FlyBase Allele Report: Dmel\Ent2[P124]

General Information

Symbol

Dmel\Ent2^P124

Species

D. melanogaster

Name

FlyBase ID

FBal0264831

Feature type

allele

Associated gene

Dmel\Ent2

Associated Insertion(s)

P{lacW}Ent2^P124

Carried in Construct

Also Known As

P124

Key Links

Genomic Maps

JBrowse

Allele class

hypomorphic allele - molecular evidence

Mutagen

P-element activity

Nature of the Allele

Allele class

hypomorphic allele - molecular evidence

(Knight et al., 2010)

Mutagen

P-element activity

(Kamyshev et al., 2000)

Progenitor genotype

Associated Insertion(s)

P{lacW}Ent2^P124

Cytology

Description

Transposon insertion in the 5' untranslated region of Ent2.

(Knight et al., 2010)

Allele components

Component

Use(s)

Inserted element

P{lacW}

enhancer trap

Encoded product / tool

lacZ

reporter enzyme

Tagged with

Tag:NLS(P)

nuclear protein localization tag

Mutations Mapped to the Genome

Curation Data

Type

Location

Additional Notes

References

transposable_element_insertion_site

2L:6,562,339..6,562,372

(Knight et al., 2010, Kamyshev et al., 2000)

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 learning | recessive

(Knight et al., 2010, Kamyshev et al., 2000)

abnormal neurophysiology | recessive | third instar larval stage

(Knight et al., 2010)

viable

(Knight et al., 2010)

Phenotype Manifest In

embryonic/larval neuromuscular junction

(Knight et al., 2010)

motor neuron | third instar larval stage

(Knight et al., 2010)

synapse

(Knight et al., 2010)

Detailed Description

Statement

Reference

Ent2^P124 mutants show defects in olfactory based associative learning. The olfactory acuity of Ent2^P124 mutants is unimpaired.

Synaptic strength and plasticity at the neuromuscular junction (NMJ) are impaired in Ent2^P124 third instar larvae. The amplitude of spontaneous miniature excitatory junction potentials (mEJPs) is not significantly different in Ent2^P124 mutants and wild-type controls. The frequency of MEJPs, however, is significantly elevated in Ent2^P124 mutants relative to controls. The amplitude of stimulus evoked excitatory junction potentials (EJPs, reflecting synaptic transmitter release) is significantly increased in Ent2^P124 mutants. Paired-pulse plasticity of Ent2^P124 mutant synapses is impaired, while post-tetanic potentiation is normal.

Calcium influx is elevated in Ent2^P124 mutant motor neurons.

(Knight et al., 2010)

In P124^P124 mutant males, in contrast to wild-type controls, the learning index is not significantly different from zero either immediately or three hours after training.

(Kamyshev et al., 2000)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Enhanced by

Statement

Reference

Ent2^P124 has abnormal neurophysiology | third instar larval stage | recessive phenotype, enhanceable by Scer\GAL4^{elav.Switch.PO}/dnc^UAS.cCa

(Knight et al., 2010)

NOT Enhanced by

Statement

Reference

Ent2^P124 has abnormal learning | recessive phenotype, non-enhanceable by AdoR¹

(Knight et al., 2010)

Suppressed by

Statement

Reference

Ent2^P124 has abnormal neurophysiology | recessive | third instar larval stage phenotype, suppressible by AdoR¹

(Knight et al., 2010)

NOT suppressed by

Statement

Reference

Ent2^P124 has viable phenotype, non-suppressible by AdoR¹

(Knight et al., 2010)

Ent2^P124 has abnormal learning | recessive phenotype, non-suppressible by AdoR¹

(Knight et al., 2010)

Phenotype Manifest In

Enhanced by

Statement

Reference

Ent2^P124 has synapse phenotype, enhanceable by Scer\GAL4^{elav.Switch.PO}/dnc^UAS.cCa

(Knight et al., 2010)

Suppressed by

Statement

Reference

Ent2^P124 has synapse phenotype, suppressible by AdoR¹

(Knight et al., 2010)

Additional Comments

Genetic Interactions

Statement

Reference

Flies homozygous for both Ent2^P124 and AdoR¹ are completely viable.

The performance index of Ent2^P124, AdoR¹ double mutants in associative learning is not significantly different from the performance indices of either the Ent2^P124 of AdoR¹ single mutants.

The synaptic defects observed in either Ent2^P124 or AdoR¹ single mutants are suppressed in Ent2^P124, AdoR¹ double mutants. EJP amplitudes are not significantly different in the double mutant and wild-type controls. Ent2^P124, AdoR¹ double mutants also show normal paired-pulse facilitation and calcium influx.

Homozygous Ent2^P124 early third instar larvae expressing dnc^Scer\UAS.cCa under the control of Scer\GAL4^{elav.Switch.PO} upon induction by RU486 (mifepristone) display more severe synaptic defects than do Ent2^P124 mutants without dnc^Scer\UAS.cCa-overexpression.

(Knight et al., 2010)

Xenogenetic Interactions

Statement

Reference

Complementation and Rescue Data

Comments

Images (0)

Mutant

Wild-type

Stocks (0)

Notes on Origin

Discoverer

Comments

Precise excision of the insertion reverts the associative learning defects.

(Knight et al., 2010)

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (3)

Reported As

Symbol Synonym

Ent2^P124

P124^P124

ent2^P124

(Knight et al., 2010)

Name Synonyms

Secondary FlyBase IDs

References (2)

Report Sections

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