FB2024_03 , released June 25, 2024
Allele: Dmel\HGTXD25
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General Information
Symbol
Dmel\HGTXD25
Species
D. melanogaster
Name
FlyBase ID
FBal0183335
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
nkx6D25
Key Links
Allele class
Nature of the Allele
Allele class
Progenitor genotype
Caused by aberration
Cytology
Description

A 25kb deletion, generated by imprecise excision of P{lacZ}HGTXP-JG, that removes the 3' end of HGTX and the complete ORF of CG13479.

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

A lineage 3 HGTXD25 mutant postembryonic neuroblast clone examined at the third larval instar stage contains the 3id axon bundle, but lacks the 3il bundle normally produced by this lineage.

In stage 16 HGTXD25 homozygous embryos, both secondary branches of the intersegmental nerve (anterior fascicle), ISNb and ISNd, are absent in a significant proportion of hemisegments. This phenotype is also seen in HGTXD25/HGTXP-JG and HGTXD25/Df(3L)fz-D21 embryos. exex expressing interneurons largely fail to project axons along the longitudinal fascicles in stage 16 HGTXD25 homozygous embryos. In HGTXD25 homozygous embryos, RP motor axons only exit the CNS 39% of hemisegments compared to 86% in wild-type. These axons often appear thinner than wild-type and the morphology of truncated axons is often aberrant - growth cones are frequently enlarged and have a club-like appearance. In 10% of mutant hemisegments, RP motor axons make dramatic guidance errors, often turning back inappropriately and extending toward the midline.

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

HGTXD25, exexKK30 has embryonic central nervous system & neuron | ectopic phenotype

Additional Comments
Genetic Interactions
Statement
Reference

A homozygous HGTXD25 mutant background does not alter the ectopic lateral fd59A[+] neurons seen when exexScer\UAS.cBa is expressed under the control of Scer\GAL4elav-C155.

Embryos doubly mutant for midGA174 and HGTXD25 exhibit gross defects in the architecture of the central nervous system.

Stage 15 exexKK30; HGTXD25 double mutant embryos have ectopic vnd expressing neurons in the central nervous system. exexKK30/exexKK30 does not enhance the expressivity of loss of secondary branches of the intersegmental nerve (anterior fascicle) - ISNb and ISNd - in stage 16 HGTXD25 homozygous embryos.

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 (7)
Reported As
Name Synonyms
Secondary FlyBase IDs
    References (9)