Allele Dmel\Psn^C2

General Information
Symbol	Dmel\Psn^C2	Species	D. melanogaster
Name		FlyBase ID	FBal0095648
Feature type	allele	Associated gene	Dmel\Psn
Also Known As	psn^c2, PS^C2

Map ( GBrowse )
Allele class
Mutagen
Recent Updates
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FB2013_03
FB2013_02
All updates	Click here to see a list of all updates to this record from FB2010_08 and on.
Nature of the Allele
Allele class
Mutagen
Mutations Mapped to the Genome

Type Location Additional Notes References point mutation 3L:20,426,095..20,426,095 reported_na_change=C?T reported_pr_change=Q52@ evidence=experimental pr_change=Q52\|Psn-PB,Q52\|Psn-PA na_change=C20426095T (Struhl and Greenwald, 1999)
Associated Sequence Data
DDBJ / EMBL / GenBank	DNA sequence Protein sequence Name

UniProtKB/Swiss-Prot
UniProtKB/TrEMBL

Progenitor genotype
Nature of the lesion	Statement Reference Amino acid replacement: Q52@. Nucleotide substitution: CAA is mutated to TAA. (Struhl and Greenwald, 1999)
Cytology
Phenotypic Data
Phenotypic Class
	lethal \| recessive (Struhl and Greenwald, 1999)
Phenotype Manifest In
	embryonic neuroblast (Struhl and Greenwald, 1999) embryonic neuroblast \| supernumerary (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 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 the genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Phenotype Manifest In
Suppressed by
Statement Reference Psn^C2 has embryonic neuroblast \| supernumerary phenotype, suppressible by Scer\GAL4^{F442A.αTub84B.T:Hsim\VP16}/N^{intra.GS.Scer\UAS} (Struhl and Greenwald, 2001)
NOT suppressed by
Statement Reference Psn^C2 has embryonic neuroblast \| supernumerary phenotype, non-suppressible by N^ECN.Scer\UAS/Scer\GAL4^{F442A.αTub84B.T:Hsim\VP16} (Struhl and Greenwald, 2001) Psn^C2 has embryonic neuroblast \| supernumerary phenotype, non-suppressible by Scer\GAL4^{F442A.αTub84B.T:Hsim\VP16}/N^Scer\UAS.cSb (Struhl and Greenwald, 2001)
Other
Statement Reference N^ECN.Scer\UAS, Psn^C2, Scer\GAL4^{F442A.αTub84B.T:Hsim\VP16} has sensory mother cell \| supernumerary phenotype (Struhl and Greenwald, 2001, Struhl and Greenwald, 2001) N^ECN.Scer\UAS, Psn^C2, Scer\GAL4^{F442A.αTub84B.T:Hsim\VP16} has wing margin phenotype (Struhl and Greenwald, 2001, Struhl and Greenwald, 2001) N^ECN.Scer\UAS, Psn^C2, Scer\GAL4^{F442A.αTub84B.T:Hsim\VP16} has wing vein phenotype (Struhl and Greenwald, 2001, Struhl and Greenwald, 2001) N^ECN.Scer\UAS, Psn^αTub84B.PS, Psn^C2, Scer\GAL4^{F442A.αTub84B.T:Hsim\VP16} has wing \| ectopic phenotype (Struhl and Greenwald, 2001, Struhl and Greenwald, 2001) N^{intra.GS.Scer\UAS}, Psn^C2, Scer\GAL4^{F442A.αTub84B.T:Hsim\VP16} has wing \| ectopic phenotype (Struhl and Greenwald, 2001, Struhl and Greenwald, 2001)
Additional Comments
Genetic Interactions
Statement Reference 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. (Struhl and Greenwald, 2001) 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. (Struhl and Greenwald, 2001)
Xenogenetic Interactions
Statement Reference
Complementation & Rescue Data
Rescued by	Psn^C2 is rescued by Psn^{NTF.αTub84B.T:Hsap\MYC}/Psn^{CTF.αTub84B.T:Ivir\HA1} (Barakat et al., 2009) Psn^C2 is rescued by Psn^{Δexon9.αTub84B.T:Ivir\HA1} (Barakat et al., 2009) Psn^C2 is rescued by Psn^{Δloop.αTub84B.T:Hsap\MYC} (Barakat et al., 2009) Psn^C2 is rescued by Psn^αTub84B.PS (Struhl and Greenwald, 1999) Psn^C2 is rescued by Psn^{αTub84B.T:Hsap\MYC} (Barakat et al., 2009) Psn^C2 is rescued by Psn^{αTub84B.T:Ivir\HA1} (Barakat et al., 2009)
Not rescued by	Psn^C2 is not rescued by Psn^{CTF.αTub84B.T:Ivir\HA1} (Barakat et al., 2009) Psn^C2 is not rescued by Psn^{NTF.αTub84B.T:Hsap\MYC} (Barakat et al., 2009)
Comments
Stocks ( 0 )

Notes on Origin
Discoverer

External Crossreferences & Linkouts
Other Crossreferences

Linkouts

Synonyms & Secondary IDs ( 5 )
Reported As
Symbol Synonym	PS^C2 (Struhl and Adachi, 2000, Struhl and Greenwald, 1999, Struhl and Greenwald, 2001) psn^c2 (Li and Baker, 2001) Psn^C2 psn^C2 (Ganguly et al., 2008, Guo et al., 2003) Psn^c2 (Barakat et al., 2009)
Name Synonym
Secondary FlyBase IDs

References ( 7 )
Research paper	Barakat et al., 2009, genesis 47(3): 161--168 Examining requirement for formation of functional Presenilin proteins and their processing events in vivo. [FBrf0207784] Ganguly et al., 2008, Hum. Mol. Genet. 17(2): 293--302 Ubiquilin antagonizes presenilin and promotes neurodegeneration in Drosophila. [FBrf0202621] Guo et al., 2003, Hum. Mol. Genet. 12(20): 2669--2678 A reporter for amyloid precursor protein gamma-secretase activity in Drosophila. [FBrf0167712] Li and Baker, 2001, Curr. Biol. 11(5): 330--338 Proneural enhancement by Notch overcomes Suppressor-of-Hairless repressor function in the developing Drosophila eye. [FBrf0134522] Struhl and Greenwald, 2001, Proc. Natl. Acad. Sci. U.S.A. 98(1): 229--234 Presenilin-mediated transmembrane cleavage is required for Notch signal transduction in Drosophila. [FBrf0132440] Struhl and Adachi, 2000, Mol. Cell 6(3): 625--636 Requirements for presenilin-dependent cleavage of Notch and other transmembrane proteins. [FBrf0132067] Struhl and Greenwald, 1999, Nature 398(6727): 522--525 Presenilin is required for activity and nuclear access of Notch in Drosophila. [FBrf0108014]

Allele Dmel\PsnC2

Allele Dmel\Psn^C2