Deletion extending from site of insertion of P{SUPor-P}KG01086 to 3' region of Stlk, deleting entire defined transcription unit of p120ctn.
p120ctn308 mutant flies (of either sex) do not exhibit a difference in survival associated with oxidative stress from Paraquat or H[[2]]O[[2]].
There is a mild but significant difference in survival between controls and p120ctn308 mutant males when exposed to increase osmotic stress due to the addition of 6% NaCl to their food, but this is not mirrored in females.
p120ctn308 mutant males and females are significantly more sensitive to heat shock (at 37[o]C) than controls.
At 25-29[o]C, there is a significant decrease in median lifespan in p120ctn308 mutant males and females. These mutants also suffer a heat-sensitive decrease in maximum lifespan.
p120ctn308 heterozygotes do not exhibit a visible phenotype nor a reduction in viability.
p120ctn308 mutant eyes display supernumerary lattice cells and a partially penetrant mis-patterning of the tertiary pigment cell niche. p120ctn308/Df(2R)244 mutant pupae exhibit a supernumerary lattice cell phenotype similar to homozygous p120ctn308 retinas.
p120ctn308 mutant pupal eyes manifest a transient separation of inter-ommatidial pigment cells (IPCs) accompanied by an apparent breakdown of adherens junctions between IPC:IPC and IPC:primary junctions.
p120ctn308 mutants are viable and fertile and exhibit normal cuticles.
A fraction of p120ctn308 mutants exhibit slight defects in cell shape during dorsal closure. Examination of dorsal closure reveals no consistent differences between p120ctn308 and wild-type embryos. However, the rate of dorsal closure is slowed in p120ctn308 mutants. On average, wild-type embryos complete dorsal closure within 75 minutes. p120ctn308 mutants are significantly slower, taking 112 minutes. Despite this, p120ctn308 mutants complete dorsal closure without apparent defects.
Mutant third instar larvae show no significant difference in the number of dendritic ends extending from the main dorsal dendrites of the vpda neurons compared to wild type.
The density of spine-like protrusions on the v'pda neurons is significantly reduced compared to wild type in mutant larvae.
Tracheal development appears normal in mutant embryos.
In many (though not all) mutant embryos the leading edge cells are irregular.
p120ctn308 has abnormal neuroanatomy phenotype, enhanceable by Rho172O/Rho1[+]
p120ctn308 has abnormal neuroanatomy phenotype, enhanceable by α-CatUAS.sgGFP/Scer\GAL4GMR.PF
p120ctn308 has abnormal neuroanatomy phenotype, enhanceable by shg[+]/shgR69
p120ctn308/Df(2R)M41A8 has abnormal cell shape | embryonic stage phenotype, suppressible by Scer\GAL4en-e16E/Arf1Q71L.UAS
p120ctn308 is an enhancer of abnormal neuroanatomy | third instar larval stage phenotype of ena46
p120ctn[+]/p120ctn308 is a suppressor of increased cell death | heat sensitive phenotype of Scer\GAL4sd-SG29.1, Src64BUY1332
p120ctn[+]/p120ctn308 is a suppressor of decreased cell growth rate | heat sensitive phenotype of Scer\GAL4sd-SG29.1, Src64BUY1332
p120ctn[+]/p120ctn308 is a suppressor of increased cell death phenotype of CskRNAi.UAS, Scer\GAL4ptc-559.1
p120ctn[+]/p120ctn308 is a suppressor | partially of increased cell death phenotype of CskRNAi.UAS, Scer\GAL4sd-SG29.1
p120ctn308 is a suppressor of abnormal neuroanatomy | third instar larval stage phenotype of Scer\GAL4109(2)80, enaUAS.cUa
p120ctn308, shg[+]/shg2 has partially lethal - majority die | recessive phenotype
p120ctn308, shg[+]/shgR69 has partially lethal - majority die | recessive phenotype
p120ctn308, shg[+]/shgg119 has partially lethal - majority die | recessive phenotype
p120ctn308, shg2 has partially lethal - majority die phenotype
p120ctn308, shgR69 has partially lethal - majority die phenotype
p120ctn308, shgg119 has partially lethal - majority die phenotype
p120ctn308 has tertiary pigment cell | increased number phenotype, enhanceable by Rho172O/Rho1[+]
p120ctn308 has interommatidial cell phenotype, enhanceable by shg[+]/shgR69
p120ctn308 has phenotype, enhanceable by shg[+]/shg2
p120ctn308 has phenotype, enhanceable by shg[+]/shgR69
p120ctn308 has phenotype, enhanceable by shg[+]/shgg119
p120ctn308/Df(2R)M41A8 has embryonic epidermis phenotype, suppressible by Scer\GAL4en-e16E/Arf1Q71L.UAS
p120ctn308 is an enhancer of embryonic/first instar larval cuticle phenotype of Rho1rev220
p120ctn308 is an enhancer of abdominal posterior ventral multidendritic neuron vdap phenotype of ena46
p120ctn308/p120ctn308 is an enhancer of embryonic ventral epidermis phenotype of shgR69
p120ctn308/p120ctn308 is an enhancer of embryonic ventral epidermis phenotype of shgg119
p120ctn308/p120ctn308 is an enhancer of embryonic ventral epidermis phenotype of shg2
p120ctn308 is a non-enhancer of embryonic/first instar larval cuticle & embryonic head phenotype of Rho1rev220
p120ctn[+]/p120ctn308 is a suppressor of wing disc phenotype of Scer\GAL4sd-SG29.1, Src64BUY1332
p120ctn[+]/p120ctn308 is a suppressor of zonula adherens & disc epithelium proper phenotype of CskRNAi.UAS, Scer\GAL4ptc-559.1
p120ctn308 is a suppressor of abdominal posterior ventral multidendritic neuron vdap phenotype of Scer\GAL4109(2)80, enaUAS.cUa
p120ctn308/p120ctn308 is a suppressor of embryonic epidermis phenotype of arm4
p120ctn[+]/p120ctn308 is a non-suppressor of eye phenotype of CskRNAi.UAS, Scer\GAL4GMR.PF
p120ctn[+]/p120ctn308 is a non-suppressor of ommatidium phenotype of CskRNAi.UAS, Scer\GAL4GMR.PF
p120ctn308 is a non-suppressor of embryonic/first instar larval cuticle & embryonic head phenotype of Rho1rev220
p120ctn308 p130CAS1 double heterozygotes do not exhibit a visible phenotype nor a reduction in viability.
p120ctn308 homozygotes in a p130CAS1 heterozygous background exhibit severely reduced viability.
p130CAS1 p120ctn308 double homozygotes exhibit severely reduced viability. These double mutants exhibit misalignment of segments and fused denticle belts, phenotypes not observed in p120ctn308 single mutants. Double mutants successfuly complete embryogensis and form larvae, but produce few pupae and no adult flies.
Expression of Scer\GAL4GMR.PF driven α-CatScer\UAS.T:Avic\GFP-sg leads to a mild enhancement of some of the p120ctn308 pupal retina patterning phenotypes.
Rho172O dominantly enhances the recessive p120ctn308 supernumerary tertiary pigment cell phenotype and increases the frequency of the inter-ommatidial cell patterning errors in the pupal retina.
p120ctn308, shgR69/+ mutant pupae exhibit disruption of the hexagonal inter-ommatidial precursor cell pattern with extra cells present in double layers around bristle cells in the retina.
p120ctn308/+ partially suppresses the loss of apical profile, delamination and subsequent migration and cell death increase seen in cells at the posterior edge of the ptc expression domain in CskIR.Scer\UAS Scer\GAL4ptc-559.1 third instar larval wing discs.
Most embryos double mutant for p120ctn308 and Rho1rev220 lack head cuticle, with the remaining cuticle differing significantly in size among different embryos.
p120ctn308 does not substantially modify the Rho1rev220 phenotype, nor is a novel double-mutant phenotype observed. The percentage of embryos with head holes is similar, for example 76.1% of Rho1rev220 mutants versus 74.6% of double mutants. However double mutants do have twice as many long cuticles as Rho1rev220 single mutants.
Rho1rev220 p120ctn308 double mutants exhibit the same range of phenotypes as Rho1rev220 single mutants during early and later stages of dorsal closure.
p120ctn308 enhances the decrease in the number of dendritic ends extending from the main dorsal dendrites of the vpda neurons which is seen in ena46/+ third instar larvae.
p120ctn308 suppresses the increase in the number of dendritic ends of the dorsal dendrites of the vpda neurons seen in third instar larvae expressing enaScer\UAS.cUa under the control of Scer\GAL4109(2)80.
In shg-/shg+ the viability of p120ctn308 homozygotes is reduced to 20-60% of their shg+/shg+ siblings.
p120ctn308 is rescued by p120ctnUbi-p63E.GFP
p120ctn308 is rescued by p120ctnUbi-p63E.GFP
Ubiquitous expression of a p120ctnUbi-p63E.T:Avic\GFP transgene completely rescues the p120ctn308 pupal retina phenotype.
Makes no mRNA as assessed by RT-PCR.