FB2026_01 , released March 12, 2026
FB2026_01 , released March 12, 2026
Allele: Dmel\eve3
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General Information
Symbol
Dmel\eve3
Species
D. melanogaster
Name
FlyBase ID
FBal0003885
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
eveR13
Key Links
Genomic Maps

Nature of the Allele
Progenitor genotype
Cytology
Description

Nucleotide substitution: C?T.

Amino acid replacement: Q106term.

Mutation that is predicted to result in a truncated protein lacking the "recognition helix" (helix 3) of the homeodomain required for DNA binding, as well as the transcriptional repression domain.

Deletion causing a frameshift that replaces the C-terminal 134 amino acid residues with 79 extraneous residues.

Mutations Mapped to the Genome
Curation Data
Type
Location
Additional Notes
References
Nucleotide change:

C9979801T

Amino acid change:

Q106term | eve-PA

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

In eveΔEL/eveΔEL, eve3/eve3 larvae, EL interneurons branch excessively off the main neurite near the soma and in the midline, which is never seen in controls; the axon is less extended than in controls, branching at ~40 microns from the soma; the dorsally projecting dendrites are significantly reduced and the ventrally projecting dendrites are significant increased.

eveΔEL/eveΔEL, Df(2R)eve/eve3 larvae show decreased crawling ability.

Cell intercalation is reduced by more than 30% in eve3 mutant embryos, accompanied by slower edge contraction.

aCC and RP2 fail to exit the CNS in eve3 mutants.

Anterior-posterior polarization of cells in the extending germband is partially disrupted in eve3 homozygous embryos.

When eve3/- males are mated with heterozygous Gug01323a mothers practically no embryos survive. These embryos die at late embryonic stage, they lose some or all of the even numbered ventral denticle belts. When the opposite cross (eve3/+ mother, Gug01323a/+ fathers) no reduction in survival is seen.

The cuticles of eve3 or eve3/Df(2R)eve embryos carrying eveEGNΔLFK, eveEGNAY or eveEGNPA resembles that of an eve hypomorph, with pair-rule defects in the pattern of abdominal denticle bands. Heterozygous embryos have abnormally narrow odd-numbered parasegments at early stages of development.

An ectopic stripe of early mitotic cells is seen at stage 8 in the presumptive parasegment 1 of eve3 mutant embryos. The cephalic furrow does not form.

The dorsolateral fat body is missing, the ventral fat body cluster is still present.

Homozygous embryos fail to form a cephalic furrow. The ventral furrow and proctodeal invagination form normally. No signs of initiator cell shortening are seen between the beginning of cycle 14 and stage 7. An irregular anterior fold is often seen in later stage embryos, at a variable position within mitotic domain 2 (MD2). This fold only arises after cells in MD2 have entered mitosis. The fold eventually resolves into a complete transversal furrow. MD2 is expanded posteriorly compared to wild-type embryos.

Reduced rate of germ band extension.

Cuticular phenotype, lawn of dentical hairs.

The ftz stripes remain broad and do not sharpen at their anterior edges.

Unsegmented 'lawn' phenotype of the cuticle. The arrays and patterns of mesodermal cells are disordered.

Unsegmented lawn of denticles.

strong allele

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhanced by
Statement
Reference

eve3 has abnormal neuroanatomy phenotype, enhanceable by unc-5[+]/unc-58

eve3 has abnormal neuroanatomy phenotype, enhanceable by unc-5[+]/beat-IaC163/beat-Ia[+]/unc-58

Suppressed by
NOT suppressed by
Statement
Reference

eve3/eve[+], trol13 has lethal phenotype, non-suppressible by CycEhs.PR

Enhancer of
Statement
Reference
Other
Phenotype Manifest In
Enhanced by
Statement
Reference

eve3 has larval intersegmental nerve phenotype, enhanceable by unc-5[+]/unc-58

eve3 has larval intersegmental nerve phenotype, enhanceable by unc-5[+]/beat-IaC163/beat-Ia[+]/unc-58

Suppressed by
Statement
Reference

eve3/eve[+], trol13 has larval brain & neuroblast phenotype, suppressible by CycEhs.PR

Enhancer of
Statement
Reference

eve3/eve[+] is an enhancer of eye phenotype of Scer\GAL4GMR.PF, fruNP0021

eve3/eve[+] is an enhancer of larval brain & neuroblast phenotype of trold8

eve3/eve[+] is an enhancer of larval brain & neuroblast phenotype of trolp4

Other
Additional Comments
Genetic Interactions
Statement
Reference

A transheterozygous combination of eve3/+, 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 8.1% to 23.1% in eve3/+, unc-58/+ transheterozygotes and eve3/+, unc-58/+, beat-IaC163/+ triple heterozygotes, respectively.

An eve3 background enhances the rough eye phenotype related to fru isoform A, found upon expression of fruNP0021 under the control of Scer\GAL4GMR.PF.

When eve3/- males are mated with heterozygous Gug01323a mothers practically no embryos survive. These embryos die at late embryonic stage, they lose some or all of the even numbered ventral denticle belts. When the opposite cross (eve3/+ mother, Gug01323a/+ fathers) no reduction in survival is seen.

The degree of rescue of the eve3 embryonic phenotype conferred by one copy of eveE+L.8.4 is reduced if the mother is heterozygous for groE48. The degree of rescue of the eve3 embryonic phenotype conferred by two copies of eveEGNΔLFK is reduced slightly if the mother is heterozygous for groE48.

The proliferation defect seen in trolp4 animals is enhanced by one copy of eve3; 100% of animals show defective proliferation. The proliferation defect seen in trold8 animals is enhanced by one copy of eve3; 88% of animals show defective proliferation. 96% of trol13/Y ; eve3/+ animals show defective proliferation of larval brain neuroblasts. The addition of CycEhs.PR (without heat shock) reduces the number of animals with defective proliferation to 35%, and expression of CycEhs.PR using a 30 minute heat shock rescues the neuroblast phenotype almost completely. Weak induction of CycEhs.PR does not rescue the enhanced lethality of trol13/Y ; eve3/+ animals. trol13/Y ; eve3/+ brains cultured in an explant assay in larval extract from eve3/+ or trol13/Y ; eve3/+ animals show a reduced amount of proliferation compared to wild-type brains cultured in larval extract from wild-type animals. In contrast, trol13/Y ; eve3/+ brains cultured in larval extract from wild-type animals have a level of proliferation close to that seen in controls (wild-type brains cultured in larval extract from wild-type animals). No trol13 brains cultured in larval extract from eve3/+ animals show normal proliferation. Addition of ecdysone rescues defective proliferation in trol13/Y ; eve3/+ brains cultured in larval extract from trol13/Y ; eve3/+ animals.

Dominantly enhances the semi-lethality of trol13/Y males and shows a transheterozygous effect in trol13/+ females, resulting in a reduction in viability. This enhancement is repressed by evetPa. Hemizygous trol13 male larvae have a normal number of S phase neuroblasts per brain lobe. If the larvae are also heterozygous for eve3 then the number of S phase neuroblasts per brain lobe is reduced.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Partially rescued by

eve3 is partially rescued by eveEGNHA

eve3 is partially rescued by eveE+L.8.4

eve3 is partially rescued by eveE+L.9.2

eve3 is partially rescued by eveE+L.8.4

Comments

Homozygosity for P{S2E.wt.eve.wt}attP2 rescues the viability of eve3 homozygotes to adulthood at a frequency of 80-85% (this is not significantly different from full 100% rescue), while the rescue frequency is lower in eve3 homozygotes carrying one copy of P{S2E.wt.eve.wt}attP2. There is no significant difference in the observed recovery of males versus females.

Homozygosity for P{S2E.wt.eve.YFP}attP2 rescues the viability of eve3 homozygotes to adulthood in more than 50% of cases.

Flies homozygous for P{S2E.MSE.eve.YFP}attP2 in a eve3 background are highly viable and fertile. However flies heterozygous for P{S2E.MSE.eve.YFP}attP2 show on average less than 5% rescue of eve3 to adulthood. In both cases there is a reduction in the recovery of males compared to females.

Flies homozygous for P{S2E.INV-MSE.eve.YFP}attP2 in a eve3 background are highly viable and fertile. However flies heterozygous for P{S2E.INV-MSE.eve.YFP}attP2 show on average less than 5% rescue of eve3 to adulthood.

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

Associated with: recessive mutations that affect fertility, as revealed in the rescued condition using eveE+L.8.4 or eveE+L.9.2.

Comments
Comments

Null mutation.

The expression of l(1)sc is altered during stage 9 in homozygous mutant embryos.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (4)
References (53)