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General Information
Symbol
Dmel\shotSF20
Species
D. melanogaster
Name
FlyBase ID
FBal0046011
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
kaksf20
Nature of the Allele
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Cytology
Nature of the lesion
Statement
Reference
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 )
Disease
Interaction
References
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
Statement
Reference

shotSF20 homozygous embryos show efficient dorsal closure, but with abnormal dynamics (i.e. a smaller dorsal hole width during dorsal closure, shown by a significant increase in the length:width ratio, and severe decrease in the fractional contribution of zippering, despite of an insignificant change in epithelial sheet translocation), as compared to controls. The dorsal-most epithelial cells of these mutants, which do not present significant changes in cell size, exhibit a slightly disorganized microtubule network (i.e. frequent abnormally long, bent and protruding microtubules at the leading edge; an increased instability of the dynamic pool of microtubules, as shown by a significant decrease in the halftime, but not in the mobile fraction, of tubulin in FRAP experiments, and by the significant increase in the growth rate, but not in the lifetime, of growing microtubules; but insignificant changes in overall microtubule directionality), and exhibit a significant decrease in the number of normal-sized filopodia and frequent long apical protrusions at the leading edge, as compared to controls.

The growth cones of shotSF20/Df(2R)MK1 primary embryonic neurons in culture show a high frequency of transverse abaxial microtubule polymerisation (19.1% of polymerisation deviates more than 45[o] from the axon axis) compared to wild-type neurons (6.7%). The axons of the neurons are reduced in length compared to wild-type controls.

shotSF20/Df(2R)MK1 primary neuronal cultures show a significantly reduced axonal length compared to controls. They also show an increase of neurons with unbundled microtubules - these microtubules display irregular trajectories and frequent loops in axons and growth cones.

shot3/Df(2R)MK1 primary neuronal cultures show a significant reduction in filopodia number.

shotSF20/Df(2R)MK1 mutants show strong reduction of output synapses at the NMJ, while this phenotype is not seen in the CNS.

Homozygous and hemizygous embryos show a paralytic phenotype. Neuromuscular junctions occupy far less surface of their respective muscles, their branches are reduced in length and boutons appear reduced in number and size in homozygous, hemizygous, shotSF20/shot91k and shotSF20/shotel3 embryos compared to wild-type. Typical presynaptic specialisations, such as T-bars, are missing in some cases in homozygous embryos. shotSF20/shotel3 neuromuscular junctions have excitatory junctional currents, indicating that neuromuscular transmission occurs. Peripheral nerves can form correctly in hemizygous and shotSF20/shotel3 embryos. The short SNb-branch has a tendency to stall in hemizygous embryos. The ipsilateral local arborisations of the RP3 neuron are almost normal, but the contralateral arborisations of the RP3 neuron are severely reduced and often form swellings or blobs in shotSF20/shotel3 or shotSF20/shot91k embryos. shotSF20/shotel3 embryos do not show any obvious defects in muscle patterning at stage 16. However, at stage 17, severe detachment of the muscles from the cuticle is seen, although the muscles remain attached to each other. The thick dendrites appear collapsed and the cilia frequently appear detached from the tip of the capsule in shotSF20/shotel3 or shotSF20/shot91k scolopidial sensory organs.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Other
Statement
Reference
Phenotype Manifest In
Other
Statement
Reference
Additional Comments
Genetic Interactions
Statement
Reference

shotSF20/+ exba2/+ primary neuronal cultures show a strong reduction in filopodia number, whereas controls heterozygous for only one of these genes display normal filopodia.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Partially rescued by
Comments

The increased length:width ratio of the dorsal hole in shotSF20 embryos is rescued by the Scer\GAL4pnr.PU-driven expression of shotLA.Scer\UAS.T:Avic\GFP, shotLA-ΔEF-hand.Scer\UAS.T:Avic\GFP, or shotRE-ΔCtail.Scer\UAS.T:Avic\GFP, but not shotLC.Scer\UAS.T:Avic\GFP, shotLA-ΔGAS2.Scer\UAS.T:Avic\GFP or shotLC-ΔGAS2.Scer\UAS.T:Avic\GFP.

The abnormal microtubules present the leading edge of the dorsal-most epithelial cells during dorsal closure of shotSF20 homozygous are rescued by the Scer\GAL4en.PU-driven expression of shotLA.Scer\UAS.T:Avic\GFP, shotLA-ΔEF-hand.Scer\UAS.T:Avic\GFP, shotRE-ΔCtail.Scer\UAS.T:Avic\GFP, shotLA-ΔGAS2.Scer\UAS.T:Avic\GFP, or shotRE-3MtLSmut.Scer\UAS.T:Avic\GFP, but not shotLC-ΔGAS2.Scer\UAS.T:Avic\GFP, shotCtail.Scer\UAS.T:Avic\GFP or shotEGG.Scer\UAS.T:Avic\GFP; expression of shotLC.Scer\UAS.T:Avic\GFP under the control of Scer\GAL4en.PU also rescues the long and bent microtubules at the apical of the dorsal-most epithelial cells during dorsal closure of shotSF20 homozygous embryos, but the cell body microtubules appear bundled, as compared to mutant and control embryos.

Expression of shotLA.Scer\UAS.T:Avic\GFP under the control of Scer\GAL4eve.RN2O significantly rescues the motor neuron stall phenotype seen in shotunspecified embryos in vivo while expression under the control of Scer\GAL4sca-537.4 completely rescues the axon extension and microtubule organisation defects of shotSF20/Df(2R)MK1 embryonic neurons in primary culture.

Expression of shotRE-ΔCtail.Scer\UAS.T:Avic\GFP under the control of Scer\GAL4eve.RN2O does not rescue the motor neuron stall phenotype seen in shotunspecified embryos in vivo and expression under the control of Scer\GAL4sca-537.4 fails to rescue the axon extension and microtubule organisation defects of shotSF20/Df(2R)MK1 embryonic neurons in primary culture.

Expression of shotRE-3MtLSmut.Scer\UAS.T:Avic\GFP under the control of Scer\GAL4eve.RN2O does not rescue the motor neuron stall phenotype seen in shotunspecified embryos in vivo and expression under the control of Scer\GAL4sca-537.4 fails to rescue the axon extension and microtubule organisation defects of shotSF20/Df(2R)MK1 embryonic neurons in primary culture.

Scer\GAL4sca-537.4-mediated expression of shotLA.Scer\UAS.T:Avic\GFP fully restores the microtubule unbundling and axonal length phenotypes of shotSF20/Df(2R)MK1 primary neuronal cultures.

Scer\GAL4sca-537.4-mediated expression of shotLA-ΔGAS2.Scer\UAS.T:Avic\GFP fails to restore the microtubule unbundling and axonal length phenotypes of shotSF20/Df(2R)MK1 primary neuronal cultures.

Scer\GAL4sca-537.4-mediated expression of shotEGG.Scer\UAS.T:Avic\GFP fails to restore the microtubule unbundling and axonal length phenotypes of shotSF20/Df(2R)MK1 primary neuronal cultures.

Scer\GAL4sca-537.4-mediated expression of shotLA.Scer\UAS.T:Avic\GFP fully rescues the reduced filopodia phenotype of shotSF20/Df(2R)MK1 primary neuronal cultures.

Scer\GAL4sca-537.4-mediated expression of shotLA-ΔGAS2.Scer\UAS.T:Avic\GFP rescues the reduced filopodia phenotype of shotSF20/Df(2R)MK1 primary neuronal cultures.

Scer\GAL4sca-537.4-mediated expression of shotEGG.Scer\UAS.T:Avic\GFP fully rescues the reduced filopodia phenotype of shotSF20/Df(2R)MK1 primary neuronal cultures.

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

M. Ashburner.

Induced with: wbSF20.

Recovered as: Second-site lethal in the wbSF20 chromosome.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (5)
References (9)