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General Information
Symbol
Dmel\apP44
Species
D. melanogaster
Name
FlyBase ID
FBal0030501
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Key Links
Nature of the Allele
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Cytology
Nature of the lesion
Statement
Reference
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

Mutants show loss of expression of P{FMRFa-EGFP.Tv}, a marker for the six Ap4 neurons in the developing ventral nerve cord, and loss of expression of eya, which identifies the four Ap cluster neurons.

The number of SE2 neurons is normal in apP44 mutant animals.

Neurons which normally express ap (Ap neurons) are still present and extend axons in apP44/apmd544 embryonic brains. However, Ap brain interneurons show defasciculation and pathfinding defects in these animals. The most severe defects are seen in the deutocerebrum, where the two pairs of Ap neuronal cell bodies are positioned incorrectly. These neurons do not appear to undergo the movements seen in wild-type embryos and never become localised on the inner surface of the developing deutocerebrum, instead remaining on the outer surface, with their axons projecting aberrantly along the frontal commissure of the stomatogastric nervous system or in rare cases along the recurrent nerve. The cell bodies of the Ap neurons in the protocerebrum appear to be positioned properly and have a normal size and shape, but many of their commissural axons fail to form commissural fascicles correctly and often leave their commissural bundle and cross over to grow along a neighbouring fascicle. This defect is seen in 30% of cases. Ap neurons that innervate the ring gland have normal axonal projection patterns. Fas2-expressing commissural fascicles are indistinguishable from wild type.

In apmd544/apP44 embryos, all neurons that normally express ap survive and extend axons, but these axons display pathfinding errors in nearly every segment, including defasciculation of axon bundles, aberrant pathway selection within the longitudinal connectives, occasional misrouting across the midline and stalling.

apmd544/apP44 flies show wing defects.

apmd544/apP44 flies have no wings but often have a ribbon- or nub-like outgrowth that lacks any recognisable structures.

apP44/apmd544 embryos show proper positioning of the thoracic ventrolateral clusters in the central nervous system and their axonal bundles appear normal.

In homozygous or apmd544/apP44 embryos, neurons that normally express ap fail to recognise their appropriate pathway and wander within the longitudinal connective, failing to fasciculate with one another. apmd544/apP44 flies have no wings, although they often have a ribbon-like outgrowth in the wing region that lacks any recognisable structures.

Neurons of homozygous embryos carrying the P{apC-tau-lacZ} exhibit pathfinding and fasciculation defects: ap neurons that project their axons along abnormal pathways and fail to fasciculate with one another. The ap neurons still project anteriorly within the connectives.

Lacks wings and halteres. In the embryo, one or more muscles of the 21--23 group, in at least one hemisegment, is absent. In the majority of embryos multiple hemisegments (from 2 to 9) were affected. Muscle 29 is absent in at least one hemisegment of 75% of mutant embryos.

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

apP44 is a suppressor of scutellar bristle | ectopic phenotype of ChiE

apP44 is a suppressor of thorax phenotype of ChiE

NOT Suppressor of
Additional Comments
Genetic Interactions
Statement
Reference

The addition of this mutant to ChiE homozygotes suppresses the thoracic left and loss of bristle phenotype seen in these flies.

The axon guidance defects seen in apmd544/apP44 embryos are not rescued by coexpression of apΔLIM.Scer\UAS and ChiΔLID.Scer\UAS.T:Hsap\MYC under the control of Scer\GAL4ap-md544. ap::ChiΔLID.ΔLIM.Scer\UAS.T:Hsap\MYC rescues pathway recognition and axon fasciculation in a majority of segments in apmd544/apP44 embryos when expressed under the control of Scer\GAL4ap-md544. The axon defects seen in Chie5.5 apmd544/apP44 double mutants are completely rescued by ap::ChiΔLID.ΔLIM.Scer\UAS.T:Hsap\MYC expressed under the control of Scer\GAL4ap-md544.

Lim3Scer\UAS.cOa expressed under the control of Scer\GAL4ap-md544 partially rescues both the wing and embryonic central nervous system phenotype of apmd544/apP44 animals at 18oC and 25oC respectively. The wing, sterility and uncoordinated behaviour phenotypes of apmd544/apP44 flies are rescued by ap::Lim3Scer\UAS.cOa expressed under the control of Scer\GAL4ap-md544 to the same extent as the rescue seen by apScer\UAS.cOa. In contrast, the axon pathfinding phenotype of apmd544/apP44 embryos is only partially rescued by ap::Lim3Scer\UAS.cOa expressed under the control of Scer\GAL4ap-md544.

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

A single copy of apScer\UAS.cOa expressed under the control of Scer\GAL4ap-md544 almost completely rescues the wing phenotype of apmd544/apP44 flies; the wing blade is normal in size, with a normal margin and vein pattern, but is held at right angles away from the body. The sterility and uncoordinated behaviour phenotypes of apmd544/apP44 flies are also rescued and the central nervous system defects of embryos are rescued. A single copy of apScer\UAS.cOa expressed under the control of Scer\GAL4ap-md544 almost completely rescues the wing phenotype of apmd544/apP44 flies; the wing blade is normal in size, with a normal margin and vein pattern, but is held at right angles away from the body. The sterility and uncoordinated behaviour phenotypes of apmd544/apP44 flies are also rescued and the central nervous system defects of embryos are rescued. The ribbon-like outgrowth seen in apmd544/apP44 flies is entirely eliminated in flies expressing apΔHD.Scer\UAS under the control of Scer\GAL4ap-md544.

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

Arose during a P{Δ2-3} mutagenesis of the P{PZ}ap41F chromosome which carries ap41F. Southern analysis indicated that P{PZ}ap41F is precisely excised in this allele. It is suggested that the P{PZ}ap41F element excised, reinserted in the 5' end of ap from where it then imprecisely excised, to create the deletion of the 5' ap exon. Four independently derived alleles (apP44, apP22, apP33 and apP39) share these properties.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (1)
References (20)