FlyBase Allele Report: Dmel\Nmdar1[EP331]

General Information

Symbol

Dmel\Nmdar1^EP331

Species

D. melanogaster

Name

FlyBase ID

FBal0191934

Feature type

allele

Associated gene

Dmel\Nmdar1

Associated Insertion(s)

P{EP}Nmdar1^EP331

Carried in Construct

Key Links

Genomic Maps

JBrowse

Allele class

hypomorphic allele - genetic evidence

Mutagen

P-element activity

Nature of the Allele

Allele class

hypomorphic allele - genetic evidence

(Xia et al., 2005)

Mutagen

P-element activity

(Xia et al., 2005)

Progenitor genotype

Associated Insertion(s)

P{EP}Nmdar1^EP331

Cytology

Description

P{EP} insertion 425bp downstream of the 3' end of the Nmdar1 transcription unit.

(Xia et al., 2005)

Allele components

Component

Use(s)

Inserted element

P{EP}

misexpression element

Regulatory region(s)

UAS

binary expression system - regulatory region

Mutations Mapped to the Genome

Curation Data

Type

Location

Additional Notes

References

transposable_element_insertion_site

3R:5,508,394..5,508,394 [+]

(Jeong et al., 2021, Ueno et al., 2017, Qin and Dubnau, 2010, Zhou et al., 2010, Xia et al., 2005)

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 Kohlschutter-Tonz syndrome

CEA with Indy³⁰²

(Jeong et al., 2021)

Modifiers Based on Experimental Evidence ( 1 )

Disease

Interaction

References

ameliorates neurodegenerative disease

modeled by mir-1000^KO1, mir-1000^KO2

(Verma et al., 2015)

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

Disease-implicated variant(s)

Phenotypic Data

Phenotypic Class

Phenotype Manifest In

Detailed Description

Statement

Reference

Nmdar1^EP3511 mutants exhibit a significant reduction of acquired tolerance to ethanol vapor-induced sedation in chronic tolerance assays, and they show a trend towards reduced tolerance in acute tolerance assays, as compared to controls.

(Maiya et al., 2012)

Mutant flies show defects in learning (memory measured immediately after conditioning) in an aversive olfactory conditioning assay. Short-term memory (assayed 1 hour after training) is also defective compared to controls. One-day memory after spaced training (long-term memory) is reduced compared to wild type, while one-day memory after massed training (anesthesia-resistant memory) is normal.

(Miyashita et al., 2012)

Nmdar1^EP331 mutants exhibit reduced short-term and long-term memory. Extinction learning appears to be normal in these mutants.

(Qin and Dubnau, 2010)

Disruption of Nmdar1 through expression of Nmdar1^EP331 under the control of Scer\GAL4^hs.PB does not result in a significant decrease in PI (preference index - with respect to light) in constant darkness conditions compared with control flies (indicating that phototaxis preference behaviour plasticity is inhibited by down-regulation of Nmdar1 during the critical period).

Nmdar1^EP331/Scer\GAL4^hs.PB flies reared in a normal light/dark cycle for 4 days at 18[o]C that are then treated with heat-shock and transferred to constant darkness exhibit no significant difference in PI (preference index - with respect to light) in constant darkness conditions compared with control flies.

(Zhou et al., 2010)

Olfactory learning after Pavlovian conditioning is reduced in Nmdar1^EP331 mutants compared to wild-type flies. However, sensorimotor responses to odors and foot shock stimuli are not affected. Expression of one copy of Nmdar1^EP331 under the control of one copy of Scer\GAL4^P26.hs, following heat shock, yields an antisense transcript of Nmdar1. This acute repression of Nmdar1 leads to a transient, severe disruption of olfactory learning. This acute repression also disrupts one day training after spaced training, while one day memory after massed training is normal, showing that long term memory is defective, but anesthesia-resistant memory is normal. Sensorimotor responses to odors and foot shock stimuli are not affected.

(Xia et al., 2005)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Enhanced by

Statement

Reference

Nmdar1^EP331 has abnormal memory phenotype, enhanceable by rut[+]/Adcy1^rut-1

(Qin and Dubnau, 2010)

Enhancer of

Statement

Reference

Nmdar1^EP331 is an enhancer of abnormal memory phenotype of Adcy1^rut-1

(Qin and Dubnau, 2010)

Suppressor of

Statement

Reference

Nmdar1^EP331/Nmdar1[+] is a suppressor | partially of short lived phenotype of mir-1000^KO2/mir-1000^KO1

(Verma et al., 2015)

Nmdar1^EP331/Nmdar1[+] is a suppressor of abnormal locomotor behavior | adult stage phenotype of mir-1000^KO2/mir-1000^KO1

(Verma et al., 2015)

Phenotype Manifest In

Additional Comments

Genetic Interactions

Statement

Reference

The climbing defects of mir-1000^KO1/mir-1000^KO2 adults are rescued if they are also carrying Nmdar1^EP331/+, and lifespan is increased (although not to control levels).

(Verma et al., 2015)

rut¹/+; Nmdar1^EP331/Nmdar1^EP331 double mutants exhibit significantly lower performance in standard Pavlovian learning assays compared to either single mutant.

(Qin and Dubnau, 2010)

Xenogenetic Interactions

Statement

Reference

Complementation and Rescue Data

Rescued by

Nmdar1^EP331 is rescued by Scer\GAL4^elav.PU/Nmdar1^UAS.cMa

(Miyashita et al., 2012)

Nmdar1^EP331 is rescued by Scer\GAL4^elav.PU/Nmdar1^N631Q.UAS

(Miyashita et al., 2012)

Nmdar1^EP331 is rescued by Nmdar1^+tCosmidC

(Xia et al., 2005)