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General Information
Symbol
Dmel\trolnull
Species
D. melanogaster
Name
FlyBase ID
FBal0197223
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
pcannull
Key Links
Allele class
Nature of the Allele
Allele class
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
Comment:

A 47,908 bp deficiency resulting from the simultaneous mobilization of P{EP}EP1619 and P{lacW}trolG0271. Site of deletion on reference sequence inferred by FlyBase curator.

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

Simultaneous mobilisation of the two progenitor insertions, resulting in a 47908bp deletion that spans the entire trol transcription unit.

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

Hemizygous embryos show ISNb motor axon guidance defects (59.9% of hemisegments) and SNa motor axon guidance defects (38.7% of hemisegments). ISNb axons fail to defasciculate at muscles 6 and 7 and some axons stall between muscles 6 and 13. SNa axons fail to reach their proper targets.

trolnull hemizygous embryonic hemocytes show decreased competence to undertake phagocytosis of apoptotic cells, as compared to controls.

Homozygous follicle cell clones have normal apical-basal polarity under normal food conditions.

Homozygous somatic follicle-cell clones often lose epithelial tissue organisation; about 50% of clones in stage 6-9 egg chambers show a multilayer phenotype.

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

The commissural axon phenotype (failure to cross the midline) seen in embryos expressing Sema-1aScer\UAS.cYa under the control of Scer\GAL4P52 in a Sema-1ak13702 null background is significantly suppressed if the embryos are also heterozygous for trolnull.

trolnull/+ ; Sema-1ak13702/+ double heterozygous embryos show ISNb motor axon guidance defects (51.0% of hemisegments) and SNa motor axon guidance defects (41.8% of hemisegments).

trolnull/+ ; Df(4)C3/+ double heterozygous embryos show ISNb motor axon guidance defects (51.5% of hemisegments) and SNa motor axon guidance defects (40% of hemisegments).

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Partially rescued by
Not rescued by
Comments

Expression of trolScer\UAS.RG under the control of Scer\GAL4elav.PU significantly rescues the ISNb and SNa motor axon guidance defects seen in trolnull embryos. Expression under the control of Scer\GAL4repo.PU only very modestly rescues the motor axon defects, and expression under the control of Scer\GAL4twi.PU fails to rescue the motor axon defects.

Images (0)
Mutant
Wild-type
Stocks (0)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (4)
References (9)