FB2026_01 , released March 12, 2026
FB2026_01 , released March 12, 2026
Allele: Dmel\tsrN96A
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General Information
Symbol
Dmel\tsrN96A
Species
D. melanogaster
Name
FlyBase ID
FBal0177371
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Key Links
Nature of the Allele
Progenitor genotype
Cytology
Description

P-element-mediated imprecise excision of the tsr locus.

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 ( 1 )
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

tsrN96A homozygous stage 16 embryos show muscle defects, including missing muscles; however, in the muscles that are present, sarcomeres are formed by embryonic stage 17, similar to controls.

tsrN96A mutant clones within mosaic third instar larval wing discs are severely smaller than control clones; these clones show a strong increase in mitotic index (Casp3 and MMP1 immunofluorescence), as compared to controls.

Homozygous mushroom body neuroblast clones that are generated in newly hatched larvae contain only 15-30 neurons in the adult, in contrast to wild-type control clones, which contain approximately 400 neurons. The neuroblasts in the homozygous clones also show severe axon growth defects, with the majority of mutant neurons failing to extend their axons beyond the peduncle. Single cell homozygous clones of γ neurons in the mushroom body show axon growth defects in the adult; 30-40% of axons do not enter the medial lobe, stopping before the α/β branch point, 35-40% fail to extend beyond the midpoint of the γ lobe and 15-20% fail to reach the end of the γ lobe. Most of the mutant axons have multiple small protrusions and swellings along the the axon shaft and at the terminal, reminiscent of filopodia and lamellipodia normally associated with developing growth cones.

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

tsr[+]/tsrN96A is a suppressor of wing disc phenotype of CskGD9345, Scer\GAL4ptc-559.1

tsr[+]/tsrN96A is a suppressor of wing disc phenotype of Scer\GAL4ptc-559.1, hepUAS.cUa

tsr[+]/tsrN96A is a suppressor | partially of eye phenotype of mbtP1

tsr[+]/tsrN96A is a suppressor of eye phenotype of mbtP3

Other
Statement
Reference
Additional Comments
Genetic Interactions
Statement
Reference

sickΔ tsrN96A double heterozygotes do not show obvious axonal growth defects in α/β axonal lobes, peduncle and ellipsoid body.

The mushroom body axons of flies that are heterozygous for Rac1J11, Rac2Δ tsrN96A sickΔ and MtlΔ fail to extend to form peduncles and lobe structures (the 'posterior arrest' phenotype).

A tsrN96A 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.

A tsrN96A/+ background suppresses the cell migration seen upon expression of Rho1Scer\UAS.cMa under the control of Scer\GAL4ptc-559.1.

A tsrN96A/+ background suppresses the cell migration seen upon expression of hepScer\UAS.cUa under the control of Scer\GAL4ptc-559.1.

tsrN96A/+; twf110/+ transheterozygotes show mildly disorganised ridges and hooked tips.

A tsrN96A heterozygous background enhances the patterning defects found in Scer\GAL4GMR.PF>cindrdsRNA.PC.PD.Scer\UAS mutants. The mean interommatidial precursor cell number and the number of cone and/or 1[o] cell errors is increased in these double mutants.

tsrN96A/+ suppresses the mild rough eye phenotype seen mbtP3 hemizygous males and largely suppresses the more severe rough eye phenotype seen in mbtP1 hemizygous males.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Partially rescued by
Comments
Images (0)
Mutant
Wild-type
Stocks (1)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (3)
References (12)