FB2026_01 , released March 12, 2026
FB2026_01 , released March 12, 2026
Allele: Dmel\bskflp147E
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General Information
Symbol
Dmel\bskflp147E
Species
D. melanogaster
Name
FlyBase ID
FBal0057730
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
bsk147e
Key Links
Nature of the Allele
Caused by aberration
Cytology
Description

This is an imprecise excision of the P-element from chico1. The 3'coding sequences are removed.

Breaks in the bsk transcription unit, removing most of the bsk coding sequence including the kinase domain.

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 ( 0 )
Disease
Interaction
References
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
 
Disease-implicated variant(s)
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
Statement
Reference

Flies containing bskflp147E mutant neuroblast clones show some β and γ mushroom body axon degeneration at 5 days post-eclosion, although most axons are still visible. This phenotype worsens in 28 day and 50 day old flies. A greater proportion of axons in bskflp147E mutant single cell γ cell clones show a "dying back" phenotype, in which they fail to reach the wild type termination point. Age matched wild type controls show no degeneration. bskflp147E mutant axons show more abnormal protrusions and swellings along the axons and terminals.

The majority of bskflp147E neuroblast clones in mushroom bodies have axons with normal projections in early stages of pupal development, but the following defects are seen from 30 hours after puparium formation: most bskflp147E axons fail to reach the wild type termination point, bskflp147E clones show discontinuous thinning along the axon tracts, and the entire axon lobe is often missing by the adult stage.

In single cell bskflp147E clones, many mushroom body neurons have fully extended axons that show thinning and breaks. Such degeneration is also seen in the main process close to the cell body.

Dorsal closure arrests early in some homozygous embryos, but dorsal closure manages to proceed further in a high percentage of the mutant embryos, sometimes even up to the zippering stage. In those mutant embryos that have a severe phenotype (little or no dorsalward net displacement and no straightening of the leading edge occurs), amnioserosa cell pulsations are sustained without damping. In embryos that manage to initiate dorsal closure, this usually happens with a significant time delay. With the onset of dorsalward leading edge movement, the leading edge begins to straighten in a manner similar to that of the wild-type but with much slower kinetics. In these mutant embryos, the damping of the amnioserosa cell pulsation also starts with a delay and is slower and parallels the behaviour of the leading edge.

bskflp147E clones generated along the A/P boundary of the wing imaginal disc, using the FLP/FRT technique, show no defects in segregation behaviour. As with wild-type clones, bskflp147E clones stay in the compartment (anterior or posterior) in which they have been generated.

Homozygous clones in the wing disc are recovered at high frequency. Homozygous clones in the pseudostratified epithelium of late-third instar wing discs have a normal shape and the actin and microtubule cytoskeletons are normal in cells of the clone.

When homozygous mutant somatic clones are made in the developing eye, a significant loss of photoreceptors and disordered ommatidia are seen.

Embryos fail to show complete elongation of the dorsal epidermis after germband retraction.

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. Homozygous clones in the eye reveal no abnormality.

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

bskflp147E/bsk[+] is a suppressor of scutum & macrochaeta phenotype of RalaS25N.UAS, Scer\GAL4sca-537.4

Other
Additional Comments
Genetic Interactions
Statement
Reference

Expression of EcRA-ΔC655.W650A.Scer\UAS under the control of Scer\GAL4ey-OK107 fails to suppress the axon degeneration seen in bskflp147E mutant mushroom body neuron clones.

Expression of zipΔHD.Scer\UAS.T:Avic\GFP-YFP under the control of Scer\GAL4ey-OK107 fails to suppress the axon degeneration seen in bskflp147E mutant mushroom body neuron clones.

Expression of two copies of thScer\UAS.cHa under the control of Scer\GAL4ey-OK107 fails to suppress the axon degeneration seen in bskflp147E mutant mushroom body neuron clones.

Expression of Iap2Scer\UAS.cLa under the control of Scer\GAL4ey-OK107 fails to suppress the axon degeneration seen in bskflp147E mutant mushroom body neuron clones.

Expression of two copies of NcΔN.C-A.Scer\UAS under the control of Scer\GAL4ey-OK107 fails to suppress the axon degeneration seen in bskflp147E mutant mushroom body neuron clones.

Expression of BuffyScer\UAS.cQa under the control of Scer\GAL4ey-OK107 fails to suppress the axon degeneration seen in bskflp147E mutant mushroom body neuron clones.

Expression of TorWT.Scer\UAS.T:Zzzz\FLAG under the control of Scer\GAL4ey-OK107 fails to suppress the axon degeneration seen in bskflp147E mutant mushroom body neuron clones.

Expression of HDAC6Scer\UAS.T:SV5\V5 under the control of Scer\GAL4ey-OK107 fails to suppress the axon degeneration seen in bskflp147E mutant mushroom body neuron clones.

Expression of ThorScer\UAS.cMa under the control of Scer\GAL4ey-OK107 fails to suppress the axon degeneration seen in bskflp147E mutant mushroom body neuron clones.

Expression of parkScer\UAS.cGa under the control of Scer\GAL4ey-OK107 fails to suppress the axon degeneration seen in bskflp147E mutant mushroom body neuron clones.

As tkv4 clones in the wing pouch do not survive due to apoptosis, and bskflp147E single mutant clones show no segregation defects in the wing, tkv4 bskflp147E clones can be used to study whether tkv4 affects segregation of cells at the A/P boundary. The majority of bskflp147E tkv4 clones of A origin in contact with the A/P boundary of the wing disc are misplaced into the P territory, causing a displacement of the A/P compartment boundary toward P. However, clones of P origin remain in the P compartment. The same defective segregation phenotype occurs in wing discs with MadB1 bskflp147E clones in contact with the A/P boundary.

The frequency of recovery of tkv4 bskflp147E double mutant clones (induced during the first larval instar) in the wing disc pouch of late-third instar larvae is only 24% compared to sibling wild-type clones, probably due to the formation of cyst-like structures followed by extrusion from the basal side of the epithelium. The double mutant clones are shorter along their apical-basal axis than normal, have lost contact to the apical epithelial surface and form cyst-like structures with the apical cell membranes facing the centre of the clone instead of the disc lumen. F-actin is enriched at the centre of the double mutant clones, whereas a dense apical network of microtubules, which is present in wild-type cells, is markedly reduced. Basal microtubules appear normal. Some tkv4 bskflp147E double mutant clones are seen in adult wings, as extruded cyst-like structures located between the dorsal and ventral wing surfaces. These mutant cells display hairs, characteristic structures of the adult epithelium, indicating that the extruded cells have undergone differentiation.

Df(2L)flp170B/Df(2L)flp147E animals in which the eyes are composed of homozygous Df(2L)flp170B clones (generated using the "eyFLP" system) and in which the deletion of bsk in Df(2L)flp170B and Df(2L)flp147E is rescued by the presence of bsk+t5 have enlarged eyes, despite the reduced size of the structures around them. Other structures in the head and body that are unaffected by the eyFLP system appear to be maintained in proportion to the chico mutant body.

bskflp147E/+ msn102/+ embryos have a dorsal open phenotype.

Xenogenetic Interactions
Statement
Reference

Expression of Mmus\wldS.Scer\UAS.T:Hsap\MYC under the control of Scer\GAL4ey-OK107 suppresses the axon degeneration seen in bskflp147E mutant mushroom body neuron clones at both 5 and 28 days post-eclosion. The 'dying back' phenotype is also suppressed; clones generated in single γ cells show that axons are able to reach the wild type termination point. The number of enlarged and supernumerary axonal protrusions seen on bskflp147E mutant axon shafts is also significantly reduced.

Expression of Mmus\Nmnat1Scer\UAS.T:Hsap\MYC under the control of Scer\GAL4ey-OK107 suppresses the axon degeneration seen in bskflp147E mutant mushroom body neuron clones at 28 days. The "dying back" phenotype is also suppressed; many of the axons now have wild type termination points. The number of enlarged and supernumerary axonal protrusions seen on bskflp147E mutant axon shafts is also significantly reduced.

Expression of Mmus\Nmnat2Scer\UAS.T:Hsap\MYC under the control of Scer\GAL4ey-OK107 fails to suppress the axon degeneration seen in bskflp147E mutant mushroom body neuron clones at 28 days.

Expression of Mmus\Nmnat3Scer\UAS.T:Hsap\MYC under the control of Scer\GAL4ey-OK107 partially suppresses the axon degeneration seen in bskflp147E mutant mushroom body neuron clones at 28 days. The number of enlarged and supernumerary axonal protrusions seen on bskflp147E mutant axon shafts is also significantly reduced.

Expression of Mmus\wldS-dead.Scer\UAS.T:Hsap\MYC under the control of Scer\GAL4ey-OK107 suppresses the axon degeneration seen in bskflp147E mutant mushroom body neuron clones at 28 days. The number of enlarged and supernumerary axonal protrusions seen on bskflp147E mutant axon shafts is also significantly reduced.

Expression of Hsap\HSPA1LScer\UAS.cWa under the control of Scer\GAL4ey-OK107 partially suppresses the axon degeneration seen in bskflp147E mutant mushroom body neuron clones at 28 days. The number of enlarged and supernumerary axonal protrusions seen on bskflp147E mutant axon shafts is also significantly reduced.

Expression of Hsp26Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4ey-OK107 partially suppresses the axon degeneration seen in bskflp147E mutant mushroom body neuron clones at 28 days.

Expression of Scer\UBP2Scer\UAS.cDa under the control of Scer\GAL4ey-OK107 fails to suppress the axon degeneration seen in bskflp147E mutant mushroom body neuron clones.

Complementation and Rescue Data
Comments

Expression of bskmTPY.Scer\UAS.T:Hsap\MYC using Scer\GAL4ey-OK107 fails to rescue the axonal phenotypes seen in bskflp147E clones.

Expression of bskScer\UAS.T:Hsap\MYC using Scer\GAL4ey-OK107 rescues the axonal phenotypes seen in bskflp147E clones. bskScer\UAS.T:Hsap\MYC needs to be provided throughout development to completely rescue.

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

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

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (4)
Reported As
Name Synonyms
Secondary FlyBase IDs
    References (17)