Open Close
General Information
Symbol
Hsap\MAPTUAS.cWa
Species
H. sapiens
Name
Saccharomyces cerevisiae UAS construct a of Wittmann
FlyBase ID
FBal0126526
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
UAS-tau, UAS-TauWT, tauWT, UAS-hTauWT, UAS-wt tau, UAS-h-tau, UAS-htau0N4R, UAS-hTau
Allele class
Nature of the Allele
Allele class
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 the full-length 0N4R isoform of Hsap\MAPT. This isoform is 383 amino acid residues long, lacks the amino terminal inserts (exons 2 and 3) and contains 4 microtubule binding repeats.
UAS regulatory sequences drive expression of wild-type Hsap\MAPT.
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 )
Modifiers Based on Experimental Evidence ( 1 )
Disease
Interaction
References
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
Statement
Reference
The expression of Hsap\MAPTScer\UAS.cWa under the control of Scer\GAL4elav-C155 leads to a significant and progressive decrease in adult locomotor activity (in negative geotaxis assays), but does not significantly affect the number of cortical neurons in the anterior medulla, as compared to controls.
The expression of Hsap\MAPTScer\UAS.cWa under the control of Scer\GAL4GMR.PU leads to lamina vacuolization compared to controls.
Expression of Hsap\APPAβ42.Scer\UAS.T:Rnor\SS-PENK driven by Scer\GAL4GMR.PF results in reduced eye size and a mild rough eye phenotype.
Expression of Hsap\MAPTScer\UAS.cWa driven by Scer\GAL4ninaE.PT (crosses carried out at 18[o]C and shifted to 25[o]C following eclosion) does not significantly affect external eye morphology in adult flies. At 1 day old, electroretinogram (ERG) recordings of light induced potentials from Scer\GAL4ninaE.PT>Hsap\MAPTScer\UAS.cWa flies are similar to controls; aged flies (day 10 and day 30) show a significant loss of light-evoked ERG response (significant reduction in depolarization amplitude) compared to controls. Scer\GAL4ninaE.PT>Hsap\MAPTScer\UAS.cWa flies do not show significant differences to controls in terms of ON transient amplitude; OFF transient amplitudes are significantly increased at day 1 but significantly decreased at day 10 and 30. The number and morphology of photoreceptors (retinae show intact ommatidia with 7 visible rhabdomeres) in Scer\GAL4ninaE.PT>Hsap\MAPTScer\UAS.cWa flies is grossly preserved at all time points, similar to controls; however photoreceptor ultrastructure (examined with TEM) in 10 day old Scer\GAL4ninaE.PT>Hsap\MAPTScer\UAS.cWa flies revealed significant subtle defects and irregularities in rhabdomeres (splitting or fraying at edges, vacuolar changes). Mutants at day 10 have similar numbers of mitochondria per ommatidium and numbers of autophagic vacuoles as controls, but have a significant increase in the percentage of photoreceptors with electron dense vacuoles (telolysosomes). Scer\GAL4ninaE.PT>Hsap\MAPTScer\UAS.cWa flies show significant disruption of photoreceptor synaptic terminal organization and morphology at 10 days old compared to controls.
Expression of Hsap\MAPTScer\UAS.cWa driven pan-neuronally by Scer\GAL4elav-C155 leads to a significantly shortened lifespan compared to control flies and flies with expression of Hsap\MAPTV337M.Scer\UAS. Scer\GAL4elav-C155>Hsap\MAPTScer\UAS.cWa flies show significant changes in the activity of antioxidant enzymes. Expression of Hsap\MAPTScer\UAS.cWa driven in mushroom bodies by Scer\GAL4c739 leads to a significant impairment in middle-term and long-term olfactory memory compared to controls.
Expression of Scer\GAL4GMR.PF>Hsap\MAPTScer\UAS.cWa is toxic in the eye resulting in the reduction of eye area compared with wild-type.
Axonal transport is disrupted in Scer\GAL4D42>Hsap\MAPTScer\UAS.cWa larvae when reared at 29[o]C. Treatment with NAP rescues axonal transport.
Limited degeneration is seen in a small subset of PPL1 dopaminergic neurons in 2 week old adults expressing Hsap\MAPTScer\UAS.cWa under the control of Scer\GAL4ple.PF. At 4 weeks after eclosion a significant loss of both PPL1 and PPM3 dopaminergic neurons is seen. Flies expressing Hsap\MAPTScer\UAS.cWa under the control of Scer\GAL4ple.PF show an age-dependent climbing deficit, with a significant loss of climbing ability compared to controls at 4-6 weeks post-eclosion. 4 week old flies also show reduced spontaneous locomotion compared to controls, appearing sluggish with an increase in the number of pauses between bouts of spontaneous locomotion and travelling short distances during each bout. 3 week old flies expressing Hsap\MAPTScer\UAS.cWa under the control of Scer\GAL4ple.PF show a modest but significant learning defect compared to control flies in an olfactory associative learning assay. 4 week old flies expressing Hsap\MAPTScer\UAS.cWa under the control of either Scer\GAL4VGlut.PD or Scer\GAL4Gad1.3.098 do not show a loss of Hsap\MAPTScer\UAS.cWa expressing cells in the brain (glutamatergic or GABAergic cells respectively). 4 week old flies expressing Hsap\MAPTScer\UAS.cWa under the control of either Scer\GAL4Hn.996 or Scer\GAL4npf.1 show a loss of the cells expressing Hsap\MAPTScer\UAS.cWa compared to wild type.
Expression of Hsap\MAPTScer\UAS.cWa under the control of Scer\GAL4C57 results in microtubule fragmentation and reduced perinuclear microtubule density in the muscles. Expression of Hsap\MAPTScer\UAS.cWa under the control of Scer\GAL4elav.PU results in a significant increase in the number of satellite boutons at the neuromuscular junction (NMJ) and a significant decrease in average NMJ length compared to controls.
Flies expressing Hsap\MAPTScer\UAS.cWa under the control of Scer\GAL4elav.PU exhibit normal learning and memory in an aversive phototaxis assay at two days after eclosion. Learning and memory are both significantly reduced at 20 days post-eclosion. Expression of Hsap\MAPTScer\UAS.cWa under the control of Scer\GAL4elav.PU results in an age-dependent decrease in locomotor activity as measured by climbing performance. At two days post eclosion no vacuolisation is observed in the brains of flies expressing Hsap\MAPTScer\UAS.cWa under the control of Scer\GAL4elav.PU. By 20 days multiple large vacuoles can be observed.
The mitochondria in the neurons of adult brains expressing Hsap\MAPTScer\UAS.cWa under the control of Scer\GAL4elav.PU are markedly elongated. Mitochondria length is on average greater than twice that of controls.
Expression of Hsap\MAPTScer\UAS.cWa under the control of Scer\GAL4GMR.PF causes age-dependent and progressive neurodegeneration in the lamina; degeneration in the lamina is undetectable or very mild in flies at 3-day old, but is prominent at 10 days old. As in wild type, mitochondria are present in the synaptic terminals of photoreceptor neurons at 3 days old. 3 day old flies expressing Hsap\MAPTScer\UAS.cWa under the control of Scer\GAL4GMR.PF show display axon pathology in the lamina. This includes the formation of vacuoles in the axons and swollen axons. In the presynaptic terminals, vacuoles and the accumulation of autophagic bodies and multivesicular bodies are seen.
Flies expressing Hsap\MAPTScer\UAS.cWa pan-neuronally under the control of Scer\GAL4elav.PU show reduced lifespan compared with control flies.
Expression of Hsap\MAPTScer\UAS.cWa in the developing retina, under the control of Scer\GAL4GMR.PF, causes a moderate rough eye phenotype, characterised by disruption of the ordered ommatidial arrangement and a moderate reduction in the size of the eye.
Overexpression of Hsap\MAPTUAS.cWa under the control of Scer\GAL4RapGAP1-OK6 in larval segmental nerves effects synaptic vesicle kinetics (there is a significant increase in synaptic vesicle pausing time, but no significant change on the directionality of the vesicular transport); there is no significant reduction in MT density; no effect on the number of mobile vesicles within axons. Emerging flies have normal wing expansion.
Expression of Hsap\MAPTScer\UAS.cWa in the developing eye under the control of Scer\GAL4GMR.PF causes a moderate rough-eye phenotype.
Expression of Hsap\MAPTScer\UAS.cWa under the control of Scer\GAL4repo.PU is lethal unless the transgene expression is temporally limited by combination with tub-Gal80[ts] (and accompanying culturing temperature manipulations) to minimize expression during development, in which case adult flies eclose but show significantly decreased lifespan and age-progressive increase in the number of apoptotic glia as well as cholinergic neurons (non-cell-autonomous effect) in the brain. Fibrillary tangles of phosphorylated tau protein are observed in the proximal as well as distal processes of glial cells in aged flies. Rearing the eclosed adults at 30[o]C for 20 days (to switch on Hsap\MAPTScer\UAS.cWa expression) and then moving them to 17[o]C for 10 days (to switch off expression) significantly reduces the number of apoptotic cells but does not decrease the number of the fibrillary inclusions in the brain. Expression of Hsap\MAPTScer\UAS.cWa under the control Scer\GAL4elav.PU (with tub-Gal80[ts] to limit time of expression to the adult stage) also results in age-progressive increase in the number of apoptotic cells in the adult brain and this increase is further enhanced when both the Scer\GAL4repo.PU and the Scer\GAL4elav.PU driver are used together: the number of apoptotic cells is much higher than when either of the two drivers is used alone.
Expression of Hsap\MAPTScer\UAS.cWa driven by Scer\GAL4Appl.G1a induces substantial axonal vesicle accumulations in larvae and results in increased lethality during development, as compared to controls.
Expression of Hsap\MAPTScer\UAS.cWa under the control of Scer\GAL4GMR.PF causes eye degeneration, characterized by a rough surface and smaller eye size.
Although the overall structure and morphology of the adult brains expressing Hsap\MAPTScer\UAS.cWa under the control of Scer\GAL4elav.PU appear unaltered, the mushroom bodies (MBs) are severely reduced or entirely absent in the majority of animals. The dendrites of MBs are prominent in controls, but not apparent in Hsap\MAPTScer\UAS.cWa-expressing animals. Other neuropils such as the protocerebral bridge in the posterior of the head and the fan-shaped body appear normal. Pan-neuronal expression of Hsap\MAPTScer\UAS.cWa under the control of Scer\GAL4elav.PU results in the loss of Kenyon cells in third-instar larval brains, whereas neurons in other parts of the central nervous system appear unaffected. MB defects are observed in 75% of the adults expressing Hsap\MAPTScer\UAS.cWa conditionally throughout development on to adulthood under the control of Scer\GAL4elav.PU and Scer\GAL80ts.αTub84B. Similarly, 70% of adults expressing Hsap\MAPTScer\UAS.cWa exclusively through embryogenesis display MB defects. In contrast, conditional expression of Hsap\MAPTScer\UAS.cWa after hatching, from early larva to adulthood results in mild MB defects in less than 5% of animals examined. Transgene expression exclusively in pupae does not result in detectable defects, and the effects of raising transgene-harboring animals at the restrictive temperature are negligible. Temperature shift experiments reveal that conditional expression of Hsap\MAPTScer\UAS.cWa under the control of Scer\GAL4elav.PU and Scer\GAL80ts.αTub84B during the first 4 h of embryogenesis at 19[o]C does not affect adult MB structure. In contrast, continued expression of Hsap\MAPTScer\UAS.cWa 8 h into embryogenesis results in MB abnormalities in adults. Continued expression of Hsap\MAPTScer\UAS.cWa up to 14 h after egg laying does not result in more severe deficits. Compared with control embryos, cells at the stereotypical mushroom body neuro-ectoderm that are known to give rise to mushroom body neuroblasts in the head of stage 9-12 Scer\GAL4elav.PU>Hsap\MAPTScer\UAS.cWa-expressing embryos are not apparent. When Hsap\MAPTScer\UAS.cWa is expressed in mushroom body neuroblasts and their progeny under the control of Scer\GAL4ey-OK107, animals with obvious MB deficits are obtained. Expression of Hsap\MAPTScer\UAS.cWa limited to the ellipsoid body under the control of Scer\GAL4Aph-4-c232 is not toxic for MB neurons.
Expression of Hsap\MAPTScer\UAS.cWa in dendritic arborization (DA) neurons under the control of Scer\GAL4109(2)80 strongly inhibits arborization.
Expression of Hsap\MAPTScer\UAS.cWa under the control of Scer\GAL4elav.PU results in severe and specific mushroom body defects. Expression of Hsap\MAPTScer\UAS.cWa under the control of Scer\GAL4Appl.G1a does not yield any detectable mushroom body defects. Expression of Hsap\MAPTScer\UAS.cWa in embryonic mushroom body (MB) neuroblasts under the control results in mild MB aberrations. Expression of Hsap\MAPTScer\UAS.cWa under the control of any one of Scer\GAL4c492b, Scer\GAL4c747, Scer\GAL4Tab2-201Y or Scer\GAL4238Y has no effect on MB morphology. Associative olfactory learning is nearly abolished in adult animals expressing Hsap\MAPTScer\UAS.cWa under the control of Scer\GAL4elav.PU. Heat-shift induced expression of Hsap\MAPTScer\UAS.cWa under the control of Scer\GAL4elav.PU and Scer\GAL80ts.αTub84B does not result in structurally altered MBs, even after continued Hsap\MAPTScer\UAS.cWa accumulation at 30[o]C for up to 7 days. However, even though these animals retain normal MB morphology, their performance in olfactory associative learning tasks is significantly impaired compared with controls.
Expression of Hsap\MAPTScer\UAS.cWa in the developing eye under the control of Scer\GAL4GMR.PF generates a moderate rough eye phenotype. Expression of Hsap\MAPTScer\UAS.cWa in the developing external sensory organs under the control of Scer\GAL4Eq1 generates a moderate bristle loss phenotype. The overall number of sensory cells is reduced in these flies. Expression of Hsap\MAPTScer\UAS.cWa in larval da neurons (under the control of Scer\GAL4ppk.PG) results in aggregate formation and dysmorphology of neurites. Oral administration of 10υM alsterpaullone significantly extends the life-span of flies expressing Hsap\MAPTScer\UAS.cWa in the nervous system (under the control of Scer\GAL4elav-C155).
Conditional expression of Hsap\MAPTScer\UAS.cWa only during the adult stages under the control of Scer\GAL4elav.PU and Scer\GAL80ts.αTub84B substantially and significantly elongates the lifespan of flies compared with wild-type.
Expression of Hsap\MAPTScer\UAS.cWa using Scer\GAL4GMR.PF produces a rough and reduced eye.
Expression with Scer\GAL4ey.PU causes a rough eye phenotype, which results in reduction of the eye tissue in extreme cases.
Expression of Hsap\MAPTScer\UAS.cWa under the control of Scer\GAL4elav.PU results in an increase in the number of apoptotic neurons in the brains of 10-day old flies, as compared to controls.
Expression of Hsap\MAPTScer\UAS.cWa in the eye under the control of Scer\GAL4GMR.PF results in a mild rough-eye phenotype.
Expression of Hsap\MAPTScer\UAS.cWa in the eye under the control of Scer\GAL4GMR.PF induces retinal degeneration and a rough eye phenotype.
Expression of Hsap\MAPTScer\UAS.cWa under the control of Scer\GAL4GMR.PF results in a rough eye phenotype and mild photoreceptor loss.
Expression of Scer\GAL4ey.PB>Hsap\MAPTScer\UAS.cWa leads to three different classes of phenotype: normal-looking eyes, abnormal eyes (characterised by abnormal shape or rough surface) and loss of eyes (no eyes). Rapamycin treatment reduces the proportion of flies without eyes, whereas increasing the proportion of flies with normal eyes. Rapamycin also increases the survival of flies expressing Hsap\MAPTScer\UAS.cWa to the adult stage.
Expression of Hsap\MAPTScer\UAS.cWa in the developing eye (under the control of Scer\GAL4GMR.PF) induces severe neurodegeneration, reflected by a severely disrupted eye phenotype.
Expression of Hsap\MAPTScer\UAS.cWa under the control of Scer\GAL4elav.PLu induces progressive neurodegeneration in flies at 30 days. Expression of Hsap\MAPTScer\UAS.cWa in the eye under the control of Scer\GAL4GMR.PF results in a rough-eye phenotype.
Flies expressing Hsap\MAPTScer\UAS.cWa under the control of Scer\GAL4GMR.PF have a disrupted eye.
Expression of Hsap\MAPTScer\UAS.cWa in the adult mushroom body and other brain neurons under the control of either Scer\GAL4c492b or Scer\GAL4c747 does not result in decreased longevity. Hsap\MAPTScer\UAS.cWa-expression does not appear to cause gross morphological abnormalities or decreased fecundity and vigor compared with controls. Degenerating cells and large vacuoles are not detected in the mushroom bodies of controls or 21 day old animals expressing Hsap\MAPTScer\UAS.cWa. 21 day old flies expressing Hsap\MAPTScer\UAS.cWa under the control of Scer\GAL4c492b do not exhibit obvious degeneration or vacuoles in the mushroom body. Mild neurodegeneration is observed in the mushroom bodies of most 60 day old flies expressing Hsap\MAPTScer\UAS.cWa using Scer\GAL4c492b. Degenerating neurons are observed in the mushroom body, but not in the ellipsoid body where the Scer\GAL4c492b driver is inactive. The performance of flies expressing Hsap\MAPTScer\UAS.cWa under the control of either Scer\GAL4c492b or Scer\GAL4c747 is not significantly different from controls in negatively reinforced associative olfactory learning tasks. The avoidance-response to electrified grids kept at 90 V or 15 V is not different between animals expressing Hsap\MAPTScer\UAS.cWa under the control of either Scer\GAL4c492b or Scer\GAL4c747 and controls. Hsap\MAPTScer\UAS.cWa-expressing animals and controls exhibit equal decrements in response to olfactory conditioned stimuli after experiencing couples conditioned plus unconditioned stimuli. Scer\GAL4c747>Hsap\MAPTScer\UAS.cWa flies exhibit a highly significant impairment in learning compared with controls. The memory of the conditioned association 90 minutes later is significantly depressed in Hsap\MAPTScer\UAS.cWa-expressing animals, and to a lesser degree at 180 minutes. Conditioned/unconditioned pairing in Scer\GAL4c747>Hsap\MAPTScer\UAS.cWa-expressing flies yields olfactory learning scores nearly 50% lower than those of controls. The Hsap\MAPTScer\UAS.cWa-expressing animals exhibit a significant decrease in memory retention after 30 minutes, despite performing at equivalent level with controls immediately after training.
Expression of Hsap\MAPTScer\UAS.cWa under the control of Scer\GAL4D42 induces the formation of vesicular aggregates in motor neuron axons.
Expression of Hsap\MAPTScer\UAS.cWa under the control of Scer\GAL4elav.PLu results in a moderate reduction in adult life span. The effect on life span is dosage sensitive. Aged flies show neurodegeneration; vacuolisation and degeneration of cells in the cortex is seen. The degeneration is progressive and the phenotype is fully penetrant. No evidence of large filamentous aggregates (neurofibrillary tangles) is seen in the brains of adults expressing Hsap\MAPTScer\UAS.cWa under the control of Scer\GAL4elav.PLu or Scer\GAL4Cha.7.4. Progressive loss of cholinergic neurons in the optic lamina is seen in adults expressing Hsap\MAPTScer\UAS.cWa under the control of Scer\GAL4Cha.7.4. 1 day old adults expressing Hsap\MAPTScer\UAS.cWa under the control of Scer\GAL4elav.PLu have a normal number of cholinergic terminals in the brain. The number of acetylcholine-positive terminals is strongly reduced in aged flies.
External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhanced by
Statement
Reference
NOT Enhanced by
Suppressed by
Statement
Reference
NOT suppressed by
Enhancer of
NOT Suppressor of
Other
Phenotype Manifest In
Enhanced by
Statement
Reference
NOT Enhanced by
Suppressed by
Statement
Reference
NOT suppressed by
Enhancer of
NOT Suppressor of
Other
Additional Comments
Genetic Interactions
Statement
Reference
Xenogenetic Interactions
Statement
Reference
The additional expression of Hsap\MAPTScer\UAS.cWa under the control of Scer\GAL4elav-C155 enhances the decreased number of anterior medulla cortical neurons resulting from the expression of Hsap\SNCANcra\QUAS.cOa under the control of Ncra\QFQF2.nSyb. Co-expressing Hsap\SNCANcra\QUAS.cOa under the control of Ncra\QFQF2.nSyb and Hsap\MAPTScer\UAS.cWa under the control of Scer\GAL4elav-C155 leads to more severe adult locomotor defects than either single expression.
The lamina vacuolization induced by the expression of Hsap\MAPTScer\UAS.cWa under the control of Scer\GAL4GMR.PU is partially suppressed by the co-expression of either CaMKIIGD9506 or Rat\CamKII-IAla.Scer\UAS and is enhanced by the co-expression of CaMKIIScer\UAS.cKa.
The small eye size and rough eye phenotype observed upon expression of Hsap\MAPTScer\UAS.cWa driven by Scer\GAL4GMR.PF is enhanced by the co-expression of Hsap\APPAβ42.Scer\UAS.T:Rnor\SS-PENK alone; this enhancement is not suppressed by also co-expressing sggGL00277. Co-expression of Hsap\MAPTScer\UAS.cWa and sggGL00277 under the control of Scer\GAL4GMR.PF results in significantly smaller eyes, as compared to controls.
Co-expression of CalpAKK104532 can protect from the toxicity of Scer\GAL4GMR.PF>Hsap\MAPTScer\UAS.cWa expression as measured by the eye area of flies. Co-expression of CalpAKK104532 in an Atg8aKG07569 mutant genetic background fails to suppress the toxicity of Scer\GAL4GMR.PF>Hsap\MAPTScer\UAS.cWa.
HDAC6KO and HDAC6KO/Df(1)ED7294 each rescue the defects in perinuclear microtubule density seen in the muscles of animals expressing Hsap\MAPTScer\UAS.cWa under the control of Scer\GAL4C57. HDAC6KO completely suppresses the increase in the number of satellite boutons at the neuromuscular junction (NMJ) and the decrease in average NMJ length caused by expression of Hsap\MAPTScer\UAS.cWa under the control of Scer\GAL4elav.PU.
Expression of NmnatScer\UAS.cZa suppresses the learning and memory deficits seen in 20 day old flies expressing Hsap\MAPTScer\UAS.cWa under the control of Scer\GAL4elav.PU. The climbing defects are suppressed to near wild type levels. The brain vacuolisation seen at 20 days post eclosion is almost completely suppressed. Expression of NmnatWR.Scer\UAS suppresses the learning and memory deficits seen in 20 day old flies expressing Hsap\MAPTScer\UAS.cWa under the control of Scer\GAL4elav.PU. The climbing defects are partially suppressed. The climbing defects are also suppressed. The brain vacuolisation seen at 20 days post eclosion is almost completely suppressed.
Expression of miltGD8116 dramatically enhances neurodegeneration in the lamina of 3 day old flies expressing Hsap\MAPTScer\UAS.cWa under the control of Scer\GAL4GMR.PF and as in flies expressing miltGD8116 alone, there is a reduction in the number of mitochondria in the synaptic terminals of photoreceptor neurons. Expression of miltGD8116 enhances the defects in axon pathology seen when Hsap\MAPTScer\UAS.cWa is expressed under the control of Scer\GAL4GMR.PF. No neurofibrillary tangles seen in these flies. This enhancement is suppressed upon co-expression of par-1dsRNA.Scer\UAS.cMDa. Expression of miltJF03022 enhances neurodegeneration in the lamina of 3 day old flies expressing Hsap\MAPTScer\UAS.cWa under the control of Scer\GAL4GMR.PF. Expression of MiroKK102189 enhances neurodegeneration in the lamina of 3 day old flies expressing Hsap\MAPTScer\UAS.cWa under the control of Scer\GAL4GMR.PF. Expression of MirodsRNA.Scer\UAS enhances neurodegeneration in the lamina of 3 day old flies expressing Hsap\MAPTScer\UAS.cWa under the control of Scer\GAL4GMR.PF. Expression of Ppyr\LUCdsRNA.Scer\UAS does not enhance neurodegeneration in the lamina of 3 day old flies expressing Hsap\MAPTScer\UAS.cWa under the control of Scer\GAL4GMR.PF.
Expression of Hsap\AK1Scer\UAS.cPa enhances the reduced lifespan seen when Hsap\MAPTScer\UAS.cWa is expressed pan-neuronally under the control of Scer\GAL4elav.PU.
Expression of Hsap\MAPTScer\UAS.cWa in neurons under the control of Scer\GAL4elav.PU significantly rescues the reduction in bouton number and terminal branches seen in muscles 6 and 7 of homozygous TBPHΔ23 third instar larvae. The rescued boutons are round with a smooth outline and beaded appearance like wild type controls. The lack of microtubule stability in distal presynaptic structures is also rescued by Hsap\MAPTScer\UAS.cWa. However, pan-neuronal expression of Hsap\MAPTScer\UAS.cWa is not able to rescue the larval motility defects seen in TBPHΔ23.
A CalpAe01545, CalpAKG05080, or Df(2R)BSC26 background suppresses the toxicity associated with expression of Hsap\MAPTScer\UAS.cWa in the developing retina under the control of Scer\GAL4GMR.PF. A CalpB17422, CalpB4062, or Df(3L)AC1 background modestly reduces the toxicity associated with expression of Hsap\MAPTScer\UAS.cWa in the developing retina under the control of Scer\GAL4GMR.PF.
Coexpression of Hsap\DAPK1K42A.Scer\UAS or Hsap\DAPK1Scer\UAS.cWa in the developing eye under the control of Scer\GAL4GMR.PF dramatically enhances Hsap\MAPTScer\UAS.cWa toxicity.
The increased number of apoptotic cells in the brain of adult flies expressing Hsap\MAPTScer\UAS.cWa under the control of Scer\GAL4repo.PU (using tub-Gal80[ts] to minimize the transgene expression during development) is significantly reduced by co-expression of either Stat92EScer\UAS.T:Avic\GFP-EGFP or Socs36EGD8929 and increased further by co-expression of Socs36EScer\UAS.P\T.cCa or by combination with a single copy of hop2.
Klc8ex94/+ enhances the partial lethality induced by the expression of Hsap\MAPTScer\UAS.cWa under the control of Scer\GAL4Appl.G1a.
One copy of lokE51 does not modify the retinal degeneration seen when Hsap\MAPTScer\UAS.cWa is expressed under the control of Scer\GAL4GMR.PF.
When co-expressed in dendritic arborization (DA) neurons, Hsap\LRRK2G2019S.Scer\UAS.cLa.T:Zzzz\FLAG causes further dendrite degeneration in DA neurons that express Hsap\MAPTScer\UAS.cWa.
Co-expression of Hsap\MAPTScer\UAS.cWa with Vha100-1GD12710 in developing eyes exposed to two days of intense light stimulation accelerates the degenerative photoreceptor phenotype.
Expression of sggA81T.Scer\UAS mitigates the Hsap\MAPTScer\UAS.cWa-induced bristle loss phenotype (with both under the control of Scer\GAL4Eq1). Expression of twsScer\UAS.cBa mitigates the Hsap\MAPTScer\UAS.cWa-induced bristle loss phenotype (with both under the control of Scer\GAL4Eq1). Bristle and sensory cell numbers increase concurrently when twsScer\UAS.cBa is co-expressed with Hsap\MAPTScer\UAS.cWa. The bristle loss phenotype found upon overexpression of Hsap\MAPTScer\UAS.cWa under the control of Scer\GAL4Eq1 is significantly abated in a sggM1-1 heterozygous background. Expression of Hsap\BΒ2Scer\UAS.cYa mitigates the Hsap\MAPTScer\UAS.cWa-induced bristle loss phenotype (with both under the control of Scer\GAL4Eq1). Bristle and sensory cell numbers increase concurrently when Hsap\BΒ2Scer\UAS.cYa is co-expressed with Hsap\MAPTScer\UAS.cWa. The Hsap\MAPTScer\UAS.cWa induced bristle loss phenotype is not suppressed by co-expression of wdb12 (both under the control of Scer\GAL4Eq1). Expression of twsScer\UAS.cBa in larval da neurons (under the control of Scer\GAL4ppk.PG) suppresses the aggregate formation and dysmorphology of neurites found upon expression of Hsap\MAPTScer\UAS.cWa. A heterozygous tauEP3597 background reduced the bristle loss phenotype found upon overexpression of Hsap\MAPTScer\UAS.cWa under the control of Scer\GAL4Eq1.
Expression of Hsap\APPAβ42.Scer\UAS and Hsap\MAPTScer\UAS.cWa in the eye under the control of Scer\GAL4GMR.PF results in a severe rough-eye phenotype, enhanced compared to over-expression of each transgene alone.
Co-expression of BacA\p35Scer\UAS.cHa suppresses the rough eye phenotype of Scer\GAL4GMR.PF>Hsap\MAPTScer\UAS.cWa. Co-expression of CycEScer\UAS.cLa strongly enhances the toxicity of Scer\GAL4GMR.PF>Hsap\MAPTScer\UAS.cWa. Co-expression of dapScer\UAS.cdNa and RbfScer\UAS.cDa substantially suppresses the Scer\GAL4GMR.PF>Hsap\MAPTScer\UAS.cWa-induced eye phenotype. Co-expression of Rheb1.1.Scer\UAS enhances the Scer\GAL4GMR.PF>Hsap\MAPTScer\UAS.cWa-induced rough eye phenotype. Co-expression of gigΔAkt-P.Scer\UAS.T:Zzzz\FLAG suppresses the Scer\GAL4GMR.PF>Hsap\MAPTScer\UAS.cWa-induced rough eye phenotype.
Expression of Hsap\APP695.T.Scer\UAS enhances the rough eye phenotype seen when Hsap\MAPTScer\UAS.cWa is expressed under the control of Scer\GAL4GMR.PF. Expression of lkb1dsRNA.Scer\UAS.cWa enhances the rough eye phenotype seen when Hsap\APP695.T.Scer\UAS and Hsap\MAPTScer\UAS.cWa are co-expressed under the control of Scer\GAL4GMR.PF.
Eye degeneration due to expression of Hsap\MAPTScer\UAS.cWa in the eye (under the control of Scer\GAL4GMR.PF) is enhanced in a loqsf00791 background.
The rough-eye phenotype observed in animals expressing Hsap\MAPTScer\UAS.cWa under the control of Scer\GAL4GMR.PF is suppressed by co-expression of dapScer\UAS.cdNa and RbfScer\UAS.cDa. The rough-eye phenotype observed in animals expressing Hsap\MAPTV337M.Scer\UAS under the control of Scer\GAL4GMR.PF is enhanced by co-expression of CycDScer\UAS.cMa. The rough-eye phenotype observed in animals expressing Hsap\MAPTV337M.Scer\UAS under the control of Scer\GAL4GMR.PF is enhanced by co-expression of CycAScer\UAS.cWa.
Co-expression of Hsap\MJDfl.Q27.Scer\UAS.T:Hsap\MYC does not suppress the mutant eye phenotype of flies expressing Hsap\MAPTScer\UAS.cWa under the control of Scer\GAL4GMR.PF.
Co-expression of Hsap\MAPTScer\UAS.cWa and par-1Scer\UAS.cSa under the control of Scer\GAL4hs.2sev exacerbates the eye phenotype compared to expression of Hsap\MAPTScer\UAS.cWa or par-1Scer\UAS.cSa alone.
Complementation and Rescue Data
Comments
Images (0)
Mutant
Wild-type
Stocks (0)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (5)
Reported As
Symbol Synonym
Hsap\MAPTScer\UAS.cWa
Hsap\MAPTUAS.cWa
Name Synonyms
Saccharomyces cerevisiae UAS construct a of Wittmann
Secondary FlyBase IDs
    References (56)