Nucleotide substitution: G to A. Amino acid replacement: R121H. R121H replacement is near the putative DNA-binding helix of the homeobox.
arg121 --> his
G9979847A
R121H | eve-PA
abdominal anterior fascicle & abdominal segment 3
abdominal anterior fascicle & abdominal segment 4
abdominal anterior fascicle & abdominal segment 5
abdominal segment 3 & somatic muscle
abdominal segment 4 & somatic muscle
abdominal segment 5 & somatic muscle
larval brain & neuroblast (with eve5)
Embryos have a pair rule phenotype. The segments that remain are about 1.4 times wider than wild-type segments and the cuticle is about 70% the length of a wild-type cuticle. The number of embryos that hatch and the number of adults eclosing is dramatically reduced compared to controls. ftz-dependent parasegments are enlarged and eve-dependent parasegments are reduced in stage 8 mutant embryos. The relative widths of enlarged and reduced parasegments remain relatively constant until germ-band retraction. Between stages 12-15 the relative widths of the smaller parasegments begin to decrease and by stage 16 reduced parasegments are no longer seen and the embryo is composed of seven enlarged parasegments. Parasegments 3 to 6 are unevenly spaced at stage 6-7 with parasegments 4 and 6 being about 1.4 times wider than wild-type and parasegments 3 and 5 being about 0.6 times the wild-type width. The wider parasegments contain about twice the number of cells of the narrower parasegments. The total width and number of cells in all four parasegments is equivalent to wild type. Each of the narrow parasegments maintains a constant relative width until around stage 12. After this time they decrease further in both width and cell number. The wide parasegments remain about 1.3-1.5 times wider and contain about 1.4 times as many cells as a normal parasegment. The pattern of cell death is abnormal in mutant embryos. Increased levels of apoptosis do not appear to be induced at or prior to stage 11 despite the earlier changes in parasegment size. By the end of stage 12 however, higher than normal levels of cell death are seen. The dying cells at this stage are almost exclusively in the wider parasegments, with few, if any, dying cells in the narrow parasegments. By stage 14, overall levels of apoptosis within the ectodermal layer have decreased. However, clusters of dying cells begin to appear below the surface of the narrow parasegments. These clusters increase in size and number at stage 15. At stage 12, cells of the narrow parasegments are seen to delaminate and move interiorly. The majority of these cells do not die until they have delaminated from the ectodermal layer, at stage 14, when the large clusters of dying cells begin to appear below the ectodermal surface.
Homozygous embryos have abnormally narrow odd-numbered parasegments at early stages of development which are eliminated at later stages.
Homozygous embryos show muscle abnormalities in abdominal segments 2 and 6. When mutant embryos are shifted to the restrictive temperature at 5 hours after egg laying most eve-expressing neurons form but the dorsal projections of motor axons are abnormal. The ISN is arrested prematurely in the ventral or dorsolateral region of the muscle field. By 9-10 hours AEL removal of eve function rarely affects ISN formation. Dorsal muscles form normally.
When eve1 embryos are shifted to the non-permissive temperature for 2 hours at early stage 11, the number of eve-expressing pericardial cells (EPCs) is reduced to on average only 24% of the wild-type number. Some of the EPCs that are present are located at some distance from the heart tube. DA1 muscle formation is also affected, but to a lesser degree. The reduction in the number of EPCs is less severe if the temperature shifts are earlier or later in development. The number of cardial cells, heart tube formation and overall body muscle formation are not significantly affected in eve1 embryos shifted to the restrictive temperature at early stage 11. Embryos shifted to the restrictive temperature at stage 11 show no morphologically detectable central nervous system defects. Temperature shifts at earlier stages perturb neural development (for example the RP2 neurons) and perturb visceral and somatic muscle formation.
Weak allele at 18oC, moderate allele at 29oC. At 18oC even-numbered denticle belts are variably deleted in homozygous embryos. At 29oC the frequency of deletions increases. At 31oC the ventral epidermis secretes a continuous lawn of denticles, which are derived from the 'fusion' of odd-numbered denticle belts. The phenotype of eve1 odd5 double homozygotes at 29oC is not an additive effect of the two mutations; the double mutant has 7 or 8 partial denticle belts, each with an apparent polarity reversal.
At the restrictive temperature of 31oC, homozygous embryos have a 'lawn of denticles' phenotype. At 25oC, homozygous embryos show a pair-rule phenotype. At 14 or 18oC, homozygous embryos show essentially normal segmentation.
Even numbered denticle bands missing.
Unsegmented lawn of denticle bands.
temperature-sensitive allele
eve1 is an enhancer of lethal | embryonic stage | maternal effect phenotype of Gug03928
eve1 is an enhancer of lethal | embryonic stage | maternal effect phenotype of Guge46-2
eve1 is an enhancer of lethal | embryonic stage | maternal effect phenotype of Gug01323a
eve1 is an enhancer of lethal | embryonic stage | maternal effect phenotype of GugrO154a
eve[+]/eve1 is an enhancer of partially lethal - majority die phenotype of trol13
eve1, ftz3-413.hs has lethal phenotype
eve1 has embryonic/first instar larval cuticle phenotype, enhanceable by Df(3R)Espl22/+
eve1 has embryonic/first instar larval cuticle phenotype, enhanceable by groE73/gro[+]
eve1 has embryonic/first instar larval cuticle phenotype, enhanceable by groE48/gro[+]
eve[+]/eve1 is an enhancer of eye phenotype of Scer\GAL4GMR.PF, fruNP0021
An eve1 background enhances the rough eye phenotype related to fru isoform B, found upon expression of fruNP0021 under the control of Scer\GAL4GMR.PF.
The number of eve1 ftz3-413.hs embryos that hatch and the number of adults eclosing is dramatically reduced compared to controls.
The severity of cuticle defects seen in eve1 embryos is increased if the mother is also heterozygous for groE48, groE73 or Df(3R)Espl22. The defects are pair rule in nature.
eve1 is partially rescued by eveE+L.8.4
eve1 is partially rescued by eveE+L.9.2
Cuticle of embryos rescued by single copy transgenes eveE+L.8.4 or eveE+L.9.2 show a high frequency of defects characteristic of hypomorphic eve mutants.
Associated with: at least one recessive mutation that affects viability, as revealed in the unrescued condition of homozygotes, compared to hemizygotes, using eveE+L.8.4 or eveE+L.9.2.
prd RNA expression has been studied in odd5 eve1 double mutant embryos.
A temperature-sensitive allele.
The authors reference FBrf0042145 for "eve[ID19]". I couldn't find "eve[ID19]" nor "eve[1]" in the retrohack of FBrf0042145, but there is another allele, eve[3] curated from that paper. In FlyBase, "eve[ID19]" has been used many times as one of the synonyms for "eve[1]", but never for "eve[3]. I checked FBrf0042145, and indeed there are more alleles of "eve" mentioned in that paper in addition to "eve[R13]" (aka eve[3]). They say that one of these vaguely described alleles (which is clearly different from "eve[R13") is a temperature sensitive allele. This description matches the description of "eve[ID19]" in the present paper as being a temperature sensitive allele, so I think it is safe to assume that "eve[ID19]" refers to eve[1] here just like in all the other relevant papers in FlyBase. ra090930.