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General Information
Symbol
Dmel\bskDN.UAS
Species
D. melanogaster
Name
FlyBase ID
FBal0097043
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
UAS-bskDN, UAS-bskDN, bskDN, UAS-Bsk-DN, UAS-JNKDN, UAS-bsk DN, bsk DN, UAS-DJNKDN, Bsk-DN
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

A nonactivatable mutant form of bsk is expressed under the control of UAS 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 ( 1 )
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
Statement
Reference

Somatic clones expressing bskDN.UAS under the control of Scer\GAL4Tub.PU contain a smaller overall number of cells and intestinal stem cells in adult flies compared to controls, but maintain a wild-type ratio of stem cells/clone.

Expression of bskDN.Scer\UAS under the control of Scer\GAL4Dll-md23 in MARCM clones in type II neuroblast lineages does not affect the clone size as compared to wild-type control clones in third instar larvae.

Expression of dominant-negative bskDN.Scer\UAS results in a robust enhancement of the regenerative response. The nerve growth response is similar, whether bskDN.Scer\UAS is expressed ubiquitously with Scer\GAL4αTub84B.Switch.PK or neuronally through Scer\GAL4elav.Switch.PO, indicating that the enhanced growth is dependent on altering neuronal signaling and not the environment.

Expression of bskDN.Scer\UAS under the control of Scer\GAL4elav.Switch.PO results in a marked decrease in the size of pigmented scar after injury.

Expression of bskDN.Scer\UAS under the control of Scer\GAL4ato.3.6 results in a decrease in the number of medulla axons compared to wild type.

Healthy egg chambers from starved flies expressing bskDN.Scer\UAS under the control of Scer\GAL4GR1 appear wild type, and dying egg chambers begin the normal process of follicle cell (FC) engulfment, including the enlargement of the FCs and uptake of the germline debris. However engulfment defects are seen later in the process. The FCs fails to enlarge and the FC nuclei become pycnotic. Nurse cell nuclei are not taken up by the FCs. The nurse cell nuclei also failed to fragment properly, making it difficult to assess the specific phases of degeneration. Very few degenerating egg chambers are seen in unstarved flies.

Males expressing bskDN.Scer\UAS under the control of Scer\GAL4en.PU display mis-oriented adult genitalia, and the acceleration of genitalia rotation is significantly impaired in these flies compared to controls.

Expression of bskDN.Scer\UAS under the control of Scer\GAL4GMR.PU has no effect on the size of the eye imaginal disc or adult eye.

Expression of bskDN.Scer\UAS under the control of Scer\GAL4opa results in thorax closure defects in the adult.

Expression of bskDN.Scer\UAS under the control of Scer\GAL4opa results in transformation of the medial edge peripodial membrane cells of the wing disc into a more broad hexagonal shape (they are elongated in wild-type discs).

Embryos expressing bskDN.Scer\UAS under the control of Scer\GAL4ptc-559.1 completely lack cell intercalation and mixer cell shifting at the segment boundary during dorsal closure (in the abdominal segments of wild-type embryos at the end of dorsal closure, a mixer cell moves across the segment boundary from the anterior compartment to the posterior compartment and two cells from the ventral ectoderm intercalate into the leading edge, posterior to the mixer cell).

Most embryos expressing bskDN.Scer\UAS under the control of Scer\GAL4ptc-559.1 are able to complete dorsal closure, but 92% of them show a high degree of segment mismatching at the dorsal midline (53% of abdominal segments A1-6 show defects).

Embryos expressing bskDN.Scer\UAS under the control of Scer\GAL4en-e16E show normal cell intercalation and mixer cell shifting at the segment boundary during dorsal closure.

Expression of bskDN.Scer\UAS using Scer\GAL4ey-OK107 results in axon defasciculation, axon degeneration and axon overextension phenotypes.

Expression of bskDN.Scer\UAS in the developing retina under the control of Scer\GAL4GMR.PF results in a few mild R axon misrouting defects.

Expression of bskDN.Scer\UAS under the control of Scer\GAL4ey.PH does not affect eye size.

Expression of one copy of bskDN.Scer\UAS, driven by Scer\GAL4ato.3.6, results in the reduction of the number of dorsal cluster neuron axons crossing toward the medulla from an average of 11.7 axons in wild-type flies to an average of 4.4 axons. Expression of two copies of the transgene results in an average of only 1.1 axons with 30% showing no axon at all. By examining axon extension at 20-30% pupal development, it is clear that extension of the axons is affected, as opposed to excessive axon retraction.

Single cell dorsal cluster neuron clones expressing bskDN.Scer\UAS under the control of Scer\GAL4ato.3.6 fail to extend axons to the medulla, but show no obvious guidance defects within the lobula.

Expression of bskDN.Scer\UAS in the posterior compartment of the wing disc, driven by Scer\GAL4en-e16E, prevents wound healing in the posterior compartment of the disc. The formation of actin-rich cables around the wound is an essential part of wound healing; in the affected posterior wing disc compartment expressing bskDN.Scer\UAS, there is an actin-rich area only at the vertex of the wound and not in the rest of the wound. Wound healing in the anterior compartment of the disc, that does not express bskDN.Scer\UAS, is unaffected.

Expression of bskDN.Scer\UAS, under the control of Scer\GAL4P2.4.Pdf, has no effect on the normal development of the terminal axonal arbour of the sLNv.

Expression of bskDN.Scer\UAS under the control of Scer\GAL4GMR.PF results in flies with small eyes.

When bskDN.Scer\UAS is driven by Scer\GAL4e22c or Scer\GAL469B a strong dorsal closure defect is observed. When bskDN.Scer\UAS is driven by Scer\GAL4A58 larvae are viable, active and do not display any morphological abnormalities. However the wound healing process is affected. No defects are seen in the early steps in wound healing, including scab formation, epidermal cell orientation toward the wound, and epidermal cell fusion to form a syncytium. However, reepithithelialization is blocked or defective, with no cytoplasmic processes or extremely fine or distorted processes and no cuticle synthesis beneath the scab 16h after wounding.

Flies that express bskDN.Scer\UAS under the control of Scer\GAL4ap-md544 show a cleft at the dorsal midline of the thorax.

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

bskDN.UAS/Scer\GAL4Act5C.PP is a suppressor of increased cell death | somatic clone | nutrition conditional phenotype of Pten117

bskDN.UAS/Scer\GAL4Act5C.PP is a suppressor of increased cell growth | somatic clone | nutrition conditional phenotype of Pten117

NOT Suppressor of
Statement
Reference
Other
Statement
Reference
Phenotype Manifest In
Enhanced by
Statement
Reference

Scer\GAL4ato.3.6, bskDN.UAS has axon & dorsal cluster neuron phenotype, enhanceable by dsh1

Scer\GAL4ap-md544, bskDN.UAS has thorax phenotype, enhanceable by Traf1[+]/Traf4ex1

NOT Enhanced by
Statement
Reference

Scer\GAL4ato.3.6, bskDN.UAS has axon & dorsal cluster neuron phenotype, non-enhanceable by Rac1N17.UAS, Scer\GAL4ato.3.6

NOT suppressed by
Statement
Reference

Scer\GAL4ato.3.6, bskDN.UAS has axon & dorsal cluster neuron phenotype, non-suppressible by Rac1N17.UAS, Scer\GAL4ato.3.6

Enhancer of
NOT Enhancer of
Suppressor of
Statement
Reference

bskDN.UAS/Scer\GAL4Act5C.PP is a suppressor of eye | somatic clone | nutrition conditional phenotype of Pten117

bskDN.UAS/Scer\GAL4GMR.PF is a suppressor | partially of eye phenotype of Ras85DKP

bskDN.UAS/Scer\GAL4ey.PH is a suppressor | partially of eye | ventral phenotype of L2

bskDN.UAS, Scer\GAL4ato.3.6 is a suppressor of axon & dorsal cluster neuron phenotype of Rac1N17.UAS, Scer\GAL4ato.3.6

bskDN.UAS is a suppressor of ventral adult lateral neuron & axon phenotype of Hsap\APPUAS.Tag:MYC, Scer\GAL4P2.4.Pdf

NOT Suppressor of
Statement
Reference

bskDN.UAS is a non-suppressor of ventral adult lateral neuron & axon phenotype of AblUAS.cFa, Scer\GAL4P2.4.Pdf

Other
Additional Comments
Genetic Interactions
Statement
Reference

Co-expressing ykiHMS00041 and bskDN.UAS under the control of Scer\GAL4dpp.blk1 does not have a major effect in the wing disc.

The co-expression of bskDN.UAS partially suppresses the third instar larval wing disc dorsal compartment apoptosis induced by the expression of pnutGD1512 from the second instar larval stage under the combined control of Scer\GAL4ap-md544 and Gal80[ts].

The co-expression of bskDN.UAS enhances the third instar larval wing disc tumors induced by the co-expression of pnutGD1512 and ykiUAS.cHa from the second instar larval stage under the combined control of Scer\GAL4ap-md544 and Gal80[ts].

The strong tumorigenic activity of Scer\GAL4Scer\FRT.Act5C>Ras85DV12.Scer\UAS;fmt1/fmt1 MARCM clones in third instar larval eye-antennal discs is strongly impeded and their invasive capacity abolished by co-expression of bskDN.Scer\UAS in the clones.

Similarly, the tumorigenicity of Ras85DV12.Scer\UAS-expressing clones is also enhanced if the clones are mutant for PpVΔ1, they display invasive behavior and increased mitotic activity; these characteristics are suppressed by co-expression of bskDN.Scer\UAS.

The partial or complete loss of the wing anterior crossvein in flies expressing fmtGD6928 under the control of Scer\GAL4ptc.PU is partially suppressed by co-expression of bskDN.Scer\UAS.

The small size of Type II neuroblast lineage MARCM clones mutant for scrib1 in third instar larvae can be rescued by expression of bskDN.Scer\UAS under the control of Scer\GAL4Dll-md23 in the mutant clones, these clones are also recovered more frequently than scrib1-only mutant clones.

The shortening of the dendritic arbor in class IV ddaC neurons in third instar larvae expressing prelScer\UAS.T:Ivir\HA1 under the control of Scer\GAL4109(2)80 is slightly enhanced by co-expression of bskDN.Scer\UAS.

The co-expression of bskDN.Scer\UAS suppresses the decreased relative clonal area of somatic clones expressing wupAJF02172 under the control of Scer\GAL4Act.PU in wandering third instar larval wing discs.

Expression of bskDN.Scer\UAS under the control of Scer\GAL4bun-GSG5961 and Scer\GAL4GSG5966 (along with RU486 to induce expression via the GeneSwitch system) in the gut fully restores growth of wild type clones in the presence of ApcQ8/ApcQ8, Apc2g10/Apc2g10 mutant clones in the posterior midgut, and suppresses the growth of ApcQ8/ApcQ8, Apc2g10/Apc2g10 mutant clones. ApcQ8/ApcQ8, Apc2g10/Apc2g10 mutant clones expressing bskDN.Scer\UAS under the control of Scer\GAL4tub.PU also show suppressed growth. Expression of bskDN.Scer\UAS in host tissue only, under the control of Scer\GAL4GSG2326, severely suppresses growth of ApcQ8/ApcQ8, Apc2g10/Apc2g10 mutant clones.

Expression of bskDN.Scer\UAS suppresses the tumor growth seen when l(2)glGD4047 is expressed under the control of Scer\GAL4en.PU in a minute background (RpL27A1). Individuals differentiate into adult pharates and a small proportion of the pupae eclose into adults with no evident phenotypic alterations.

Expression of bskDN.Scer\UAS in enteroblasts under the control of Scer\GAL4Su(H).GBE reduces tumor formation in the anterior midgut of Sox21a6 mutant flies. Expression of bskDN.Scer\UAS in enterocytes under the control of Scer\GAL4Myo31DF-NP0001 also suppresses tumor formation and the presence of delaminating enterocytes.

Co-expression of egrScer\UAS.cIa and bskDN.Scer\UAS under the control of Scer\GAL4GMR.PU results in a moderate hanging eye phenotype.

Expression of TaceGD572 enhances the hanging eye phenotype seen when egrScer\UAS.cIa and bskDN.Scer\UAS are co-expressed under the control of Scer\GAL4GMR.PU. The majority of these triple mutant animals die in late pupal stages and show a ring of necrotic tissue around the eyes.

Expression of TacedsRNA.Scer\UAS enhances the hanging eye phenotype seen when egrScer\UAS.cIa and bskDN.Scer\UAS are co-expressed under the control of Scer\GAL4GMR.PU. The majority of these triple mutant animals die in late pupal stages and show a ring of necrotic tissue around the eyes.

Expression of bskDN.Scer\UAS suppresses the increased cell death seen in eye-antennal disc clones expressing Ras85DV12.Scer\UAS under the control of Scer\GAL4Act.PU in a Sec151 mutant background. Tumor growth is not restored to that seen in clones expressing Ras85DV12.Scer\UAS alone.

The number of medulla axons in animals co-expressing both bskDN.Scer\UAS and NECN.Scer\UAS under the control of Scer\GAL4ato.3.6 is similar to that seen in animals expressing bskDN.Scer\UAS alone under the control of Scer\GAL4ato.3.6.

The number of medulla axons in animals co-expressing both bskDN.Scer\UAS and PakScer\UAS.T:Myr-Src64B under the control of Scer\GAL4ato.3.6 is similar to that seen in animals expressing bskDN.Scer\UAS alone under the control of Scer\GAL4ato.3.6.

Expression of bskDN.Scer\UAS in Pten117 eye clones (using the MARCM system) efficiently blocks apoptosis and enhanced the overgrowth phenotype.

Co-expression of bskDN.Scer\UAS suppresses the wing disc overgrowth caused by expression of Vha44Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4ap-md544.

Co-expression of bskDN.Scer\UAS partially suppresses the dissemination of hindgut cells seen in flies expressing Ras85DV12.Scer\UAS under the control of Scer\GAL4byn-Gal4.

Expression of bskDN.Scer\UAS suppresses the enhancement of aversive long term memory seen when hiwΔRING.Scer\UAS is expressed under the control of Scer\GAL4NP4132. Learning is unaffected.

Expression of bskDN.Scer\UAS using Scer\GAL4αTub84B.PL suppresses the frequency of ensheathment defects in raw134.47/raw155.27 mutants.

Co-expression of bskDN.Scer\UAS does not suppress the small, rough eye phenotype found upon expression of nopoScer\UAS.cUa under the control of Scer\GAL4GMR.PF.

egrScer\UAS.cIa-induced cell death is partially suppressed by co-expression of bskDN.Scer\UAS under the control of Scer\GAL4GMR.PF.

Co-expression of bskDN.Scer\UAS in the Scer\GAL4ey.PU, vitoGD10890 background partially suppresses the increased apoptosis phenotype, but eye disc size is not rescued.

Expression of bskDN.Scer\UAS under the control of Scer\GAL4Act.PU in the cells surrounding scrib1 clones in the eye-antennal disc significantly suppresses the elimination of the mutant scrib1 clones compared to that seen when the cells surrounding the clone are wild type.

Expression of bskDN.Scer\UAS does not suppress the increase in circulating lamellocytes seen when ND75KK108222 is expressed under the control of Scer\GAL4Antp-10.

Co-expression of bskDN.Scer\UAS dramatically rescues the increase in cell death seen in the third larval instar eye disc of animals expressing Hsap\APPAβ42.Scer\UAS.cUa under the control of Scer\GAL4GMR.PU and also strongly rescues the reduced size of the adult eye.

Expression of bskDN.Scer\UAS in Ras85DV12.Scer\UAS, Scer\GAL4Scer\FRT.Act5C /dorC107 clones suppresses the enhanced tumour overgrowth and metastasis.

Wing pouch clones expressing bskDN.Scer\UAS under the control of Scer\GAL4tub.PU in a l(2)gl4 mutant background do not show increased apoptosis, but are smaller in size than wild type controls. In contrast, clones in the proximal regions of the wing disc lose polarity and overgrow.

Co-expression of bskDN.Scer\UAS and Dcp-1Scer\UAS.cKa (insertion line P{UAS-Dcp-1.K}19-2) under the control of Scer\GAL4GMR.PF is lethal.

Inhibition of the JNK pathway through expression of bskDN.Scer\UAS under the control of Scer\GAL4e22c suppresses the cell death induced by ectopic hppyScer\UAS.cLa expression.

Co-expression of bskDN.Scer\UAS suppresses the ectopic apoptosis in cells expressing Rho1Scer\UAS.cMa under the control of Scer\GAL4dpp.blk1.

Co-expression of bskDN.Scer\UAS in wing discs expressing GliScer\UAS.cPa under the control of Scer\GAL4ap-md544 completely suppresses cell migration and apoptosis.

Expression of bskDN.Scer\UAS suppresses the tumors seen in scrib1 mutant eye-antennal disc clones that simultaneously express Ras85DV12.Scer\UAS under the control of Scer\GAL4Act.PU.

Expression of bskDN.Scer\UAS does not suppress the tumors seen in eye-antennal disc clones that simultaneously express Ras85DV12.Scer\UAS and upd1Scer\UAS.cUa under the control of Scer\GAL4Act.PU.

Expression of bskDN.Scer\UAS in eye-antennal disc clones that express Ras85DV12.Scer\UAS under the control of Scer\GAL4Act.PU, and in which adjacent cells are mutant for scrib1, partially suppresses the tumor phenotype. Few scrib1 cells remain in the tissue at late stages.

Co-expression of bskDN.Scer\UAS in the 'eyeful' (Scer\GAL4ey.PH, DlScer\UAS.cDa, psqGS88A8, lolaGS88A8) background leads to tumors in 61% of eyes and an approximately 7-fold increase in metastasis.

Co-expression of bskDN.Scer\UAS in a Scer\GAL4ey.PH DlScer\UAS.cDa background leads to the induction of tumors and metastasis.

Co-expression of bskDN.Scer\UAS in a atoScer\UAS.cJa 'eyeful' (Scer\GAL4ey.PH, DlScer\UAS.cDa, psqGS88A8, lolaGS88A8) background leads to a suppression of the inhibitory effects of atoScer\UAS.cJa on the 'eyeful' tumor phenotype, restoring tumor formation and enhancing metastasis.

Expression of bskDN.Scer\UAS under the control of Scer\GAL4elav.PLu partially suppresses the high levels of autophagy and bouton number found upon expression of Atg1Scer\UAS.cSa under the control of Scer\GAL4elav.PLu.

The eye phenotype in Ras85DKP mutant flies is partially suppressed by ectopic expression of bskDN.Scer\UAS in the eye under the control of Scer\GAL4GMR.PF.

Co-expression of bskDN.Scer\UAS suppresses the invasive behaviour of clones in the eye antennal disc which are expressing Ras85DV12.Scer\UAS under the control of Scer\GAL4Act5C and are also homozygous for scrib1.

Expression of bskDN.Scer\UAS under the control of Scer\GAL448Y significantly suppresses the defects in left-right asymmetry of the anterior midgut that are seen in homozygous pucGS16811 embryos.

Expression of bskDN.Scer\UAS under the control of Scer\GAL4Gap1-NP3392 significantly suppresses the defects in left-right asymmetry of the anterior midgut that are seen in homozygous pucGS16811 embryos. This suppression is stronger if the embryos are also carrying bsk1/+.

Co-expression of bskDN.Scer\UAS and Ras85DV12.Scer\UAS in scrib1 mutant clones completely blocks the invasion of the ventral nerve cord as well as secondary tumour foci formation.

Expression of Ras85DV12.Scer\UAS, egrScer\UAS.cIa and bskDN.Scer\UAS, under the control of Scer\GAL4Act5C.PI in shgk03401 mutant larval cephalic complexes (brain, eye and antennal discs) induces tumor invasion of the ventral nerve cord.

Expression of bskDN.Scer\UAS under the control of Scer\GAL4ey.PH results in rescue of the ventral eye loss of L2/+ mutants in 36% of cases.

Coexpression of bskDN.Scer\UAS and Rac1N17.Scer\UAS under the control of Scer\GAL4ato.3.6 results in the few dorsal cluster neuron axons crossing the optic chiasm, which is the same phenotype seen as single bskDN.Scer\UAS expression and is opposite to that seen when only Rac1N17.Scer\UAS is expressed.

Expression of one copy of bskDN.Scer\UAS, under the control of Scer\GAL4ato.3.6, in dsh1 mutant animals results in a synergistic reduction of extension of dorsal cluster neuron axons, with 60% showing no axons crossing the optic chiasm.

Expression of bskDN.Scer\UAS clones blocks the cell invasive phenotype of Scer\GAL4Act5C.PI>Ras85DV12.Scer\UAS, scrib1 eye/antennal imaginal disc clones. These clones still overgrow in the discs but never leave this structure. bskDN.Scer\UAS expression also rescues the larval lethality of Scer\GAL4Act5C.PI>Ras85DV12.Scer\UAS, scrib1 clone-bearing animals, with rescued animals progressing through most of metamorphosis and dying as pharate adults.

Expression of bskDN.Scer\UAS, has no effect on Scer\GAL4P2.4.Pdf>AblScer\UAS.cFa-induced axonal arborization of the sLNv.

Expression of bskDN.Scer\UAS, under the control of Scer\GAL4ap-md544, in a Traf1ex1/+ background results in an enhancement of the thorax closure defect seen in Scer\GAL4ap-md544>bskDN.Scer\UAS flies. The Scer\GAL4ap-md544>bskDN.Scer\UAS, Traf1ex1 flies have a larger cleft and the notum structure is disruoted.

The addition of bskDN.Scer\UAS to egrGS9830, Scer\GAL4GMR.PF animals leads to a strong suppression of the eye phenotype.

Does not suppress the phenotype caused by tkvCA.Scer\UAS expressed under the control of Scer\GAL471B.

Xenogenetic Interactions
Statement
Reference

The additional co-expression of bskDN.Scer\UAS does not modify the adult wing defects and the rough eye phenotype observed upon the co-expression of HPV18\E6Scer\UAS.T:Hsap\MYC and Hsap\UBE3AScer\UAS.cRa under the control of Scer\GAL4ap.PU and Scer\GAL4GMR.PU, respectively.

Expression of bskDN.Scer\UAS under the control of Scer\GAL4hs.2sev has no effect on the reduced adult eye size phenotype found in Scer\GAL4hs.2sev->Mmus\Gria1Lc.Scer\UAS flies.

Expression of bskDN.Scer\UAS suppresses the Scer\GAL4P2.4.Pdf>Hsap\APPScer\UAS.T:Hsap\MYC-dependent arborization of the sLNv.

Complementation and Rescue Data
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    References (95)