FlyBase Allele Report: Dmel\Psn[I2]

General Information

Symbol

Dmel\Psn^I2

Species

D. melanogaster

Name

FlyBase ID

FBal0324912

Feature type

allele

Associated gene

Dmel\Psn

Associated Insertion(s)

Carried in Construct

Also Known As

Psn¹²

Key Links

Genomic Maps

JBrowse

Allele class

loss of function allele

Mutagen

ethyl methanesulfonate

Nature of the Allele

Allele class

loss of function allele

(Ye et al., 1999)

Mutagen

ethyl methanesulfonate

(Lukinova et al., 1999, Ye et al., 1999)

Progenitor genotype

Cytology

Description

Amino acid replacement: W278term.

(Lukinova et al., 1999)

Mutation is predicted to result in a truncated protein ending in the middle of the sixth transmembrane domain.

(Lukinova et al., 1999)

Nucleotide substitution: G?A.

(Lukinova et al., 1999)

Mutations Mapped to the Genome

Curation Data

Type

Location

Additional Notes

References

point_mutation

3L:20,433,860..20,433,860 [+]

Nucleotide change:

G20433860A

Reported nucleotide change:

TGG?TGA

Amino acid change:

Reported amino acid change:

W278term

(Lukinova 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 Alzheimer's disease

CEA

(McBride et al., 2010)

Modifiers Based on Experimental Evidence ( 1 )

Disease

Interaction

References

model of Alzheimer's disease

is ameliorated by Ipp³

(McBride et al., 2010)

is ameliorated by mGluR^112b

(McBride et al., 2010)

is ameliorated by Ipp¹

(McBride et al., 2010)

ameliorates Alzheimer's disease 1

modeled by Hsap\APP^695.UAS

(Gunawardena et al., 2013)

modeled by Hsap\APP^{695-Swedish.UAS}

(Gunawardena et al., 2013)

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

Disease-implicated variant(s)

Phenotypic Data

Phenotypic Class

Phenotype Manifest In

larva | third instar larval stage

(Ye et al., 1999)

prepupa | prepupal stage P4(i)

(Lukinova et al., 1999)

sensory mother cell

(Ye et al., 1999)

wing disc

(Koelzer and Klein, 2006, Ye et al., 1999)

wing disc (with Psn^B3)

(Klein et al., 2000)

wing margin (with Psn^B3)

(Klein et al., 2000)

Detailed Description

Statement

Reference

Young (less than 10 days old) males heterozygous for Psn^I2 do not show any defects in their courtship behavior or locomotor activity compared to wild-type. Their learning index during training with mated unreceptive female is also normal as is their immediate recall memory (assayed by measuring courtship behavior of a male which has just completed a training with a mated unreceptive female toward a receptive virgin female) and 60 min short-term memory (courtship of the trained male is assayed after a 60 min break).

Aged (30 or more days old) males heterozygous for Psn^I2 also do not show any defects in the level or quality of naive courtship, locomotor activity, phototaxis or chemotaxis, however they display learning defects (fail to demonstrate the typical decrease in courtship activity when paired with an mated unreceptive female) as well as loss of short-term (60 min) memory is impaired (immediate recall memory is normal though).

(McBride et al., 2010)

The dorsal/ventral boundary fails to form correctly in Psn^I2 mutant wing discs.

(Koelzer and Klein, 2006)

Psn^B3/Psn^I2 wing discs lack all cell fates distal to the wg expression domain, i.e. the wing pouch and margin.

(Klein et al., 2000)

Hemizygotes show late prepupal lethality, at the P4(i) prepupa stage.

(Lukinova et al., 1999)

Mutant larvae secrete a pupal case and complete the last stages of larval development but do not form any adult structures. They collapse into a homogeneous oily mass within the pupal case. The phenotype closely resembles that of Su(H) mutants. Wing margin structures are missing from mutant wing discs. Size of wing pouch is reduced. Clusters of supernumerary SOP cells arise at the position of normal SOP cell emergence. Lateral inhibition in the clusters is impaired.

(Ye et al., 1999)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Suppressed by

Statement

Reference

Psn^I2 has abnormal learning | male | adult stage | progressive phenotype, suppressible by mGluR^112b/mGluR[+]

(McBride et al., 2010)

Psn^I2 has abnormal memory | male | adult stage | progressive phenotype, suppressible by mGluR^112b/mGluR[+]

(McBride et al., 2010)

Psn^I2 has abnormal learning | male | adult stage | progressive phenotype, suppressible by Ipp³/Ipp[+]

(McBride et al., 2010)

Psn^I2 has abnormal memory | male | adult stage | progressive phenotype, suppressible by Ipp³/Ipp[+]

(McBride et al., 2010)

Psn^I2 has abnormal memory | male | adult stage | progressive phenotype, suppressible by Itpr^wc361/Itp-r83A[+]

(McBride et al., 2010)

Psn^I2 has abnormal memory | male | adult stage | progressive phenotype, suppressible by Itpr^wc703/Itp-r83A[+]

(McBride et al., 2010)

Psn^I2 has abnormal memory | male | adult stage | progressive phenotype, suppressible by Itpr^90B.0/Itp-r83A[+]

(McBride et al., 2010)

NOT suppressed by

Statement

Reference

Psn^I2 has abnormal learning | male | adult stage | progressive phenotype, non-suppressible by Itpr^wc703/Itp-r83A[+]

(McBride et al., 2010)

Psn^I2 has abnormal learning | male | adult stage | progressive phenotype, non-suppressible by Itpr^90B.0/Itp-r83A[+]

(McBride et al., 2010)

Psn^I2 has abnormal learning | male | adult stage | progressive phenotype, non-suppressible by mGluR^2b/mGluR[+]

(McBride et al., 2010)

Psn^I2 has abnormal memory | male | adult stage | progressive phenotype, non-suppressible by mGluR^2b/mGluR[+]

(McBride et al., 2010)

Psn^I2 has abnormal learning | male | adult stage | progressive phenotype, non-suppressible by Ipp¹/Ipp[+]

(McBride et al., 2010)

Psn^I2 has abnormal memory | male | adult stage | progressive phenotype, non-suppressible by Ipp¹/Ipp[+]

(McBride et al., 2010)

Psn^I2 has abnormal learning | male | adult stage | progressive phenotype, non-suppressible by Itpr^wc361/Itp-r83A[+]

(McBride et al., 2010)

Enhancer of

Statement

Reference

Psn^I2 is an enhancer of abnormal neuroanatomy | embryonic stage phenotype of Tace¹⁹

(Zang et al., 2022)

NOT Enhancer of

Statement

Reference

Psn^I2 is a non-enhancer of abnormal neuroanatomy | embryonic stage phenotype of Tace¹⁹

(Zang et al., 2022)

Suppressor of

Statement

Reference

Psn^I2/Psn[+] is a suppressor | partially of visible | heat sensitive phenotype of Dcr-2^UAS.cDa, Eogt^GD5084, Scer\GAL4^en.PU

(Müller et al., 2013)

Psn^I2/Psn[+] is a suppressor of abnormal learning | male | adult stage phenotype of Ipp³

(McBride et al., 2010)

NOT Suppressor of

Statement

Reference

Psn^I2 is a non-suppressor of abnormal neuroanatomy | embryonic stage phenotype of Tace¹⁹

(Zang et al., 2022)

Psn^I2/Psn[+] is a non-suppressor of abnormal learning | male | adult stage phenotype of Itpr^90B.0

(McBride et al., 2010)

Psn^I2/Psn[+] is a non-suppressor of abnormal learning | male | adult stage phenotype of Itpr^wc361

(McBride et al., 2010)

Psn^I2/Psn[+] is a non-suppressor of abnormal learning | male | adult stage phenotype of Itpr^wc703

(McBride et al., 2010)

Phenotype Manifest In

Suppressed by

Statement

Reference

Psn^I2 has wing disc phenotype, suppressible by H^E31

(Koelzer and Klein, 2006)

Psn^I2/Psn^B3 has wing disc phenotype, suppressible by H^E31

(Klein et al., 2000)

Psn^I2/Psn^B3 has wing margin phenotype, suppressible by H^E31

(Klein et al., 2000)

Psn^I2/Psn^B3 has wing margin phenotype, suppressible by N^int.SH.UAS/Scer\GAL4^dpp.blk1

(Klein et al., 2000)

Psn^I2/Psn^B3 has wing disc phenotype, suppressible by N^int.SH.UAS/Scer\GAL4^dpp.blk1

(Klein et al., 2000)

NOT suppressed by

Statement

Reference

Psn^I2/Psn^B3 has wing disc phenotype, non-suppressible by Delta^UAS.cHa/Scer\GAL4^dpp.blk1

(Klein et al., 2000)

Psn^I2/Psn^B3 has wing margin phenotype, non-suppressible by Delta^UAS.cHa/Scer\GAL4^dpp.blk1

(Klein et al., 2000)

Enhancer of

Statement

Reference

Psn^I2 is an enhancer of axon | embryonic stage phenotype of Tace¹⁹

(Zang et al., 2022)

Psn^I2 is an enhancer of larval EW neuron | embryonic stage phenotype of Tace¹⁹

(Zang et al., 2022)

NOT Enhancer of

Statement

Reference

Psn^I2 is a non-enhancer of larval EW neuron | embryonic stage phenotype of Tace¹⁹

(Zang et al., 2022)

Psn^I2 is a non-enhancer of axon | embryonic stage phenotype of Tace¹⁹

(Zang et al., 2022)

Suppressor of

Statement

Reference

Psn^I2/Psn[+] is a suppressor | partially of wing blade posterior compartment | heat sensitive phenotype of Dcr-2^UAS.cDa, Eogt^GD5084, Scer\GAL4^en.PU

(Müller et al., 2013)

NOT Suppressor of

Statement

Reference

Psn^I2 is a non-suppressor of larval EW neuron | embryonic stage phenotype of Tace¹⁹

(Zang et al., 2022)

Psn^I2 is a non-suppressor of axon | embryonic stage phenotype of Tace¹⁹

(Zang et al., 2022)

Additional Comments

Genetic Interactions

Statement

Reference

The wing blistering phenotype seen in the posterior compartment of wings in flies expressing Eogt^GD5084 under the control of Scer\GAL4^en.PU in the presence of Dcr-2^Scer\UAS.cDa is dominantly partially suppressed if the flies are also heterozygous for Psn^I2.

(Müller et al., 2013)

The learning defects (measured in a courtship behavior assay) observed in Psn^I2, Ipp¹ or Ipp³ single heterozygote 30 day-old males are suppressed in the Psn^I2/+;Ipp³/+ and the Psn^I2/+;Ipp¹/+ double heterozygotes. Combination with a single copy of Ipp³ (but not Ipp¹) can also restore the short-term memory defects characteristic for the Psn^I2 aged heterozygote males.

The age-onset learning and memory defects (measured in a courtship behavior assay) characteristic for Psn^I2 heterozygote males are suppressed by combination with a single copy of the mGluR^112b allele but not with the mGluR^2b allele.

The learning defects observed in Psn^I2, Itp-r83A^wc361, Itp-r83A^wc703 and Itp-r83A^90B.0 single heterozygote 30 day-old males are not suppressed in the Psn^I2/+;Itp-r83A^wc361/+, Psn^I2/+;Itp-r83A^wc703/+ or Psn^I2/+;Itp-r83A^90B.0/+ double heterozygotes. Combination with a single copy of any of these alleles: Itp-r83A^wc361 or Itp-r83A^wc703 or Itp-r83A^90B.0 can, however, restore the short-term memory defects characteristic for aged Psn^I2 heterozygote males (Itp-r83A^90B.0 can do so both at 30 and 40 days of age).

(McBride et al., 2010)

In contrast to Psn^I2 single mutants, the dorsal/ventral boundary forms correctly in H^E31; Psn^I2 double mutants.

(Koelzer and Klein, 2006)

Xenogenetic Interactions

Statement

Reference

Complementation and Rescue Data

Comments

Images (0)

Mutant

Wild-type

Stocks (2)

5463

108255

Notes on Origin

Discoverer

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (9)

Reported As

Symbol Synonym

(Lukinova et al., 1999)

PS¹²

Psn¹²

(Koelzer and Klein, 2006)

Psn^I2

(Müller et al., 2013)

l(3)77CDb^I2

(Lukinova et al., 1999)

psn I2

(McBride et al., 2010)

psn¹²

(Zang et al., 2022, Neuhaus-Follini and Bashaw, 2015)

psn^I2

(Restrepo et al., 2022)

psn^I

(Gunawardena et al., 2013)

Name Synonyms

Secondary FlyBase IDs

FBal0102924
FBal0097198

References (12)

Report Sections

Open Close