdc42³/+ and Exn^EY01953/+ in a GluRIIA^SP16 mutant genetic background. There is no deficit in synaptic bouton number in Cdc42³/+ , Exn^EY01953/+, GluRIIA^SP16 triple mutants, compared to wild-type or GluRIIA^SP16 controls.

Synaptic homeostasis is completely blocked in larvae that are double heterozygotes for Cdc42⁴/+ and Exn^EY01953/+ in a GluRIIA^SP16 mutant genetic background.

The heterozygous Exn^EY01953/+ mutation alone does not significantly change the recessive GluRIIA^SP16 phenotype involving the synaptic homeostatic compensation at the neuromuscular junction (NMJ).

The combination of Exn^EY01953/+ and Eph^x652/+ heterozygous mutations does not significantly change the GluRIIA^SP16 phenotype involving spontaneous miniature release event (mepsp) amplitudes, while it does partially suppress the GluRIIA^SP16 quantal content phenotype at the neuromuscular junction (NMJ).

(Frank et al., 2009)

Xenogenetic Interactions

Statement

Reference

Complementation and Rescue Data

Rescued by

Exn^EY01953 is rescued by Scer\GAL4^elav-C155/Exn^UAS.EYFP

(Frank et al., 2009)

Comments

Presynaptic expression of Exn^{Scer\UAS.T:Avic\GFP-EYFP} driven by the pan-neuronal driver Scer\GAL4^elav-C155 in a GluRIIA^SP16; Exn^EY01953 double mutant background is sufficient to fully rescue the Exn^EY01953 specific components in the abnormal neuromuscular junction synaptic homeostasis phenotypes associated with GluRIIA^SP16; Exn^EY01953 double mutants.

(Frank et al., 2009)

Images (0)

Mutant

Wild-type

Stocks (1)

Bloomington

15385

y¹ w^67c23; P{EPgy2}Exn^EY01953

Notes on Origin

Discoverer

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (4)

Reported As

Symbol Synonym

CG3799^EY01953

Exn^EY01953

(Howell et al., 2012)

exn^EY01953

(Frank et al., 2009)

exn^EY10953

(Wentzel et al., 2018)

Name Synonyms

Secondary FlyBase IDs

References (4)

Report Sections

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