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General Information
Symbol
Dmel\bsk2
Species
D. melanogaster
Name
FlyBase ID
FBal0001322
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Allele class
Nature of the Allele
Allele class
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
point mutation
Nucleotide change:

A10247899T

Reported nucleotide change:

A?T

Amino acid change:

K316term | bsk-PB; K316term | bsk-PE; K316term | bsk-PF

Reported amino acid change:

K316term

Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Cytology
Nature of the lesion
Statement
Reference

Mutation maps within kinase subdomain XI.

Nucleotide substitution: A?T.

Amino acid replacement: K316term.

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
Detailed Description
Statement
Reference

bsk2 mutant clones in sensory neurons in adult wing do not display any defects in injury-induced axon degeneration (following an axotomy, the severed axons are cleared away normally).

bsk2 heterozygosity does not significantly affect the mitotic index in the adult midgut epithelium, as compared to controls.

bsk2/bsk2 clones (in adult mushroom body γ lobe) are deficient in axon (but not dendrite) pruning compared to wild type.

bsk2 heterozygous mutants exhibit extreme sensitivity to 1-octen-3-ol. These flies survive for approximately 14 days when exposed to 0.5ppm 1-octen-3-ol, significantly lower than the 18 days-long survival span observed for exposed wild-type flies.

Single cell bsk2 clones in mushroom bodies have axons with wild type projections.

A bsk2/+, background suppressed the rough eye phenotype found upon expression of TgA.Scer\UAS under the control of Scer\GAL4GMR.PS.

bsk2 embryos show a severe dorsal closure defect.

The denticle belt patterning is not perturbed in bsk2 mutant embryos.

The cleft notum phenotype caused by expression of Nf-YAdsRNA.231-399.Scer\UAS.WIZ under the control of Scer\GAL4pnr-MD237 is enhanced by bsk2/+.

bsk1/bsk2 mutant embryos exhibit defective dorsal closure. F-actin cable formation in the peripheral amnioserosa is less prominent and the outer (ventral) edge of the peripheral amnioserosa is able to maintain a higher activity of filopodia.

Single cell bsk2 dorsal cluster neuron clones, created using the MARCM technique, show no axonal outgrowth.

A greater number of bsk2/+ mutant flies die after feeding with paraquat than wild-type flies.

Homozygous embryos have a dorsal open phenotype. The dorsal hole extends posterior to 50% egg length in 24% of embryos.

Initial phases of dorsal closure are normal, but the first rows under the leading cell row of the dorsal edge show only a partial lengthening cell shape change or no cell shape change at all. The defect is more pronounced in anterior cells.

Mutant embryos show a dorsal hole due to a defect in dorsal closure. Dorsoventral patterning is not defective.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Suppressed by
Statement
Reference

bsk2 has chemical sensitive | dominant phenotype, suppressible by pucE69/puc[+]

Enhancer of
Statement
Reference

bsk2/bsk[+] is an enhancer of lethal | recessive phenotype of Src42AJp45

NOT Enhancer of
Statement
Reference
Suppressor of
Statement
Reference

bsk2/bsk[+] is a suppressor of neuroanatomy defective | larval stage phenotype of Eaat1hypo

bsk2/bsk[+] is a suppressor | partially of visible phenotype of DrefUAS.cSa, Scer\GAL4GMR.PS

bsk2/bsk[+] is a suppressor | partially of visible phenotype of Rab11mo

bsk2 is a suppressor | partially of lethal | recessive phenotype of flw6

bsk2/bsk[+] is a suppressor | partially of visible phenotype of Rala35d

bsk2 is a suppressor of visible phenotype of RetMEN2A.GMR

bsk2 is a suppressor of visible phenotype of RetMEN2B.GMR

bsk2/bsk[+] is a suppressor of chemical resistant | dominant phenotype of pucE69

bsk2/bsk[+] is a suppressor | partially of planar polarity defective phenotype of peb1

bsk2/bsk[+] is a suppressor of planar polarity defective phenotype of dshhs.sev.B

NOT Suppressor of
Other
Statement
Reference
Phenotype Manifest In
Enhancer of
NOT Enhancer of
Statement
Reference

bsk2/bsk[+] is a non-enhancer of wing hair phenotype of Scer\GAL4en-e16E, kermitGS2053

bsk2/bsk[+] is a non-enhancer of ommatidium phenotype of MtlUAS.cMa, Scer\GAL4hs.2sev

bsk2 is a non-enhancer of photoreceptor cell | precursor & nucleus phenotype of Scer\GAL4unspecified, msnDN.UAS

bsk2/bsk[+] is a non-enhancer of dorsal appendage phenotype of bwk08482/bwk151

Suppressor of
Statement
Reference

bsk2/bsk[+] is a suppressor of NMJ bouton | supernumerary | larval stage phenotype of Eaat1hypo

bsk2/bsk[+] is a suppressor of wing disc phenotype of CskGD9345, Scer\GAL4ptc-559.1

bsk2/bsk[+] is a suppressor of wing disc phenotype of Scer\GAL4ptc-559.1, Sin3AKK100700

bsk2/bsk[+] is a suppressor | partially of eye phenotype of DrefUAS.cSa, Scer\GAL4GMR.PS

bsk2/bsk[+] is a suppressor of eye phenotype of Scer\GAL4GMR.PS, TgA.UAS

bsk2/bsk[+] is a suppressor of ommatidium phenotype of Scer\GAL4GMR.PS, TgA.UAS

bsk2/bsk[+] is a suppressor | partially of eye phenotype of Rab11mo

bsk2/bsk[+] is a suppressor | partially of ommatidium phenotype of ecspok

bsk2/bsk[+] is a suppressor | partially of microchaeta phenotype of Rala35d

bsk2/bsk[+] is a suppressor of macrochaeta phenotype of Rala35d

bsk2/bsk[+] is a suppressor | partially of eye phenotype of pucA251.1F3

bsk2 is a suppressor of eye phenotype of RetMEN2A.GMR

bsk2 is a suppressor of eye phenotype of RetMEN2B.GMR

bsk2/bsk[+] is a suppressor | partially of eye phenotype of rprGMR.PW

bsk2/bsk[+] is a suppressor | partially of ommatidium phenotype of rprGMR.PW

bsk2/bsk[+] is a suppressor | partially of ommatidium phenotype of peb1

bsk2 is a suppressor of ommatidium phenotype of Rac1V12.hs.sev

bsk2/bsk[+] is a suppressor of ommatidium phenotype of dshhs.sev.B

bsk2/bsk[+] is a suppressor of scutum & macrochaeta phenotype of RalaS25N.UAS, Scer\GAL4sca-537.4

bsk2 is a suppressor of phenotype of dshhs.sev.B

NOT Suppressor of
Statement
Reference

bsk2/bsk[+] is a non-suppressor of wing hair phenotype of Scer\GAL4en-e16E, kermitGS2053

bsk2/bsk[+] is a non-suppressor of ommatidium phenotype of MtlUAS.cMa, Scer\GAL4hs.2sev

bsk2/bsk[+] is a non-suppressor of dorsal appendage phenotype of bwk08482/bwk151

bsk2 is a non-suppressor of phenotype of dshΔC.hs.sev

Other
Additional Comments
Genetic Interactions
Statement
Reference

The axon degeneration in sensory neurons clones in the adult wing expressing Ect4ΔARM.Scer\UAS.T:Hsap\MYC under the control of Scer\GAL4nSyb.PS can be suppressed by combination with bsk2.

bsk2 heterozygosity suppresses the increased mitotic index in the adult midgut epithelium induced by the adulthood-only expression of UvragHMS01357 under the control of Scer\GAL4esg-NP5130 (and Gal80[ts], for the temporal control of expression).

A bsk2 heterozygous mutant background suppresses the actin remodelling and subsequent basolateral invasion of epithelial cells seen in flies expressing CskGD9345 in a stripe of cells at the anterior/posterior boundary of the larval wing disc under the control of Scer\GAL4ptc-559.1.

The cell invasion phenotype seen when Sin3AKK100700 is strongly expressed (using a line in which the transgene has been mobilised to the third chromosome) under the control of Scer\GAL4ptc-559.1 is suppressed in a bsk2/+ background.

The rough eye phenotype caused by expression of DrefScer\UAS.cSa under the control of Scer\GAL4GMR.PS is weakly but significantly suppressed by by bsk2/+.

bsk2/+ is unable to suppress the Scer\GAL4pnr-MD237>POSHScer\UAS.cSa lethality phenotype.

The eye defects seen in Rab11mo homozygotes are partially suppressed by bsk2/+.

The reduced eye size caused by expression of Rab11N124I.Scer\UAS under the control of Scer\GAL4GMR.PF is partially suppressed by bsk2/+.

Homozygous bsk2 border follicle cell clones that are also expressing PvrDN.Scer\UAS under the control of Scer\GAL4slbo.2.6 show defects in migration that are more severe than border follicle cells expressing PvrDN.Scer\UAS under the control of Scer\GAL4slbo.2.6 in an otherwise wild-type background.

The ommatidial rotation defects observed in ecspok hemizygous adult eyes are partially suppressed by bsk2/+.

bsk2 does not protect Df(1)su(s)R194/+ clones in the eye; Df(1)su(s)R194/+ ; bsk2 clones are not recovered in the adult eye in animals with mosaic eyes containing two genotypes of cells with respect to RpL36; cells which are Df(1)su(s)R194/+ and cells in which the haplo-insufficiency of Df(1)su(s)R194/+ for RpL36 has been rescued by RpL36+t4 (in a wild-type background the Df(1)su(s)R194/+ clones are eliminated by cell competition and are not seen in the adult eye in these animals). Also, the proportion of Df(1)su(s)R194/+ cells in the larval eye disc is not increased by the presence of bsk2.

Trans-heterozygotic combination between lkb1X5 and bsk2 induces a significant dorsal open phenotype in unhatched first instar larvae.

A bsk2/+ background enhances the splitting wing hair phenotype of flies that express trcT453A.Scer\UAS under the control of Scer\GAL4ap-md544.

7% of animals expressing msnDN.Scer\UAS in the developing eye, combined with bsk2/+ exhibit a R-cell nuclear migration phenotype.

Heterozygosity for bsk2 partially rescues pucA251.1F3 mutant eye tissue.

Shows no interaction with Mpk21.

The mutant dorsal appendage phenotype seen in bwk151/bwk08482 eggs is not significantly modified by bsk2/+.

pucE69/+, bsk2/+ mutant flies have a decreased mortality rate in response to paraquat compared to bsk2/+ single mutants and an increased mortality rate compared to pucE69/+ single mutants..

The addition of bsk2/+ to egrGS9830, Scer\GAL4GMR.PF animals leads to a suppression of the eye phenotype.

The rprGMR.PW eye phenotypes are significantly suppressed by heterozygosity for bsk2.

bsk2 suppresses the ommatidial polarity defects seen in dshhs.sev.B flies grown at 29oC. About 85% of ommatidia are in their correct polarity compared to 55% in dshhs.sev.B flies alone. Dominantly suppresses the ommatidial polarity phenotype seen in flies with msnEP549 driven by Scer\GAL4hs.2sev, producing near wild-type ommatidial arrays.

bsk2/+ msn102/+ embryos have a dorsal open phenotype.

bsk2 dominantly enhances the cnomis1/cno3 phenotype; bsk2/+ ; cnomis1/cno3 embryos have a dorsal open phenotype bsk2 dominantly enhances the cnomis1/cno3 phenotype; bsk2/+ ; cnomis1/cno3 embryos have a dorsal open phenotype.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Comments

The dorsal hole defect, though not embryonic lethality, can be partly rescued by bskhs.PS.

Images (0)
Mutant
Wild-type
Stocks (2)
Notes on Origin
Discoverer
Comments
Comments

Cuticle phenotypes reveal an allelic series: bskJ27 < bsk1 < bsk2 < bskflp147E.

External Crossreferences and Linkouts ( 3 )
Crossreferences
GenBank Nucleotide - A collection of sequences from several sources, including GenBank, RefSeq, TPA, and PDB.
GenBank Protein - A collection of sequences from several sources, including translations from annotated coding regions in GenBank, RefSeq and TPA, as well as records from SwissProt, PIR, PRF, and PDB.
UniProt/Swiss-Prot - Manually annotated and reviewed records of protein sequence and functional information
Synonyms and Secondary IDs (6)
References (68)