Nucleotide substitution: C3844T. Amino acid replacement: P1113L.
Amino acid replacement: P1112L.
Nucleotide substitution: C3335T. Amino acid replacement: P1112L. (numbering relates to the type II 5' splicing alternative, FBrf0043895). This amino acid residue is in the tyrosine kinase domain.
C21558286T
C3844T
P1113L | Egfr-PA; P1162L | Egfr-PB
P1113L
Egfrf1 homozygous mutant embryos transferred from 18[o]C to 29[o]C at any stage prior to stage 10 show severe cuticle defects. Shifting slightly older (approx. stage 11) Egfrf1 mutant embryos to 29[o]C, however, results in a less severe mutant phenotype comprising a smaller head hole, distinct from other defects in the dorsal surface, and a less severe defect in germband retraction. In addition, these embryos consistently display creases or 'puckers' in the dorsal surface, which together with the mild germband retraction defect, gave them a bowed appearance. Approximately 52% of Egfrf1 embryos exhibit a bowed phenotype in a temperature shift experiment where a 2.5hr collection of embryos is aged at 18[oc for 12 hours and then shifted to 29[o]C (corresponding to later stage 10/11 at the time of the temperature shift). Of these bowed embryos, half exhibit an additional phenotype of a hole or scab in the dorsal surface. Few defects are seen in the dorsal surface of Egfrf1 embryos when they are shifted to 29[o]C at stage 12 or later.
In Egfrf1 stage 15 embryos, the genital disc precursor cells are completely missing.
When mutants are raised to the non-permissive temperature at ES 9, then a strong loss of midbrain phenotype is seen. When Egfr is removed at late ES 12, there is no gross loss of midbrain, however the circumesophageal connectives are sometimes disrupted.
Heat pulses between 3 and 6 hours of development in Egfrf1 embryos result in defects in head development, but leave the visual system intact. Heat pulses at 6-8 hours of development result in non-disjunction of the Bolwig's organ and optic lobe. Heat pulses from 8-10 hours of development do not affect optic placode morphogenesis but result in a reduction in Bolwig's neurons.
Leg disc development is severely affected when the temperature is increased to the restrictive temperature at 6 hours after egg laying (AEL). Only a mild defect is found in leg discs when embryos are shifted to the restrictive temperature at 7 hours AEL.
When Egfrf1/Egfrt1 flies are raised at the non-permissive temperature (29oC)a vein-loss phenotype is seen. There is a large truncation in wing vein L4 which is similar to the Egfrt1/Deficiency phenotype. This phenotype is seen if heat shocking occurs from 6 to 18 hours APF (after puparium formation).
Egfrf1 embryos grown at 25oC generates a hypomorphic, embryonic lethal phenotype.
Embryos shifted to 29oC at 6-7 hours of development fail to develop the LL1 muscle precursor. Embryos shifted to 29oC at 5-6 hours of development fail to develop the LL1, DA1 and VA2 muscle precursors.
Shifting mutant embryos to the restrictive temperature after germ band retraction causes abnormal midgut development.
sna-positive neuroblasts are often missing in homozygous embryos. Loss of RP2 motor neurons is also seen.
Homozygous embryos shifted to the restrictive temperature (25oC) at 6 hours of development give rise to larvae with residual denticle belts in their abdomens, often with 2-4 disordered rows of tapered denticles per belt. The regions of naked cuticle in between the denticle belts tend to be wider than in wild-type embryos.
Embryonic muscle pattern is severely disrupted.
Homozygotes exhibit complete absence of ventral denticle belts.
Homozygotes show a severe embryonic lethal phenotype at 29oC and a weak embryonic lethal phenotype at 18oC. Enhances the female sterility and adult morphological defects of Egfrt1. Rarely survives as transheterozygote with the semi-viable Egfrtop-CA allele.
Embryos shifted from the restrictive temperature to the permissive temperature after 5 hours of development display defective germband retraction and defective dorsal/ventral patterning. The cell fate of ventral cells is shifted to lateral cells.
Partially suppresses the "Ellipse" phenotype at both restrictive and permissive temperatures.
Homozygotes show a weak zygotic embryonic lethal phenotype at the permissive temperature (18oC). They show a moderate or severe embryonic lethal phenotype, with all denticles being reduced in size at the restrictive temperature (29oC).
At the permissive temperature, homozygous Egfrf1 embryos do not hatch, but the cuticle and CNS is similar to wild-type. At the restrictive temperature the cuticle and CNS show a severe phenotype, comparable to null Egfr alleles: the germ band does not retract, and the longitudinal axon tracts of the CNS are disarrayed. Temperature shifts at different times show that the phenotype can be dissected into at least five temporally and spatially distinct components, which affect many processes, including germ band retraction, CNS development, differentiation of cuticle secreting epidermal cells, differentiation of head structures, and differentiation and survival of midline glial cells.
Homozygotes and hemizygotes display a weak 'flb' phenotype. Embryos produced from heteroallelic combination with Egfrt1 have a severe ventralised phenotype, reduction in size of their dorsal appendage.
Weak lethal phenotype: embryos lack some head and telson structures and have some development of the ventral cuticle.
weak allele
Egfrf1 has somatic muscle cell | embryonic stage phenotype, enhanceable by SIIN
Egfrf1, spi1 has somatic muscle cell | embryonic stage phenotype, enhanceable by S[+]/SIIN
Egfrf1, SIIN has somatic muscle cell | embryonic stage phenotype, enhanceable by spi1
Egfrf1 has ventral denticle belt phenotype, suppressible by aope2d
Egfrf1 is an enhancer of ommatidium phenotype of gro1
Egfrf1 is an enhancer of interommatidial bristle phenotype of gro1
Egfrf1 is an enhancer of prothoracic leg phenotype of gro1
When Egfrf1/Egfrt1; rhove-1/rhove-1 flies are raised at the permissive temperature (18oC) a wing vein phenotype is seen that is similar to (but slightly more severe than) rhove-1/rhove-1 alone; wing veins L4 and L5 have prominent distal truncations, L2 and L3 remain largely intact. When raised at the non-permissive temperature (29oC) there is an enhancement of the wing vein phenotype with all wing veins showing major truncations. This phenotype is seen if heat shocking occurs from 0 to 24 hours APF (after puparium formation).
Enhances the eye reduction phenotype caused by WGMR.PG.
Egfrf1; gro1/gro1 flies display an enhanced gro phenotype: ectopic compound eyes, fused or bifurcated legs. These phenotypes are almost exclusively restricted to males. The ectopic eyes are organised into arrays of ommatidia. They are frequently adjacent to the endogenous eye but separated by a discrete border and exhibit defects in ommatidial packing and the distribution of interommatidial bristles.
Does not alter the denticle phenotype of wgl-17 larvae.
Selected as: Embryonic lethal.
Weak allele.
Temperature shift analysis identifies two distinct times at which Egfr is required for embryonic development. Germline clone analysis indicates that there is very little, if any, requirement for Egfr in the germline.
Class I allele.