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General Information
Symbol
Dmel\exexKK30
Species
D. melanogaster
Name
FlyBase ID
FBal0137268
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
hb9KK30, dHb9KK30
Key Links
Nature of the Allele
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
Nucleotide change:

C7949011T

Reported nucleotide change:

C646T

Amino acid change:

Q216term | exex-PA

Reported amino acid change:

Q?term

Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Cytology
Nature of the lesion
Statement
Reference

Nucleotide substitution: C646T.

Amino acid replacement: Q?term.

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

exexKK30/exexGal4 embryos show motorneuron axon targeting defects. In 34.4% of hemisegments, Fas2-positive ISNb motorneuron axons do not correctly defasciculate from each other, resulting in the stalling of thicker axon bundles between muscles 6 and 13 and a failure to innervate the muscle 12/13 cleft. In 36.2% of hemisegments, ISNb or TN axons extend processes that form abnormal contacts between them.

68.3% of exexKK30/exexJJ154 mutant anterior dMP2 neurons fail to undergo apoptosis. Other aspects of dMP2 specification appear unaffected; they are able to project neurons posteriorly along the most medial fascicle, and exit the VNC to innervate the hindgut correctly.

Two ectopic eve-positiver neurons appear per hemisegment, in the vicinity of the aCC/pCC pair, at late stage 11. One remains immediately posterior to aCC/pCC, the other migrates posteriorly. The ectopic neurons arise from the NB1-1 lineage. ISNb projects aberrantly after defasciculating from the ISN, or fails to defasciculate at all.

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

exex[+]/exexKK30 is a non-enhancer of abnormal neuroanatomy | dominant phenotype of vvldfr-B129

NOT Suppressor of
Statement
Reference
Phenotype Manifest In
Enhanced by
Enhancer of
NOT Enhancer of
NOT Suppressor of
Statement
Reference
Other
Statement
Reference

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

Additional Comments
Genetic Interactions
Statement
Reference

The penetrance of the phenotype seen in both OliΔ9 (19.3%) and exexKK30/exexGal4 (34.4%) single mutant embryos where ISNb motorneuron axons do not correctly defasciculate from each other and fail to innervate the muscle 12/13 cleft is increased in double mutants to 68.5%.

The number of ectopic CO[[2]] neurons on the maxillary palp in animals containing prosIG2227 clones is unaffected if they are also carrying exexKK30/+.

Embryos doubly mutant for H15nmr-210 or midGA174 and exexKK30 do not show enhancement of the respective single mutant central nervous system phenotypes.

Stage 15 exexKK30; HGTXD25 double mutant embryos have ectopic vnd expressing and eve expressing neurons in the central nervous system.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Comments

Expression of exexScer\UAS.cOa from embryonic stage 16 onwards under the control of Scer\GAL4Vap.P0201 fails to rescue the apoptosis defects seen in exexKK30/exexJJ154 mutant anterior dMP2 neurons. Expressing exexScer\UAS.cOa from stage 10 under the control of Scer\GAL4odd-106 does rescue this apoptosis.

Images (0)
Mutant
Wild-type
Stocks (2)
Notes on Origin
Discoverer
Comments
Comments

Allele is a protein null.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (6)
References (12)