FB2025_01 , released February 20, 2025
Allele: Dmel\Antp25
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General Information
Symbol
Dmel\Antp25
Species
D. melanogaster
Name
FlyBase ID
FBal0000566
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
AntpW10, AntpRW10, Antennapedia25
Key Links
Nature of the Allele
Progenitor genotype
Cytology

Polytene chromosomes normal.

Description
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

Homozygous clones in second leg discs fall into two categories; those that are well integrated into the disc epithelium and whose borders are interdigitated with their wild-type neighbours and those that are rounded up and have smooth borders. The interdigitated cones occur in all regions of the leg disc and appear to develop completely normally. The rounded up clones often have borders that coincide with novel folds in the disc. These rounded up clones almost always show some connection to the proximal ring that co-expresses Dll, hth and exd and are transformed to antenna (as assayed by marker expression).

The posterior signaling center is absent in Antp25/Antp17 mutant larvae.

In Antp25 embryos, thoracic neuroblast 3-3 (NB3-3T) fails to enter quiescence during mid-embryogenesis. Correspondingly, NB3-3T generates an increased number of GMCs and EL neurons compared to wild type.

Single cell class IV dendrite arborisation (da) neuron clones that are homozygous for Antp25 show no significant defects in dendrite development.

Loss of Antp function in Antp25 mutants does not affect the NB6-4t lineage in any of the thoracic segments.

Late homozygous embryos have normal oenocyte clusters.

Thoracic BrdU incorporation associated with ventrolateral/lateral neuroblasts is normal in homozygous embryos. However, additional staining is detected in ventral positions.

Severe disorganisation of T2 and T3 muscle pattern and absence of the first midgut constriction.

Expression of nub in endoderm is wild type.

Staining with antibodies reveals that Antp25 is necessary for many thoracic es organs, it is required for lch3 axonal projection and contributes to ch organs in T2 and T3.

No salivary gland defects.

Homozygous clones in the leg show deletions of structures from the femur, tibia and proximal part of the basitarsus.

Hemizygotes lack the anterior constriction of the midgut. In hemizygotes Scr expression is very much reduced.

X ray induced somatic clones homozygous for Antp25 demonstrate that loss of Antp function results in the development of only a restricted portion of the thorax and mesothoracic legs are transformed to an antennal identity.

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

Antp25, Ubx1 double mutant embryos lack a DA3 muscle in all thoracic and abdominal A1-A2 segments.

Scr4 Antp25 embryos show a wild-type oenocyte pattern.

UbxIa.Scer\UAS.T:Hsim\VP16 driven by a weak expressing line of Scer\GAL4arm.PS (arm-GAL4r), in a Antp25 mutant background, displays a normal Antp loss of function phenotype. When driven by a strong expressing line of Scer\GAL4arm.PS (arm-GAL4), the Antp25 is rescued almost to wild type; T2 and T3 are rescued to their normal appearances, though some head segments develop small patches of T2-like denticles.

In heterozygous combination with ctL188 or ctC145, ectopic structures project (usually unilaterally) from the position of the anterior spiracle on the dorsal prothorax, and are associated with malformation of absence of the two macrochaetaes on the humeral callus. The phenotype is incompletely penetrant and not as severe as for Antp11.

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

Scer\GAL4e22c-mediated expression of AntpScer\UAS.cCa rescues the muscle defects in T2.

Images (0)
Mutant
Wild-type
Stocks (1)
Notes on Origin
Discoverer

Wakimoto.

Comments
Comments

Reduced levels of tsh transcripts are found in parasegments 4 and 5.

The A and B glial cells do not show a pattern defect.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (9)
References (69)