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General Information
Symbol
Dmel\DCTN1-p150Δ.UAS
Species
D. melanogaster
Name
FlyBase ID
FBal0102986
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
UAS-GluedDN, UAS-Glued-DN, UAS-DNGlued, UAS-D82glued
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

Expression of a 2897bp truncated Gl cDNA, carrying only the N-terminal 922 amino acids, is governed by UASt regulatory sequences.

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 ( 0 )
Disease
Interaction
References
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In

eye photoreceptor cell & nucleus, with Scer\GAL4Glass38-1

giant fibers & nerve terminal

giant fibers & nerve terminal, with Scer\GAL4c17

giant fibers & synapse

giant fibers & synapse, with Scer\GAL4c17

larval Bolwig's organ & nucleus, with Scer\GAL4elav.PLu

synapse & neuromuscular junction, with Scer\GAL4elav-C155

Detailed Description
Statement
Reference

The expression of DCTN1-p150Δ.Scer\UAS under the control of Scer\GAL4shot-OK307 results in shorter and thinner giant fiber terminals, as compared to controls. Expression under the control of Scer\GAL4GMR68A06 leads to a severe impairment of the axonal transport of Nrg-positive vesicles in giant fibers, as compared to controls.

Expression of DCTN1-p150Δ.Scer\UAS under the control of Scer\GAL4btl.PU in embryos leads to defects in dorsal branch tube fusion.

Expression of GlΔ.Scer\UAS under the control of Scer\GAL4D42 results in a reduced number of type 1b boutons at the neuromuscular junction in third-instar larvae.

Third instar larvae expressing GlΔ.Scer\UAS under the control of Scer\GAL4D42 have axonal blockages.

Centrosome dynamics during cell division in pI (sensory organ precursor) cells in the notum expressing GlΔ.Scer\UAS under the control of Scer\GAL4neur-P72 proceed normally from prophase to anaphase. However, in telophase both centrosomes fail to move towards the apex of the pI daughter cells.

Survival data from virgin females expressing GlΔ.Scer\UAS under the control of Scer\GAL4RapGAP1-OK6 generated on standard laboratory food demonstrate that Gl1 mutants have significant reduction in survival including changes in median and maximum lifespan compared with wild-type.

Survival data from virgin females expressing GlΔ.Scer\UAS in motor neurons under the control of Scer\GAL4D42 generated on standard laboratory food demonstrate that Gl1 mutants have significant reduction in survival including changes in median and maximum lifespan compared with wild-type.

Flies expressing GlΔ.Scer\UAS in CM9 motor neurons under the control of Scer\GAL4E49 exhibit an accelerated decline in motor function with age. Quantification of the proboscis extension reflex shows no significant difference at 7 and 21 days of age between mutant and control flies. However, analysis from days 21 and 42 show an accelerated deterioration of proboscis extension in Scer\GAL4E49>GlΔ.Scer\UAS flies which results in a highly significant reduction in the rate of motor reflex response.

Flies expression Scer\GAL4E49>GlΔ.Scer\UAS exhibit progressive deterioration of proboscis muscle CM9 neuromuscular junctions (NMJs). Unlike in wild-type, synaptic area significantly decreases in the mutant with age. The mutant presynaptic nerve terminals appear disorganised in 72 day old flies compared with wild-type. The mutant NMJs display significantly more presynaptic sprouts per CM9 NMJ compared with controls at both 21 and 42 days of age. The number of synaptic retractions per CM9 NMJ is only increased at 42 day old mutant NMJs compared with wild-type. No abnormal age related changes are seen in the number of myo-nuclei, or gross organization of T-tubules in the mutant muscle compared to wild-type. Bristle-tracking reveals that Scer\GAL4E49>GlΔ.Scer\UAS flies have a significant reduction in average proboscis velocity compared with age-matched controls.

Scer\GAL4E49>GlΔ.Scer\UAS mutant CM9 NMJs have impaired neurotransmission. The average amplitudes of evoked endplate junctional potentials (EJPs) are significantly reduced at NMJs from Scer\GAL4E49>GlΔ.Scer\UAS flies compared with wild-type. The amplitudes of miniature EJPs (mEJPs), also referred to as quantal size, are found to significantly reduced at the NMJs in the mutant flies raised at diluted (0.5X) diet compared with wild-type flies on the same diet. Analysis of quantal content, a measure of presynaptic release determined by dividing the EJP amplitudes by the mEJP amplitudes, reveals no significant difference in vesicle release in mutant flies compared to controls.

Expression of GlΔ.Scer\UAS under the control of Scer\GAL4Ccap.PP results in a failure of wing expansion.

Expression of GlΔ.Scer\UAS under the control of Scer\GAL4OK6 results in neuromuscular junctions indistinguishable from wild-type. At 7 and 9 hours after puparium formation there is no obvious change in synaptic vesicle distribution (compared to a redistribution in wild-type). These mutants also show considerably larger synaptic areas compared to wild-type.

The number of SE2 neurons is normal in animals expressing GlΔ.Scer\UAS under the control of Scer\GAL4elav-C155.

Axonal sprouting of the injured axon after a crush injury to the segmental nerve in third instar larvae is significantly inhibited in animals expressing GlΔ.Scer\UAS under the control of Scer\GAL4unspecified.

Expression of GlΔ.Scer\UAS under the control of Scer\GAL4GMR.PF results in adult flies with smaller eyes than normal. The eyes contain fused ommatidia and misarrayed eye bristles.

Adults expressing GlΔ.Scer\UAS under the control of Scer\GAL4A307 have defects in giant fiber axon morphology; the characteristic terminal bend is missing and the axon tips are swollen.

Adults expressing GlΔ.Scer\UAS under the control of Scer\GAL4A307 have electrophysiological defects in the giant fiber system; some flies fail to respond to brain stimulation and those that do respond show a long response latency and show only a single response or poor following to repetitive stimuli

Targeted expression of GlΔ.Scer\UAS driven by Scer\GAL4αTub84B.PP results in abnormalities in the architecture of the CSD interneuron (CSDn). The ipsilateral dendrites are greatly increased in number and the presynaptic terminals are reduced compared to wild-type.

Expression of GlΔ.Scer\UAS in the developing eye using the MARCM system (under the control of Scer\GAL4Act5C.PP) has a modest effect on R7 tiling.

Expression of GlΔ.Scer\UAS in the presynaptic membrane, driven by Scer\GAL4elav-C155, causes an increase in the rate of synapse retraction.

In the retinal photoreceptors of late third instar GlΔ.Scer\UAS; Scer\GAL4Glass38-1 larvae, the region of the photoreceptor containing the nucleus often leaves the retina and travels through the optic stalk towards the brain. Bolwig's organ photoreceptor nuclei in second instar GlΔ.Scer\UAS; Scer\GAL4elav.PLu larvae are mislocalised: instead of being located at the anterior tip of the larva they sit on the surface of the eye/antennal disc.

When GlΔ.Scer\UAS is driven by Scer\GAL4ap-md544, a blockade of axonal transport is seen in the embryonic nervous system.

When GlΔ.Scer\UAS is driven by Scer\GAL4dimm-929 animals survive to pupal stage and about 50% eclose. Many of the eclosed adults exhibit uncoordinated movements and some do not inflate their wings.

GlΔ.Scer\UAS; Scer\GAL4elav-C155 animals have normal patterns of motor neuron fasciculation and innervation of target muscles. However at the third instar larval stage they have small synapses at neuromuscular junctions and detachments of the pre- and postsynaptic membrane around active zones.

The addition of GlΔ.Scer\UAS driven by Scer\GAL4elav-C155 leads to an increase in synaptic fingerprints (seen after synapses retract) at the synapses of muscles 6 and 7. No significant effect is seen on numbers of apoptotic nuclei in these animals. There are disruptions seen specifically in the presynaptic microtubule skeleton. When GlΔ.Scer\UAS is driven by Scer\GAL4elav-C155, a reduction of more than 30% is seen in boutons per synapse (at the neuromuscular junctions of muscles 6 and 7). Active zone number per bouton is also decreased by about 50% compared to wild-type. Presynaptic boutons are filled with large vesicles and vacuoles of varying size. Post-synaptically the subsynaptic membrane folds (SSR) are much less compact than seen in wild-type, and can be invaded my mitochondrion. In the distal regions of the synapse, with severe SSR disruption, the presynaptic profiles are often very small and devoid of fully formed active zones. Also an 8 fold increase in the percentage of active zone that is detached is seen. When GlΔ.Scer\UAS is driven by Scer\GAL4elav-C155, No alteration is seen in quantal size or mEPSP frequency, but quantal content is reduced by about 40%. When GlΔ.Scer\UAS is driven by Scer\GAL4elav-C155 no effect on synaptic development or bouton size is seen.

When expression is driven by Scer\GAL4c311 and the larvae raised at 29oC the larval lethality is fully penetrant and the eye disc phenotype is severely enhanced. Morphogenetic furrow progression is reduced or eliminated, and mitotic patterns are disrupted. Eye development is not completely blocked.

When expression is driven in the eye by Scer\GAL4GMR.PF or Scer\GAL4hs.2sev the eyes are reduced and roughened. When expression is driven by Scer\GAL4A307 the giant fibers fail to show their characteristic bend in the second thoracic neuromere, and the axons have swellings at their terminals of up to three times the normal axon diameter. The axons are distorted by large vesicles. Arborization of the dendritic field is normal. When expression is driven by Scer\GAL4c17 a similar, though less extreme, phenotype is seen to that caused when expression is driven by Scer\GAL4A307. These abnormalities in giant fibers appear late in development. Morphology is normal up to 24hr APF, indicating no defects in growth and pathfinding in the brain and connective. By 48hr APF the defects are becoming apparent. When expression is driven by Scer\GAL4c17 or Scer\GAL4A307 dye coupling between the giant fibre and the TTM (tergotrochanteral motoneuron) is reduced and abolished, respectively. When expression is driven by Scer\GAL4c17 or Scer\GAL4A307 and the GF-TTM synapse characteristics are examined, changes occur in response latency (becomes variable), refractory period (increased) and following frequency (decreased). The effect is more pronounced for Scer\GAL4A307 than for Scer\GAL4c17. DLM muscle response is normal.

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

DCTN1-p150Δ.UAS, Scer\GAL4A307 has giant fiber neuron phenotype, non-enhanceable by EG28EG28/EG28[+]

Suppressed by
Statement
Reference

DCTN1-p150Δ.UAS, Scer\GAL4Glass38-1 has eye photoreceptor cell & nucleus phenotype, suppressible | partially by Khc[+]/Khc8

DCTN1-p150Δ.UAS, Scer\GAL4elav.PLu has larval Bolwig's organ & nucleus phenotype, suppressible | partially by Khc[+]/Khc8

DCTN1-p150Δ.UAS, Scer\GAL4elav.PLu has larval Bolwig's organ & nucleus phenotype, suppressible | partially by Khc[+]/Khck13314

DCTN1-p150Δ.UAS, Scer\GAL4Glass38-1 has eye photoreceptor cell & nucleus phenotype, suppressible by Khc[+]/Khck13314

NOT suppressed by
Statement
Reference

DCTN1-p150Δ.UAS, Scer\GAL4A307 has giant fiber neuron phenotype, non-suppressible by SG16[+]/SG16SG16

Other
Statement
Reference
Additional Comments
Genetic Interactions
Statement
Reference

The reduction in the number of type 1b boutons at the neuromuscular junction seen in third-instar larvae expressing GlΔ.Scer\UAS under the control of Scer\GAL4D42 is enhanced if the flies are also carrying a single copy of CG4562EY09703, bbgEY05191, Arfipd04252, Arfip12, klarEY01576, CG42575EY04050 or TM9SF4EY00960.

The reduction in the number of type 1b boutons at the neuromuscular junction seen in third-instar larvae expressing GlΔ.Scer\UAS under the control of Scer\GAL4D42 is enhanced if the flies are also carrying a single copy of ArfipEY11874, P{EPgy2}EY20330 or CoopEY13293. The number of synaptic retractions is suppressed.

The reduction in the number of type 1b boutons at the neuromuscular junction seen in third-instar larvae expressing GlΔ.Scer\UAS under the control of Scer\GAL4D42 is enhanced if the flies are also carrying a single copy of fanc04756, Sirt2c03323, B4EY14645, nesdEY11086 or P{EPgy2}EY12448. The number of synaptic retractions is also enhanced.

The reduction in the number of type 1b boutons at the neuromuscular junction seen in third-instar larvae expressing GlΔ.Scer\UAS under the control of Scer\GAL4D42 is suppressed if the flies are also carrying a single copy of P{EPgy2}EY06888 or AkhREY11371. The number of synaptic retractions are also suppressed.

Co-expression of ArfipScer\UAS.WT enhances the reduction in the number of type 1b boutons at the neuromuscular junction seen in third-instar larvae expressing GlΔ.Scer\UAS under the control of Scer\GAL4D42.

Scer\GAL80Scer\FRT.αTub84B has no effect on the wing expansion defect caused by expression of GlΔ.Scer\UAS under the control of Scer\GAL4Ccap.PP. When FLPase is used to remove the Scer\FRT cassette in Scer\GAL80Scer\FRT.αTub84B, generating Scer\GAL80αTub84B.PB which expresses Scer\GAL80, the failure of wing expansion caused by expression of GlΔ.Scer\UAS under the control of Scer\GAL4Ccap.PP is completely suppressed.

The eye phenotype caused by expression of GlΔ.Scer\UAS under the control of Scer\GAL4GMR.PF is dominantly suppressed by SG13SG13, SG16SG16, SG46SG46 or aPKCSG58.

The eye phenotype caused by expression of GlΔ.Scer\UAS under the control of Scer\GAL4GMR.PF is dominantly enhanced by EG162EG162, Su(H)EG37, EG28EG28, EG165EG165, EG7EG7, EG56EG56, EG79EG79 or EG149EG149.

Both the lack of a terminal bend and the swollen axon tip phenotypes of giant fiber axons that are seen in adults expressing GlΔ.Scer\UAS under the control of Scer\GAL4A307 are suppressed by either SG13SG13/+ or SG46SG46/+.

aPKCSG58/+ mildly suppresses the swollen tip phenotype of giant fiber axons expressing GlΔ.Scer\UAS under the control of Scer\GAL4A307, but the lack of a terminal bend phenotype is not rescued.

The giant fiber axon defects seen in adults expressing GlΔ.Scer\UAS under the control of Scer\GAL4A307 are not rescued by SG16SG16/+.

The giant fiber axon defects seen in adults expressing GlΔ.Scer\UAS under the control of Scer\GAL4A307 are partially suppressed by aPKCk06403/+ and by aPKCEY22946/+.

20% of giant fiber axons fail to exit the brain in adults expressing GlΔ.Scer\UAS under the control of Scer\GAL4A307 in a EG28EG28/+ background.

Heterozygosity for SG13SG13 or SG46SG46 partially suppresses the giant fiber system electrophysiological defects in animals expressing GlΔ.Scer\UAS under the control of Scer\GAL4A307; all preparations respond to brain stimulation and the response latency is shorter than in flies expressing GlΔ.Scer\UAS under the control of Scer\GAL4A307 in a wild-type background.

Heterozygosity for aPKCSG58 partially suppresses the giant fiber system electrophysiological defects in animals expressing GlΔ.Scer\UAS under the control of Scer\GAL4A307; all preparations respond to stimulation, there is a slight reduction in the long response latency and a corresponding increase in following to repetitive stimuli.

When neighboring wild-type R7 axons are removed through the presence of sevV1, GlΔ.Scer\UAS mutant R7 axons extend into adjacent columns.

The loss of photoreceptor nuclei from the retina in late third instar GlΔ.Scer\UAS; Scer\GAL4Glass38-1 larvae is significantly suppressed by Khck13314/+ and almost completely suppressed by Khc8/+. Mislocalisation of the Bolwig's organ nuclei in GlΔ.Scer\UAS/Scer\GAL4elav.PLu second instar larvae is partially suppressed by Khck13314/+ or Khc8/+.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Comments
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Mutant
Wild-type
Stocks (1)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (3)
Reported As
Symbol Synonym
DCTN1-p150Δ.Scer\UAS
DCTN1-p150Δ.UAS
GlΔ.Scer\UAS
Name Synonyms
Secondary FlyBase IDs
    References (33)