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.
C9979801T
Q106term | eve-PA
abnormal locomotor behavior | larval stage (with Df(2R)eve), with eveΔEL
pair rule phenotype (with Df(2R)eve), with eveEGNAY
pair rule phenotype (with Df(2R)eve), with eveEGNPA
pair rule phenotype (with Df(2R)eve), with eveEGNΔLFK
embryo (with Df(2R)eve), with eveEGNΔLFK
ventral denticle belt (with Df(2R)eve), with eveEGNAY
ventral denticle belt (with Df(2R)eve), with eveEGNPA
ventral denticle belt (with Df(2R)eve), with eveEGNΔLFK
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.
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
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
eve3/eve[+], trol13 has decreased occurrence of cell division | third instar larval stage phenotype, suppressible | partially by CycEhs.PR
eve3 is an enhancer of lethal | embryonic stage | maternal effect phenotype of Gug01323a
eve3 is an enhancer of lethal | embryonic stage | maternal effect phenotype of Gug03928
eve3 is an enhancer of lethal | embryonic stage | maternal effect phenotype of Guge46-2
eve3 is an enhancer of lethal | embryonic stage | maternal effect phenotype of GugrO154a
eve3/eve[+] is an enhancer of decreased occurrence of cell division | larval stage phenotype of trold8
eve3/eve[+] is an enhancer of decreased occurrence of cell division | larval stage phenotype of trolp4
eve3/eve[+] is an enhancer of partially lethal - majority die phenotype of trol13
eve3/eve[+], trol13 has decreased occurrence of cell division | third instar larval stage phenotype
eve3/eve[+], trol13 has decreased occurrence of cell division | larval stage phenotype
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
Gug01323a, eve3 has abdominal 4 ventral denticle belt phenotype
Gug01323a, eve3 has abdominal 8 ventral denticle belt phenotype
Gug01323a, eve3 has abdominal 2 ventral denticle belt phenotype
Gug01323a, eve3 has abdominal 6 ventral denticle belt phenotype
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.
eve3 is rescued by eve-6.6.+9.8
eve3 is rescued by eveMSE.-6.6.+9.8.SYFP2
eve3 is rescued by eveINV-MSE.-6.6.+9.8.SYFP2
eve3 is rescued by eveΔS2E/eveDpse\eve.S2E
eve3 is rescued by eveeve.S2E/eveΔS2E
eve3 is rescued by eveΔS2E/eveDyak\eve.S2E
eve3/Df(2R)eve is rescued by eveE+L.8.4
eve3 is rescued by eveE+L.8.4
eve3 is partially rescued by eve-6.6.+9.8.SYFP2
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
eve3 is not rescued by eveΔS2E/eveDere\eve.S2E
eve3/Df(2R)eve is not rescued by eveEGNΔLFK
eve3 is not rescued by eveEGNΔLFK
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.
Associated with: recessive mutations that affect fertility, as revealed in the rescued condition using eveE+L.8.4 or eveE+L.9.2.
Null mutation.
The expression of l(1)sc is altered during stage 9 in homozygous mutant embryos.