FlyBase Allele Report: Dmel\Psn[C2]

General Information

Symbol

Dmel\Psn^C2

Species

D. melanogaster

Name

FlyBase ID

FBal0095648

Feature type

allele

Associated gene

Dmel\Psn

Associated Insertion(s)

Carried in Construct

Also Known As

PS^C2

Key Links

Genomic Maps

JBrowse

Allele class

Mutagen

Nature of the Allele

Allele class

Mutagen

Progenitor genotype

Cytology

Description

Nucleotide substitution: C?T.

(Struhl and Greenwald, 1999)

Amino acid replacement: Q52term.

(Struhl and Greenwald, 1999)

Mutations Mapped to the Genome

Curation Data

Type

Location

Additional Notes

References

point_mutation

3L:20,432,995..20,432,995 [+]

Nucleotide change:

C20432995T

Reported nucleotide change:

C?T

Amino acid change:

Reported amino acid change:

Q52term

(Struhl and Greenwald, 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 ( 0 )

Disease

Interaction

References

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

Disease-implicated variant(s)

Phenotypic Data

Phenotypic Class

abnormal learning | adult stage | male | progressive

(McBride et al., 2010)

lethal | recessive

(Struhl and Greenwald, 1999)

Phenotype Manifest In

embryonic neuroblast

(Struhl and Greenwald, 1999)

embryonic neuroblast | increased number

(Struhl and Greenwald, 2001)

epidermis

(Struhl and Greenwald, 1999)

epidermoblast

(Struhl and Greenwald, 1999)

neurogenic region

(Struhl and Greenwald, 1999)

neuron & eye | supernumerary | somatic clone

(Li and Baker, 2001)

Detailed Description

Statement

Reference

Young (less than 10 days old) males heterozygous for Psn^C2 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).

30-day old males heterozygous for Psn^C2 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).

(McBride et al., 2010)

homozygous somatic clones in the eye lead to an intermediate neural hyperplasia in the adult eye.

(Li and Baker, 2001)

In Psn^C2 embryos, most or all ventral ectoderm cells segregate as neuroblasts.

(Struhl and Greenwald, 2001)

Psn^- embryos (lacking maternal and zygotic Psn product) are identical to those lacking maternal and zygotic N product. Clusters of neuroblasts segregate at positions usually occupied by single neuroblasts. Extensive neural hyperplasia occurs, larvae lack dorsal and ventral cuticle. Number of embryonic midline cells is reduced.

(Struhl and Greenwald, 1999)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Phenotype Manifest In

Suppressed by

Statement

Reference

Psn^C2 has embryonic neuroblast | increased number phenotype, suppressible by Scer\GAL4^{VP16.F442A.αTub84B}/N^intra.GS.UAS

(Struhl and Greenwald, 2001)

NOT suppressed by

Statement

Reference

Psn^C2 has embryonic neuroblast | increased number phenotype, non-suppressible by N^ECN.UAS/Scer\GAL4^{VP16.F442A.αTub84B}

(Struhl and Greenwald, 2001)

Psn^C2 has embryonic neuroblast | increased number phenotype, non-suppressible by Scer\GAL4^{VP16.F442A.αTub84B}/N^UAS.cSb

(Struhl and Greenwald, 2001)

Other

Statement

Reference

N^ECN.UAS, Psn^C2, Scer\GAL4^{VP16.F442A.αTub84B} has wing vein phenotype

(Struhl and Greenwald, 2001)

N^ECN.UAS, Psn^C2, Scer\GAL4^{VP16.F442A.αTub84B} has wing margin phenotype

(Struhl and Greenwald, 2001)

N^ECN.UAS, Psn^C2, Scer\GAL4^{VP16.F442A.αTub84B} has sensory mother cell | increased number phenotype

(Struhl and Greenwald, 2001)

N^ECN.UAS, Psn^αTub84B.PS, Psn^C2, Scer\GAL4^{VP16.F442A.αTub84B} has wing | ectopic phenotype

(Struhl and Greenwald, 2001)

N^intra.GS.UAS, Psn^C2, Scer\GAL4^{VP16.F442A.αTub84B} has wing | ectopic phenotype

(Struhl and Greenwald, 2001)

Additional Comments

Genetic Interactions

Statement

Reference

In Psn^C2 wing disc clones that also express N^ECN.Scer\UAS (under the control of Scer\GAL4^{F442A.αTub84B.T:Hsim\VP16}) formation of multiple sensory organ mother cell (SMCs) is seen in place of single SMCs.

Psn^C2 clones that also express N^ECN.Scer\UAS, give adult wing phenotypes: clones that cross the wing margin lead to wing notching, whereas clones within the dorsal compartment of the blade can form abnormally thick veins. If Psn^αTub84B.PS is also added, a double dorsal wing outgrowth develops, flanked by adjacent rows of dorsal wing margin bristles.

Psn^C2 clones that also express N^{intra.GS.Scer\UAS} lead to double dorsal wing outgrowth.

In Psn^C2 clones that also express N^ECN.Scer\UAS (under the control of Scer\GAL4^{F442A.αTub84B.T:Hsim\VP16}) formation of multiple sensory organ mother cell (SMCs) is seen in place of single SMCs. Psn^C2 clones that also express N^ECN.Scer\UAS, give wing phenotypes. clones that cross the wing margin lead to wing notching. Clones within the dorsal compartment of the blade can form abnormally thick veins. If Psn^αTub84B.PS is also added, a double dorsal wing outgrowth , flanked by adjacent rows of dorsal wing margin bristles. Psn^C2 clones that also express N^{intra.GS.Scer\UAS} lead to double dorsal wing outgrowth.