FB2024_03 , released June 25, 2024
Allele: Dmel\eveΔRP2A
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General Information
Symbol
Dmel\eveΔRP2A
Species
D. melanogaster
Name
FlyBase ID
FBal0155322
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
eveΔRP2, RP2A
Key Links
Transgenic product class
Nature of the Allele
Transgenic product class
Progenitor genotype
Carried in construct
Cytology
Description

Sequence from +8.2kb to +9.2kb (coordinates relative to the eve transcription start site) of the eve genomic region has been deleted, thus sequences from -6.4kb to +8.2kb of eve are present.

Allele components
Component
Use(s)
Regulatory region(s)
Encoded product / tool
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

aCC and RP2 fail to exit the CNS in eveΔRP2A mutants.

eveΔRP2A mutants exhibit a failure of aCC/RP2 motoneurons to project out of the ventral nerve cord. In aCC, these effects are highly penetrant and observed at several stages, whereas in RP2 the effects are partially penetrant at stage 12 and almost absent at stage 15.

Homozygous Df(2R)eve embryos carrying two copies of eveΔRP2A show defects in the RP2, aCC and pCC neurons.

Homozygous Df(2R)eve embryos carrying both eveΔRP2A and eveΔRP2B show defects in the RP2, aCC and pCC neurons.

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

eveΔRP2A, beat-Ia[+], eve[+], beat-Ia3 is an enhancer of abnormal neuroanatomy phenotype of unc-58

eveΔRP2A/eve[+] is an enhancer of abnormal neuroanatomy phenotype of unc-58

Other
Phenotype Manifest In
Additional Comments
Genetic Interactions
Statement
Reference

A transheterozygous combination of eveΔRP2A/+, unc-58/+ reduces beat-Ia levels to 50% and significantly increases the defects seen in intersegmental nerves, with the number of axons exhibiting stalling increasing from 3% to 7.5% in eveΔRP2A/+, unc-58/+ transheterozygotes and eveΔRP2A/+, unc-58/+, beat-Ia3/+ triple heterozygotes, respectively.

Expression of unc-5Scer\UAS.T:Ivir\HA1,T:SS-wg in an eveΔRP2A mutant background results in 11% of hemisegments exhibiting dual motoneuron exit. These mutants exhibit an increase in dorsal projections in 67% of hemisegments.

Expression of beat-IaScer\UAS.cFa in an eveΔRP2A mutant background results in the exit of a single motoneuron of the pair in each hemisegment. These mutants exhibit an increase in dorsal projections in 36% of hemisegments.

Expression of Fas2Scer\UAS.cLa in an eveΔRP2A mutant background results in the exit of a single motoneuron of the pair in each hemisegment. These mutants exhibit an increase in dorsal projections in 25% of hemisegments.

Expression of Nrg180.I.Scer\UAS in an eveΔRP2A mutant background results in the exit of a single motoneuron of the pair in each hemisegment.

Removing one copy of eve in Nrgl7/Y mutants results in more severe intersegmental nerve guidance defects with a significant increase in axon stalling upon the addition of eveΔRP2A.

eveΔRP2A, Df(2R)eve/+ ; unc-58/+ double heterozygous embryos show guidance defects in the intersegmental nerve.

Expression of grnScer\UAS.cBa in the aCC/RP2 neurons, under the control of Scer\GAL4eve.RN2 does not rescue the failure of aCC to project its axon out of the ventral nerve cord in eveΔRP2A mutants.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Partially rescues
Comments

Two copies of eveΔRP2A fully rescue segmentation function in eve null mutants. However, at the extended germband stage, eve expression in the mesoderm is often weak or missing.

Homozygous Df(2R)eve embryos carrying two copies of eveΔRP2A show defects in the RP2, aCC and pCC neurons.

eve null mutants carrying a copy of eveΔRP2A and eveΔRP2C in trans show normal mesodermal expression of eve and normal segmentation and are efficiently rescued to adulthood.

Images (0)
Mutant
Wild-type
Stocks (0)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (4)
Reported As
Symbol Synonym
Df(2R)eveΔRP2A
eveΔRP2A
Name Synonyms
Secondary FlyBase IDs
    References (6)