FlyBase Allele Report: Dmel\Psn[C1]

General Information

Symbol

Dmel\Psn^C1

Species

D. melanogaster

Name

FlyBase ID

FBal0095649

Feature type

allele

Associated gene

Dmel\Psn

Associated Insertion(s)

Carried in Construct

Also Known As

PS^C1

Key Links

Genomic Maps

JBrowse

Allele class

Mutagen

Nature of the Allele

Allele class

Mutagen

Progenitor genotype

Cytology

Description

Insertion of 8bp (GATATATA) in place of CG immediately downstream of the codon E438 (GAA). The insertion is predicted to destroy a slice donor and to truncate the protein before the last two transmembrane domains.

(Struhl and Greenwald, 1999)

Mutations Mapped to the Genome

Curation Data

Type

Location

Additional Notes

References

delins

3L:20,434,712..20,434,713 [+]

Inserted_sequence:

GATATATA

Comment:

Insertion of 8bp (GATATATA) in place of CG immediately downstream of the codon E438 (GAA). The insertion is predicted to destroy a splice donor and to truncate the protein before the last two transmembrane domains

(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)

abnormal memory | adult stage | male | progressive

(McBride et al., 2010)

lethal | recessive

(Struhl and Greenwald, 1999)

Phenotype Manifest In

cytoskeleton & follicle cell | somatic clone

(Lopez-Schier and St. Johnston, 2002)

egg chamber | somatic clone

(Lopez-Schier and St. Johnston, 2001)

embryonic neuroblast

(Struhl and Greenwald, 1999)

epidermis

(Struhl and Greenwald, 1999)

epidermoblast

(Struhl and Greenwald, 1999)

eye disc

(Klein, 2003)

follicle cell | somatic clone

(Lopez-Schier and St. Johnston, 2001)

neurogenic region

(Struhl and Greenwald, 1999)

proneural cluster

(Koelzer and Klein, 2003)

sensory mother cell | increased number

(Klein, 2003)

wing

(Struhl and Greenwald, 1999)

wing disc

(Koelzer and Klein, 2006)

wing margin bristle

(Struhl and Greenwald, 1999)

wing vein

(Struhl and Greenwald, 1999)

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 female toward a receptive virgin female) and 60 min short-term memory (courtship of the trained male is assayed after a 60 min break).

30-day old males heterozygous for Psn^C1 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^C1 mutant wing discs.

(Koelzer and Klein, 2006)

Mutant wing discs display larger proneural clusters that are often fused.

(Koelzer and Klein, 2003)

In mutant clones in the follicle cells the normal organization of the spectrin cytoskeleton is disrupted.

(Lopez-Schier and St. Johnston, 2002)

Large homozygous mutant clones that presumably include the polar cell precursors lead to fusions between adjacent egg chambers. Mutant epithelial follicle cells continue to divide after stage 6. When mutant clones include the follicle cells at the posterior of the egg chamber, the germinal vesicle often fails to migrate and remains at the posterior pole.

(Lopez-Schier and St. Johnston, 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. Clones of Psn^- cells induced in imaginal discs cause phenotypes similar to those caused by the N^- condition: in the wing scalloping and vein thickening occur, margins are interrupted and veins are miss-spaced.

(Struhl and Greenwald, 1999)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Suppressor of

Statement

Reference

Psn^C1/Psn[+] is a suppressor | partially of visible phenotype of Scer\GAL4^Bx-MS1096, Ubqn^{RNAi.3'UTR.UAS}

(Ganguly et al., 2008)

Psn^C1/Psn[+] is a suppressor | partially of visible phenotype of Scer\GAL4^Bx-MS1096, Ubqn^RNAi.CDS.UAS

(Ganguly et al., 2008)

Psn^C1/Psn[+] is a suppressor of visible phenotype of Scer\GAL4^GMR.APP, grim^UAS.cYa

(Guo et al., 2003)

Psn^C1 is a suppressor of decreased cell number | somatic clone | larval stage phenotype of l(2)gd1^d7

(Klein, 2003)

NOT Suppressor of

Statement

Reference

Psn^C1/Psn[+] is a non-suppressor of visible phenotype of Scer\GAL4^GMR.PF, grim::rpr^gr.UAS

(Guo et al., 2003)

Psn^C1/Psn[+] is a non-suppressor of visible phenotype of grim^GMR.PH

(Guo et al., 2003)

Phenotype Manifest In

NOT Enhanced by

Statement

Reference

Psn^C1 has eye disc | increased number phenotype, non-enhanceable by l(2)gd1^d7

(Klein, 2003)

Psn^C1 has sensory mother cell | increased number phenotype, non-enhanceable by l(2)gd1^d7

(Klein, 2003)

Suppressed by

Statement

Reference

Psn^C1 has wing disc phenotype, suppressible by Su(H)^del47

(Koelzer and Klein, 2006)

NOT suppressed by

Statement

Reference

Psn^C1 has eye disc | increased number phenotype, non-suppressible by l(2)gd1^d7

(Klein, 2003)

Psn^C1 has sensory mother cell | increased number phenotype, non-suppressible by l(2)gd1^d7

(Klein, 2003)

NOT Enhancer of

Statement

Reference

Psn^C1 is a non-enhancer of proneural cluster phenotype of Su(H)^del47

(Koelzer and Klein, 2003)

Suppressor of

Statement

Reference

Psn^C1/Psn[+] is a suppressor | partially of wing phenotype of Scer\GAL4^Bx-MS1096, Ubqn^{RNAi.3'UTR.UAS}

(Ganguly et al., 2008)

Psn^C1/Psn[+] is a suppressor | partially of wing vein phenotype of Scer\GAL4^Bx-MS1096, Ubqn^{RNAi.3'UTR.UAS}

(Ganguly et al., 2008)

Psn^C1/Psn[+] is a suppressor | partially of wing phenotype of Scer\GAL4^Bx-MS1096, Ubqn^RNAi.CDS.UAS

(Ganguly et al., 2008)

Psn^C1/Psn[+] is a suppressor | partially of wing vein phenotype of Scer\GAL4^Bx-MS1096, Ubqn^RNAi.CDS.UAS

(Ganguly et al., 2008)

Psn^C1/Psn[+] is a suppressor | partially of leg joint | ectopic phenotype of l(2)gd1^d7/l(2)gd1^SH0495

(Jaekel and Klein, 2006)

Psn^C1/Psn[+] is a suppressor | partially of tarsal segment phenotype of l(2)gd1^d7/l(2)gd1^SH0495

(Jaekel and Klein, 2006)

Psn^C1/Psn[+] is a suppressor of eye phenotype of Scer\GAL4^GMR.APP, grim^UAS.cYa

(Guo et al., 2003)

Psn^C1 is a suppressor of wing disc phenotype of l(2)gd1^d7

(Klein, 2003)

NOT Suppressor of

Statement

Reference

Psn^C1/Psn[+] is a non-suppressor of eye phenotype of Scer\GAL4^GMR.PF, grim::rpr^gr.UAS

(Guo et al., 2003)

Psn^C1/Psn[+] is a non-suppressor of eye phenotype of grim^GMR.PH

(Guo et al., 2003)

Psn^C1 is a non-suppressor of proneural cluster phenotype of Su(H)^del47

(Koelzer and Klein, 2003)

Additional Comments

Genetic Interactions

Statement

Reference

Psn^C1/+ strongly suppresses the wing defects caused by expression of Ubqn^{miRNA.CDS.Scer\UAS} or Ubqn^{miRNA.3'UTR.Scer\UAS} under the control of Scer\GAL4^Bx-MS1096.

(Ganguly et al., 2008)

Heterozygosity for Psn^C1 weakens the l(2)gd1^SH0495/l(2)gd1^d7 leg phenotypes.

(Jaekel and Klein, 2006)

In contrast to Psn^C1 single mutants, the dorsal/ventral boundary forms correctly in Su(H)^del47; Psn^C1 double mutants.

(Koelzer and Klein, 2006)

Psn^C1/+ suppresses the small eye phenotype caused by expression of grim^Scer\UAS.cYa under the control of Scer\GAL4^{GMR.T:Hsap\APP}, but does not suppress the small eye phenotype caused by expression of grim^GMR.PH or by expression of grim::rpr^gr.Scer\UAS under the control of Scer\GAL4^GMR.PF.

(Guo et al., 2003)

The overproliferation seen in l(2)gd1^d7 wing disc cells is suppressed by the addition of Psn^C1. The neurogenic phenotype seen in Psn^C1 is unaffected by the addition of l(2)gd1^d7. The small eye disc phenotype also resembles that of Psn^C1.

(Klein, 2003)

Xenogenetic Interactions

Statement

Reference

Complementation and Rescue Data

Rescued by

Psn^C1 is rescued by Psn^αTub84B.PS

(Struhl and Greenwald, 1999)

Comments

Images (0)

Mutant

Wild-type

Stocks (0)

Notes on Origin

Discoverer

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (4)

Reported As

Symbol Synonym

PS^C1

(Lieber et al., 2002, Noll et al., 2000, Struhl and Adachi, 2000, Struhl and Greenwald, 1999)

Psn^C1

(Schnute et al., 2022, Jia et al., 2014, Yamakawa et al., 2012, Kaspar et al., 2008, Jaekel and Klein, 2006, Koelzer and Klein, 2006)

psn C1

(McBride et al., 2010)

psn^C1

(Ganguly et al., 2008, Sun and Deng, 2005, Guo et al., 2003, Lopez-Schier and St. Johnston, 2002)

Name Synonyms

Secondary FlyBase IDs

References (18)

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