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General Information
Symbol
Dmel\NICN.UAS
Species
D. melanogaster
Name
FlyBase ID
FBal0090559
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
UAS-Nact, UAS-NICD, UAS-Nintra, UAS-NICD, UAS-Ni, NACT, Nintra, uas-Nintra, UAS-Nic, UAS-Notch-ICD
Key Links
Nature of the Allele
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Carried in construct
Cytology
Nature of the lesion
Statement
Reference

UAS regulatory sequences drive expression of a constitutively active form of N in which the extracellular domain including the signal peptide and transmembrane domain is deleted.

Allele components
Product class / Tool use(s)
Encoded product / tool
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
Modifiers Based on Experimental Evidence ( 1 )
Disease
Interaction
References
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
 
Disease-implicated variant(s)
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In

neuroblast | supernumerary & larval brain | somatic clone, with Scer\GAL4Act5C.PI

Detailed Description
Statement
Reference

At stage 11 expression of NICN.UAS under the control of Scer\GAL4da.G32 leads to a reduction in neuroblast numbers when compared to control embryos.

Expressing NICN.UAS under the control of Scer\GAL4dpp.blk1 leads to misshapen wing discs; sone cells originating from the wing disc's Dpp-positive domain show an invasive phenotype.

Third instar larval eye-antennal disc clones expressing NICN.Scer\UAS under the control of Scer\GAL4Act5C.PI exhibit ectopic epithelial folding when located in a normally non-folding region. The cells at the ectopic fold show apical constriction and reduced apical and basolateral volumes, as compared to controls, and appear more similar to cells at the A1 fold.

The expression of NICN.Scer\UAS under the control of Scer\GAL4E(spl)m6-BFM.PF leads to significantly increased numbers of abdominal lateral and dorsal, but not ventral, adult muscle precursor cells in mid-third instar larvae, as compared to controls; this expression does not affect the number of mitotic adult muscle precursor cells at embryonic stages, as compared to controls.

Ectopic expression of NICN.UAS under the control of Scer\GAL4ct-PG142 (in combination with a Gal80[ts] transgene to overcome embryonic and larval lethality) in spiracular branch growth zone 3 leads to an excessive proliferation.

Expression of NICN.Scer\UAS under the control of Scer\GAL4ey.PU results in rough eye phenotype with irregular and fused ommatidia and extra or missing interommatidial bristles in the adult eye and leads to eye (Scer\GAL4ey.PU driver) or wing (Scer\GAL4ap.PU driver) disc overgrowth in third instar larvae.

Expression of NICN.Scer\UAS under the control of Scer\GAL4ap-md544 results in an increase in size of the wing disc.

Expression of NICN.Scer\UAS driven by Scer\GAL4ey.PS results in an enlarged adult eye, and increased cell proliferation, associated with enlargement of the morphogenetic furrow, in third instar larva eye discs, which do not show any obvious differentiation defects.

Expression of NICN.Scer\UAS under the control of Scer\GAL4ey.PH results in a loss of photoreceptors in the eye disc.

The overall number and positioning of the longitudinal glia in the embryo is not altered by expression of NICN.Scer\UAS under the control of Scer\GAL4htl.POS.

Expression of NICN.Scer\UAS under the control of Scer\GAL4ey.PU results in hyperplasia of the eye disc.

Expression of NICN.Scer\UAS under the control of Scer\GAL4btl.PS arrests outgrowth of the dorsal tracheal branch and results in the stalling of cells near the base. Some dorsal branches completely fail to bud in the posterior metameres.

Expression of NICN.Scer\UAS in eye discs using the Scer\GAL4GMR.PF driver greatly reduces the number of elav-positive cells, indicating a strong inhibition of photoreceptor recruitment.

Third instar clones expressing NICN.Scer\UAS have a similar number of cells in the larval outer optic anlage compared to control clones but have a reduced number of neurons in clones derived from post-embryonic neuroblasts (inhibits neuronal differentiation).

Expression of NICN.Scer\UAS in clones under the control of Scer\GAL4Act5C.PI leads to the overproliferation of larval neuroblasts.

Expression of NICN.Scer\UAS in all the prohemocytes using the Scer\GAL4srp.D.cCa driver does not generate more crystal cells. Expression of NICN.Scer\UAS in all the plasmatocytes using the Scer\GAL4svr-PG33 driver does not generate more crystal cells.

Cells in regions of the late third instar wing disc which are normally insensitive to irradiation induced apoptosis become sensitive to it if they are part of NICN.Scer\UAS; Scer\GAL4Act5C.PI somatic clones. (40Gy of γ rays; assayed after 4hrs)

Cells within Scer\GAL4Act5C.PP > NICN.Scer\UAS Flip-out somatic clones generated along the furrow and posterior to the furrow of the eye-antennal disc, using Scer\FLP1hs.PG, incorporate BrdU cell-autonomously. More cells within the clone enter S-phase than surrounding wild-type cells. Clones of the same genotype generated anterior to the furrow are non-autonomous, as both cells within the clone and cells surrounding the clone incorporate increased levels of BrdU and enter S-phase at an increased rate. Flip-out Scer\GAL4Act5C.PP > NICN.Scer\UAS somatic clones generated in the eye-antennal discs, using Scer\FLP1ey.PN, have a growth advantage over wild-type tissue, thus covering most of the eye tissue. Such discs are severly hyperplasic and lose much of their normal morphology. Cells across the disc appear to be proliferating in an asynchronous manner, instead of such proliferation being restricted to the region of the disc anterior to the furrow. There is no significant cellular differentiation within such discs. However, the antennal and eye primordia are correctly patterned. Resulting pharate adults have overgrown tissue within the head, with no discernable features or structure, exept for a few residual pigment cells.

NICN.Scer\UAS; Scer\GAL4en-e16E embryos lack C1 chordotonal organ precursor cells and have no larval oenocyte precursors.

NICN.Scer\UAS; Scer\GAL4Act5C.PI clones in the eye disc can induce overgrowth when located anterior to the morphogenetic furrow. Clones near the lateral margin cause non-autonomous overgrowth, whereas centrally located clones cause only local overgrowth.

NICN.Scer\UAS; Scer\GAL41151 pupae lack dorsal-ventral indirect flight muscle founder myoblasts.

Overexpression of NICN.Scer\UAS, under the control of Scer\GAL4Mef2.PR, causes a marked increase in lymph-gland size in late-stage-15 embryos.

When NICN.Scer\UAS is driven by Scer\GAL4hs.PB a dramatic increase is seen in the number of crystal cell precursors in the lymph gland. They are also seen in the second lobe, where they are rarely seen in wild-type.

Expression of NICN.Scer\UAS under the control of Scer\GAL4dpp.blk1 results in gross overgrowth of the eye disc in both dorsal and ventral domains.

When NICN.Scer\UAS is driven by Scer\GAL4ptc-559.1 a row of ectopic sensory organ precursors (SOPs) are induced in the wing disc.

Expression of NICN.Scer\UAS under the control of Scer\GAL4byn-Gal4 in the embryo results in the entire large intestine differentiating into boundary cells. The large intestine becomes short and thick in these animals.

Expression of NICN.Scer\UAS driven by Scer\GAL4ey.PH leads to pupal lethality. Those few that do escape lethality show hyperplasia of the eyes, with a significant increase in the number of facets. At larval stages the eye dics are overgrown. About 16% of escapers formed ectopic eyes on the rostral membrane of the head.

When expression is driven by Scer\GAL4btl.PS the branching pattern of the embryonic trachea is normal but the metameres remain unconnected at the end of embryogenesis. Fusion cell fate has been abolished. When expression is driven by Scer\GAL4p127 63% of the dorsal branches do not fuse and 48% of the branches do not express the hdc fusion cell marker.

Flies expressing NICN.Scer\UAS under the control of Scer\GAL4T113 have slightly enlarged eyes. Largely suppresses the wing defects seen in flies expressing HScer\UAS.cGa under the control of Scer\GAL4vg.int2.1. Larvae expressing NICN.Scer\UAS under the control of Scer\GAL4vg.int2.1 have enlarged wing discs compared to wild-type. This phenotype is associated with elevated mitotic activity in the disc. Elevated mitotic activity is also seen in the wing disc when NICN.Scer\UAS is expressed under the control of Scer\GAL4dpp.blk1, Scer\GAL471B, Scer\GAL430A or Scer\GAL4c766. The dorsal side of the wing pouch is enlarged in larvae expressing NICN.Scer\UAS under the control of Scer\GAL4A9. Larvae expressing NICN.Scer\UAS under the control of Scer\GAL4T113 have enlarged wing discs compared to wild-type, and the leg discs appear abnormal.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhanced by
Statement
Reference
Suppressed by
NOT suppressed by
Enhancer of
NOT Enhancer of
Suppressor of
NOT Suppressor of
Other
Phenotype Manifest In
Enhanced by
Statement
Reference

NICN.UAS, Scer\GAL4ey.PS has eye phenotype, enhanceable by Apcc00746

Suppressed by
NOT suppressed by
Enhancer of
Suppressor of
NOT Suppressor of
Other
Statement
Reference
Additional Comments
Genetic Interactions
Statement
Reference

The small size of GATAe1 homozygote MARCM clone in adult posterior midgut is not rescued by expression of NICN.Scer\UAS under the control of Scer\GAL4Act5C.PI.

The co-expression of MycKK103869 and NICN.Scer\UAS under the control of Scer\GAL4E(spl)m6-BFM.PF leads to significantly decreased numbers of abdominal lateral, dorsal and ventral adult muscle precursor cells in third instar larvae, as compared to controls.

Expression of maheScer\UAS.T:Ivir\HA1 partially suppresses the highly proliferated eye tissue phenotype seen when NICN.Scer\UAS is expressed under the control of Scer\GAL4ey.PU.

The wing nicking phenotype caused by expression of Rbf280.Scer\UAS under the control of Scer\GAL4bbg-C96 is suppressed if the flies are also co-expressing NICN.Scer\UAS.

The wing nicking phenotype caused by expression of domdsRNA.Sym.Scer\UAS under the control of Scer\GAL4bbg-C96 is suppressed if the flies are also co-expressing NICN.Scer\UAS.

The nuclear translocation of Notch-ICD (intracellular part of the N receptor) in somatic MARCM clones expressing NICN.Scer\UAS under the control of Scer\GAL4tub.PU in third instar larval brain is blocked when the clones are also homozygous mutant for Kap-α3D93.

The adult eye defects - irregularities in size and spacing of ommatidia and aberrant numbers of interommatidial bristles - as well as decreased eclosion rate and reduced adult life-span observed in flies expressing NICN.Scer\UAS under the control of Scer\GAL4ey.PU is exacerbated further by co-expression of Kap-α3Scer\UAS.T:Ivir\HA1. The neoplastic overgrowth of both eye and wing discs induced by NICN.Scer\UAS expression (controlled by either the Scer\GAL4ey.PU or the Scer\GAL4ap.PU driver, respectively) is also strongly enhanced by Kap-α3Scer\UAS.T:Ivir\HA1 co-expression.

Expression of NICN.Scer\UAS under the control of Scer\GAL4bab1-Gal4 (limited to the adult stages using Scer\GAL80ts.αTub84B) significantly suppresses the germline stem cell and cap cell loss seen in InR339/InRE19 mutant week old females.

Co-expression of NICN.Scer\UAS results in enlarged wing discs containing a larger field (30-40% of disc surface area) of differentiating ectopic eye precursors compared to expression of eyScer\UAS.cHa alone under the control of Scer\GAL4ap-md544.

Expression of NICN.Scer\UAS under the control of Scer\GAL4arm.PS in pcx3 embryos which lack maternal and zygotic pcx function partially rescues the neurogenic phenotype: 44% of embryos are rescued, 48% are partially rescued and 8% are not rescued. The endoplasmic reticulum defects are also rescued.

Expression of NICN.Scer\UAS under the control of Scer\GAL41151 suppresses the planar polarity defects seen in the notum of chas1 flies.

Expression of NICN.Scer\UAS under the control of Scer\GAL4Act5C.PU partially suppresses the oocyte polarity defect seen when the posterior follicle cells are mutant for flwFP41.

The co-expression of panΔN.Scer\UAS suppresses the enlarged eye in adults and the increased proliferation and enlarged morphogenetic furrow in third instar larva eye discs expressing NICN.Scer\UAS driven by Scer\GAL4ey.PS.

Apcc00746 or the co-expression of either wgd08266 or armS10.Scer\UAS.T:Hsap\MYC enhance the eye defects in adults expressing NICN.Scer\UAS driven by Scer\GAL4ey.PS, with associated wrinkling and distortion in third instar larva eye discs, but no obvious differentiation defects are visible in these discs.

hipk3/hipk3 suppresses the loss of photoreceptors in the eye disc caused by expression of NICN.Scer\UAS under the control of Scer\GAL4ey.PH.

Expression of NICN.Scer\UAS and par-1Scer\UAS.cBa under the control of Scer\GAL4ey.PU results in profound hyperplasia of the eye disc.

Homozygous mutant auxI670K eye discs that also express NICN.Scer\UAS (under the control of Scer\GAL4GMR.PF) exhibit a reduction in the number of elav-positive cells, indicating that N is epistatic to aux.

The absence of oenocyte formation in NICN.Scer\UAS; Scer\GAL4en-e16E embryos is rescued by rhoScer\UAS.cdCa. The absence of chordotonal organ precursor C1 formation is not.

NICN.Scer\UAS; Scer\GAL4dpp.blk1 partially restores eye development in eyg1/eygM3-12 flies.

When NICN.Scer\UAS are expressed in scrib1 clones, massive overproliferation of the scrib1 tissue is seen inducing larval/pupal lethality.

Lsi strongly suppresses the overgrowth of the ventral part of the eye disc in animals expressing NICN.Scer\UAS under the control of Scer\GAL4dpp.blk1, but has little effect on dorsal outgrowth of the eye discs in these animals.

The addition of dxΔPRM.Scer\UAS does not suppress the ectopic SOP phenotype seen in NICN.Scer\UAS, Scer\GAL4ptc-559.1 animals.

Expression of AntpScer\UAS.cBa and NICN.Scer\UAS driven by Scer\GAL4ey.PH is lethal. About 1/4 of those few escapers that do survive are found to have ectopic wings on their heads that usually consisted of dorsal and ventral wing blades bordered by bristles of the wing margin, but lacking wing veins. About 17% of these flies showed ectopic leg structures induced by secondary transformation of the ectopic antennal tissue into leg structures, an additional 10% showed a transformation of the original antenna to leg structures.

Larvae expressing both NICN.Scer\UAS and vgScer\UAS.cKa under the control of Scer\GAL4T113 show striking overgrowth of the eye discs. Other imaginal discs also show overgrowth. This overgrowth phenotype is also seen if the Scer\GAL4dpp.blk1 driver is used instead of Scer\GAL4T113.

Xenogenetic Interactions
Statement
Reference

Co-expression of Hsap\NUMBScer\UAS.PTBS-PRRS partially suppresses the inhibition of neuronal differentiation seen in clones with expression of NICN.Scer\UAS in third instar larval neuroblasts.

Co-expression of Hsap\NUMBScer\UAS.PTBS-PRRL increases the number of neuroepithelial cells but does not suppress the inhibition of neuronal differentiation seen in clones with expression of NICN.Scer\UAS in third instar larval neuroblasts.

Complementation and Rescue Data
Comments
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Mutant
Wild-type
Stocks (0)
Notes on Origin
Discoverer
Comments
Comments

Carried in plasmid " pUAST:NotchICD " and transfected into S3 cells.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (4)
Reported As
Symbol Synonym
Name Synonyms
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    References (67)