FB2025_01 , released February 20, 2025
Allele: Dmel\bskK53R.UAS
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General Information
Symbol
Dmel\bskK53R.UAS
Species
D. melanogaster
Name
FlyBase ID
FBal0119311
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
UAS-bskDN, UAS-JNKDN, UAS-BskDN, UAS-bskK53R, BskDN, JnkDN, UASbskDN, UASBskDN, Bsk-DN, UAS::bskDN
Key Links
Nature of the Allele
Progenitor genotype
Carried in construct
Cytology
Description

UASt regulatory sequences drive expression of a dominant negative form of bsk (carries the amino acid replacement K53R).

Allele components
Component
Use(s)
Encoded product / tool
Mutations Mapped to the Genome
Curation Data
Type
Location
Additional Notes
References
Variant Molecular Consequences
Associated Sequence Data
DNA sequence
Protein sequence
 
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 ( 0 )
Disease
Evidence
References
Modifiers Based on Experimental Evidence ( 1 )
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
 
Disease-implicated variant(s)
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
Statement
Reference

Expressing bskK53R.UAS under the control of Scer\GAL4tey-5053A (together with Dicer-2, for efficient RNAI) provides significant protection against (injury-induced) Wallerian degeneration of third instar larval motoneurons.

Expressing bskK53R.UAS under the control of Scer\GAL4C587 (together with Dicer-2, for a more efficient RNAi) does not induce any obvious L3 spermatogenesis defects.

The expression of bskK53R.UAS under the control of Scer\GAL4hh-Gal4 does not lead to any obvious phenotype in the wing disc, as compared to controls.

The expression of bskK53R.Scer\UAS under the control of Scer\GAL4Bx-MS1096 does not result in any obvious size or viability defects in third instar larval wing discs, as compared to controls.

The expression of bskK53R.Scer\UAS in third instar larval wing discs does not result in any obvious cell migration defects (when expression is driven by Scer\GAL4dpp.PU) and does not lead to any obvious signs of basal delamination, such as embedment in the extracellular matrix or extrusion from the epithelium (when expression is driven by Scer\GAL4C-765), as compared to controls.

The temporally regulated expression (by Gal80[ts]) of bskK53R.UAS for 6 days under the control of Scer\GAL4NP5130 leads to a decrease in the proportion of mitotic cells in the adult midgut, as compared to controls.

Expression of Scer\GAL4Myo31DF-NP0001>bskK53R.Scer\UAS restores lipid levels in aging flies to levels seen in young animals.

Aging flies are more sensitive to starvation, which correlates with age-related changes in glucose and lipid metabolism. Expression of Scer\GAL4Myo31DF-NP0001>bskK53R.Scer\UAS in enterocytes has no effect on starvation resistance in young animals but leads to significantly improved starvation resistance in older flies compared with wild-type controls.

Expression of bskK53R.Scer\UAS under the control of Scer\GAL4BG380 has no effect on maximum bouton diameter at the larval neuromuscular junction.

Expression of bskK53R.Scer\UAS in neuronal cells under the control of Scer\GAL4Cha.7.4 results in a reduced survival rate compared to controls when flies undergo severe wounding.

Expression of bskK53R.Scer\UAS under the control of Scer\GAL4C855a does not cause any mutant phenotype in the larval optic lobe.

Compared with controls, female flies expressing bskK53R.Scer\UAS under the control of Scer\GAL4bun-GSG5961 show a moderate, but significant, reduction in intestinal cell proliferation at old age. These flies are significantly longer lived when exposed to RU486 than isogenic siblings exposed to mock treatment.

Axonal sprouting of the injured axon after a crush injury to the segmental nerve in third instar larvae is significantly inhibited in animals expressing bskK53R.Scer\UAS under the control of Scer\GAL4tey-5053A.

Flies expressing bskK53R.Scer\UAS under the control of Scer\GAL4Ilp2.PR show a significantly reduced repression of growth (assayed by measuring wing area) when shifted from 25[o]C to 29[o]C compared to wild-type flies.

Flies expressing bskK53R.Scer\UAS under the control of Scer\GAL4Ilp2.PR are significantly more sensitive to paraquat than control flies.

Flies expressing bskK53R.Scer\UAS under the control of Scer\GAL4Ilp2.Switch.PK show increased sensitivity to paraquat compared to controls in the presence of RU486.

Wing imaginal discs expressing bskK53R.Scer\UAS under the control of Scer\GAL4Bx-MS1096-KE are reduced in size compared to controls.

Overexpression of bskK53R.Scer\UAS under the control of Scer\GAL4en-e16E has no effect on the wing.

The size and number of paraquat-induced autophagosomes are reduced in bskK53R.Scer\UAS-expressing clones in the larval midgut epithelium compared to controls.

Clones of larval intestinal epithelial cells or fat body cells expressing bskK53R.Scer\UAS show a similar induction of autophagy as in wild type clones upon starvation.

Clones of larval fat body cells expressing bskK53R.Scer\UAS show a similar induction of autophagy as in wild type clones at the late third instar stage - a stage when animals prepare to pupate and sustained autophagy is observed in these cells.

Expression of bskK53R.Scer\UAS pan-neuronally under the control of Scer\GAL4elav-C155 severely reduces synapse size.

Inactivation of the JNK pathway by overexpression of bskK53R.Scer\UAS, under the control of Scer\GAL4ap-md544 in the notum results in a thoracic cleft phenotype.

When bskK53R.Scer\UAS is driven by Scer\GAL4αTub84B.PL adult flies exhibit a mild eye disorganisation phenotype.

Expression of bskK53R.Scer\UAS under the control of Scer\GAL4elav-C155 results in a 25-30% decrease in EJC amplitude (synaptic strength) and bouton number at the larval neuromuscular junction.

The cuticles of bskK53R.Scer\UAS; Scer\GAL4arm.PS embryos display classic dorsal closure phenotypes (a large dorsal hole of variable size). The prominent actin cable seen in leading edge cells during dorsal closure in wild-type embryos is reduced in these mutants.

When expression is driven by Scer\GAL4hs.2sev the eye shows an eye planar polarity phenotype. Some ommatidia are misrotated, and show chirality flips or are symmetrical with variable frequencies. This phenotype is exacerbated by bsk2.

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

Scer\GAL4Bx-MS1096-KE/bskK53R.UAS is a suppressor | partially of actin filament & dorsal mesothoracic disc phenotype of Scer\GAL4Bx-MS1096-KE, Vps4DN.UAS.Tag:HA

NOT Suppressor of
Statement
Reference

Scer\GAL4tey-5053A/bskK53R.UAS is a non-suppressor of axon | third instar larval stage | conditional phenotype of rawdcp-1

bskK53R.UAS/Scer\GAL4shot-OK307 is a non-suppressor of synapse phenotype of ben1

Other
Additional Comments
Genetic Interactions
Statement
Reference

rawdcp-1 homozygotes show protection against (injury-induced) Wallerian degeneration in third instar larval motor neurons, which is not significantly suppressed by the expression of bskK53R.UAS under the control of Scer\GAL4tey-5053A; in these double mutants, injured axons exhibit severely decreased new growth/sprouting compared to controls, as well as varicosities.

Co-expression of egrUAS.cUa and bskK53R.UAS under the control of Scer\GAL4rn-GAL4-5 (in combination with tub-Gal80[ts] to restrict expression to early stages of third instar larvae) does not lead to ectopic wings compared to controls.

The co-expression of bskK53R.Scer\UAS suppresses the tumor phenotype and tissue disorganization resulting from the expression of dlg1HMS01954, but not from the expression of aPKCΔN.Scer\UAS, under the control of Scer\GAL4Bx-MS1096.

The synaptic overgrowth phenotype (increase in bouton number) seen at the neuromuscular junction in larvae derived from homozygous SkpAGD65 females is partially suppressed by expression of bskK53R.Scer\UAS under the control of Scer\GAL4elav.PU.

The co-expression of bskK53R.Scer\UAS does not suppressed the following defects resulting from the expression of biScer\UAS.cBa in third instar larval wing discs: long distance cell migration and scattering, from expression either under the control of Scer\GAL4dpp.PU or in clones under the control of Scer\GAL4Act5C.PI; and the basal delamination of cells, resulting from the expression under the control of Scer\GAL4C-765.

Expression of bskK53R.Scer\UAS suppresses the cell invasion phenotype seen in wing discs when Sin3AKK100700 is expressed under the control of Scer\GAL4ptc-559.1.

Co-expression of CskdsRNA.Scer\UAS and Sin3AKK100700 (with Dcr-2Scer\UAS.cDa) results in a much stronger wing disc cell migration phenotype than is seen when either transgene is expressed alone. Upon co-expression of bskK53R.Scer\UAS, massive overgrowth is seen, but the invasion phenotype is suppressed.

Expression of bskK53R.Scer\UAS in the insulin-producing cells under the control of Scer\GAL4Ilp2.PR rescues the starvation resistance seen in itgr[ku] (Itp-r83Aka1091/Itp-r83Aug3) mutant flies.

Expression of bskK53R.Scer\UAS under the control of Scer\GAL4elav.PU suppresses the increase in bouton number seen at the neuromuscular junction in shot3/shotVV third instar larvae.

Co-expression of PvrCA.Scer\UAS and bskK53R.Scer\UAS in 3-5 day old adult flies, under the control of Scer\GAL4esg-NP5130 and Scer\GAL80ts.αTub84B phenocopies the proliferation of Scer\GAL4esg-NP5130>GFP-positive cells observed upon expression of PvrCA.Scer\UAS alone.

Expression of bskK53R.Scer\UAS enhances the synaptic degeneration phenotype seen when α-SpecKK101541 is expressed under the control of Scer\GAL4elav-C155.

Expression of bskK53R.Scer\UAS under the control of either Scer\GAL4en-e16E or Scer\GAL4puc-GAL4E69 partially suppresses the "black dot" phenotype seen in MAPk-Ak2Δ43 larvae.

Co-expression of Ilp2GD15756 efficiently rescues the repression of growth when shifted from 25[o]C to 29[o]C in flies expressing bskK53R.Scer\UAS under the control of Scer\GAL4Ilp2.PR.

Co-expression of Ilp2GD15756 rescues the increased sensitivity to paraquat of flies expressing bskK53R.Scer\UAS under the control of Scer\GAL4Ilp2.PR.

The disruption of the actin cytoskeleton that is seen in the wing imaginal discs of animals expressing Vps4DN.Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4Bx-MS1096-KE is partially suppressed by co-expression of bskK53R.Scer\UAS.

Wing imaginal discs co-expressing both bskK53R.Scer\UAS and Vps4DN.Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4Bx-MS1096-KE overgrow and are larger in size compared to controls.

The reduced eye size caused by expression of Rab11N124I.Scer\UAS under the control of Scer\GAL4GMR.PF is significantly suppressed by co-expression of bskK53R.Scer\UAS.

Overexpression of both bskK53R.Scer\UAS and cln3Scer\UAS.cTa under the control of Scer\GAL4en-e16E produces clones of cells in the wings with multiple bristles.

Co-expression of bskK53R.Scer\UAS and sggA81T.Scer\UAS pan-neuronally under the control of Scer\GAL4elav-C155 severely and significantly reduces synapse size compared to synapses in Scer\GAL4elav-C155-sggA81T.Scer\UAS flies.

Expression of bskK53R.Scer\UAS in a ben1 mutant background does not suppress the giant fiber axonal overgrowth phenotype found in these mutants.

Expression of bskK53R.Scer\UAS (under the control of Scer\GAL4BG380) suppresses the hiwND8 synaptic phenotype, reducing the number of synaptic boutons and branches and increasing bouton size and the intensity of synaptic vesicle markers.

Ectopic expression of bskK53R.Scer\UAS, under the regulatory control of Scer\GAL4Ddc.PL in hep1 mutants restores the morphology of dorsomedial dopaminergic neuron. The thoracic cleft formation observed in parkScer\UAS.T:Hsap\MYC overexpression mutants (Scer\GAL4ap-md544) and bskK53R.Scer\UAS mutants is mutually enhanced by their co-expression.

Downregulation of JNK signaling in clones of scribunspecified mutant tissue by overexpression of bskK53R.Scer\UAS suppresses apoptosis (from 16.6% to wild-type levels of 25%) and increases the overgrowth of the tissue, even compared to wild-type, resulting in scribunspecified bskK53R.Scer\UAS clones contributing over 70% of the tissue in third instar eye imaginal discs.

The small, deformed eye phenotype of foxoScer\UAS.cPa; Scer\GAL4GMR.PF adults is largely suppressed by bskK53R.Scer\UAS.

When bskK53R.Scer\UAS is driven by Scer\GAL4αTub84B.PL in scrib1 clones in the eye, a significant increase in the size of scrib1 clones is seen. However, this combination leads to pupal lethality.

Xenogenetic Interactions
Statement
Reference

The enlarged wing disc posterior compartment observed upon exposure to ionizing radiation of individuals expressing BacA\p35UAS.cHa alone, or in combination with either okrKK107487 or mei-41GD4258, is suppressed by the additional co-expression of bskK53R.UAS.

The additional co-expression of bskK53R.UAS suppresses the longer DNA damage response to an exposure to ionizing radiation (assessed by phospho-H2Av immunostaining) in the wing disc posterior compartment observed in individuals co-expressing BacA\p35UAS.cHa and either okrKK107487 or mei-41GD4258 under the control of Scer\GAL4en.PU.

The BacA\p35Scer\UAS.cHa-WScer\UAS.cUa invasive cell phenotype is completely suppressed by co-expression of bskK53R.Scer\UAS.

Complementation and Rescue Data
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Mutant
Wild-type
Stocks (1)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (5)
Reported As
Symbol Synonym
bskK53R.Scer\UAS
bskK53R.UAS
Name Synonyms
Secondary FlyBase IDs
    References (78)