FB2026_01 , released March 12, 2026
FB2026_01 , released March 12, 2026
Allele: Dmel\trh10512
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General Information
Symbol
Dmel\trh10512
Species
D. melanogaster
Name
FlyBase ID
FBal0009624
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
l(3)10512
Key Links
Genomic Maps

Nature of the Allele
Progenitor genotype
Associated Insertion(s)
Cytology
Description

P{PZ} is inserted in the 5' non-coding part of the first trh exon, 674bp upstream to the designated initiator ATG.

Allele components
Component
Use(s)
Inserted element
Encoded product / tool
Mutations Mapped to the Genome
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

Trachea are absent in homozygous trh10512 embryos, yet peripheral glial migration phenotype is normal.

A trh10512 heterozygous background dominantly suppresses the tracheal phenotypes found in ago1/ago3 mutants.

trh10512 mutant clones in the distal leg are frequently associated with morphological defects in the pretarsus, such as loss of claws and malformation of the pulvilli. When large trh10512 mutant clones are generated in a Minute background loss of claws and partial ta4/ta5 fusion is seen. Clones in more proximal segments of the leg show no discernible abnormalities. No morphological defects are observed in trh10512 mutant antenna.

One third of the lateral chordotonal (lch5) neuron clusters fail to project normally beyond the TP1 choice point in trh10512 homozygous mutant embryos. In these segments the growth cones fail to leave the region of the lch5 cluster or they extend ventrally but along an aberrant route. Occasionally, the lch5 axons fasciculate with the axon of v'ch1 and contribute to the segmental nerve (SN). In most hemisegments of trh10512 mutant embryos, the lch5 axon bundle does reach the intersegmental nerve (ISN) and the morphology of the fascicle appears normal in most cases.

Salivary glands form closed sacs that are not connected to the foregut. The filzkorper do not elongate and tracheal pits do not form. The oesophagus, gastric caecae and Malpighian tubules are unaffected.

Germline clones produce eggs with patterning defects: trachea are missing.

Tracheal structures are not formed in the embryo. Phenotype is more severe than for trh1.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Phenotype Manifest In
Suppressor of
Statement
Reference
NOT Suppressor of
Statement
Reference
Additional Comments
Genetic Interactions
Statement
Reference

trh10512/+ does not lead to a significant reduction in the penetrance of Scer\GAL4btl.PS VhldsRNA.Scer\UAS tracheal phenotypes.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Comments
Images (0)
Mutant
Wild-type
Stocks (1)
Notes on Origin
Discoverer

A. Spradling.

Comments
Comments

Complements: l(3)0596700315a. Complements: l(3)0624006240. Complements: Prm10631. Complements: l(3)neo11.

Reversion studies prove that the P{PZ} insertion is the cause of the trh10512 mutant phenotype. trh alleles fall into an allelic series. Two lethal lines were derived that complement trh mutants, along with wild type revertants and new trh alleles. From strongest to weakest: trh1 = trh8 > trh7 > trh10512 > trh6 > trh5 > trh4.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (7)
References (24)