Amino acid replacement: W15R. Amino acid replacement: L24V. Amino acid replacement: A887T. Figure 1 and the text concerning this allele are at odds - the text is correct (note from N. Baker).
T21523131C
T43C
W15R | Egfr-PA
W15R
One of three nucleotide substitutions affecting the amino acid sequence in the EgfrE3 mutant relative to the reference sequence.
G21557607A
G3165A
A887T | Egfr-PA; A936T | Egfr-PB
A887T
One of three nucleotide substitutions affecting the amino acid sequence in the EgfrE3 mutant relative to the reference sequence.
C21523158G
C70G
L24V | Egfr-PA
L24V
One of three nucleotide substitutions affecting the amino acid sequence in the EgfrE3 mutant relative to the reference sequence.
EgfrE3/+ produces a small rough eye phenotype compared with wild-type.
Adult wings carrying EgfrE3 mutations exhibit extra wing veins.
EgfrE3/+ adults have extra vein tissue at the distal end of L2.
EgfrE3/+ mutants have eyes that are reduced in size with fewer photoreceptors than wild type. Additionally these mutants have, on average, more than two extra crossveins at the tip of L2 in the wing. EgfrE3/Egfrt1 transheterozygotes show a less severe wing phenotype, with the majority of flies exhibiting either no, or one extra crossvein. This phenotype is reduced further in EgfrE3/Egfrtop-18A transheterozygotes, with the vast majority of flies showing no extra crossveins. Flies that are EgfrE3/+ and also carry the deficiency Df(3L)Ar14-8 have a slightly reduced wing phenotype, with a quarter of flies exhibiting no extra crossveins, while a quarter of these flies still exhibit more than two extra crossveins in the wing.
Eye of EgfrE3/+ heterozygotes is rough. Extra wing veins form.
Few ommatidia are seen in homozygous eye discs, in a background of G2-arrested cells. Some mitotic cells are seen adjacent to differentiating ommatidia. Apoptotic cells are seen in columns 7-15 of the developing eye disc.
Mutant flies develop wing with ectopic wing material. EgfrE3 dominantly causes an abnormal eye phenotype. The eye is rough lacking the occasional outer photoreceptor.
Heterozygous mutant wings have ectopic wing vein material.
Heterozygous mutants do not cause any defects in the ocellar sensory system (OSS) neurogenesis or axon guidance.
Heterozygous flies have rough eyes and show a slight overproduction of wing vein material. The eyes of homozygotes are severely reduced in size and contain very few ommatidia. Homozygotes are poorly viable.
Homozygous embryos have slightly more midline glia cells than normal, at least until stage 15. Homozygous first instar larvae have a normal number of midline glia.
Extra wing veins close to the wing margin.
Clonal analysis reveals phenotypes in the adult including loss of wing vein, ectopic wing vein, reduced cell size, extra bristles, cell lethality and tergite bristle abnormalities. Phenotype is cell autonomous. rl1/Df(2R)rl10a suppresses the wing phenotype of EgfrE3.
Rough eye phenotype, which is characterised by disorganised ommatidia and reduction in the size of the eye.
Eyes are reduced and roughened.
Eyes contain only 10% of normal ommatidial complement. This is first evident in the imaginal disc where areas of ommatidia are separated by large distances creating completely isolated groups of ommatidia. Axons from these isolated photoreceptor clusters with no near neighbours can project to the larval brain via the optic stalk.
Homozygous clones in the eye disc are rescued by surrounding heterozygous or wild type cells.
Homozygous eye discs have fewer ommatidia than wild-type. Outgrowth of photoreceptor axons is disturbed, occurring in many directions. Cell death is abundant in the region approximately corresponding to columns 10-15 in wild-type. The pattern of cell division in the eye disc is altered. In the adult eye the ommatidia are separated by numerous pigment cells and mechanosensory bristles. Wing veins show thickening and plexus formation. The eye and wing phenotype is more extreme in the homozygote than the heterozygote.
A morphogenetic furrow crosses the eye disc in homozygotes, but very few ommatidia form. Adults have smaller eyes than normal, with a small number of ommatidia, many of which have the normal cellular constitution. Ommatidia are separated by pigment cells and bristle organs.
The array of ommatidia is less regular in heterozygotes than in wild-type flies, and there is a slight disturbance in the wing vein pattern. Homozygotes have much smaller eyes than normal, containing many fewer ommatidia, and some regions lack ommatidia entirely. These regions contain cells resembling the pigment cells that normally surround each ommatidium, and also mechanosensory bristles. Most ommatidia contain the normal number and arrangement of cells.
EgfrE3 has visible | dominant phenotype, suppressible by brmK804R.Tag:HA/brm[+]
EgfrE3 has visible phenotype, suppressible by Ppm1UAS.Tag:HA/Scer\GAL4Bx-MS1096
EgfrE3 has visible | semidominant phenotype, suppressible by ShcBG/Shc[+]
EgfrE3 has visible | semidominant phenotype, suppressible by Shc111-40/Shc[+]
EgfrE3 has visible phenotype, non-suppressible by Ppm1D228A.UAS.Tag:HA/Scer\GAL4Bx-MS1096
EgfrE3 has increased cell death | larval stage phenotype, non-suppressible by Hsap\CDKN1AGMR.PH
EgfrE3 has eye phenotype, enhanceable by geminin[+]/geminink03202b
EgfrE3 has wing vein phenotype, enhanceable by ash2S112411/ash2S112411
EgfrE3 has wing phenotype, enhanceable by ash2S112411/ash2S112411
EgfrE3 has wing vein | increased number phenotype, enhanceable by ed[+]/ed1X5
EgfrE3 has phenotype, enhanceable by netunspecified/netunspecified
EgfrE3 has phenotype, enhanceable by pxunspecified/pxunspecified
EgfrE3 has eye phenotype, suppressible by brmK804R.Tag:HA/brm[+]
EgfrE3 has wing vein | ectopic phenotype, suppressible by Ppm1UAS.Tag:HA/Scer\GAL4Bx-MS1096
EgfrE3 has crossvein | increased number phenotype, suppressible by Pcyt116919/Cct1[+]
EgfrE3 has crossvein | increased number phenotype, suppressible by Scer\GAL4sd-SG29.1/Pcyt1Ala.UAS
EgfrE3 has crossvein | increased number phenotype, suppressible by Cct1[+]/Pcyt1EP831
EgfrE3 has eye photoreceptor cell phenotype, suppressible by Pcyt116919/Cct1[+]
EgfrE3 has wing | ectopic phenotype, suppressible by Scer\GAL432B/kayFbz.UAS
EgfrE3 has wing vein | ectopic phenotype, suppressible by Sps1k11320
EgfrE3 has phenotype, suppressible by rhounspecified/rhounspecified
EgfrE3 has phenotype, suppressible by kniunspecified/kniunspecified
EgfrE3 has wing vein | ectopic phenotype, non-suppressible by Ppm1D228A.UAS.Tag:HA/Scer\GAL4Bx-MS1096
EgfrE3 has eye disc | larval stage phenotype, non-suppressible by Hsap\CDKN1AGMR.PH
EgfrE3/Egfr[+] is an enhancer of wing phenotype of ash2S112411
EgfrE3/Egfr[+] is an enhancer of wing vein | ectopic phenotype of ash2S112411
EgfrE3/Egfr[+] is an enhancer of wing vein | increased number phenotype of Mkp31/Mkp32
EgfrE3/EgfrE3 is an enhancer of phenotype of netunspecified
EgfrE3/Egfr[+] is a non-enhancer of axon & ocellus sensory structure phenotype of Scer\GAL4sca-537.4, htlDN.UAS.cMb
EgfrE3/EgfrE3 is a suppressor | partially of wing vein phenotype of rhounspecified, vnunspecified
EgfrE3/Egfr[+] is a suppressor of phenotype of kniunspecified
EgfrE3/Egfr[+] is a non-suppressor of axon & mechanosensory neuron & adult head phenotype of Scer\GAL4sca-537.4, htlDN.UAS.cMb
The small rough eye phenotype of EgfrE3/+ is suppressed by expression of the brmK804R.T:Ivir\HA1 genomic construct.
The small rough eye phenotype of EgfrE3/+ is suppressed by brm2/+.
geminink03202b/+ enhances the EgfrE3/+ small rough eye phenotype.
EgfrE3/+ adults have extra vein tissue at the distal end of L2. This phenotype is enhanced by ash2S112411/ash2S112411 - the resulting wings are more reduced and have more ectopic veination than ash2S112411/ash2S112411 animals.
EgfrE3/+, Cct116919/+ double mutants show reduced loss of photoreceptors in the eye compared to EgfrE3/+ single mutants. Additionally, the eyes of the double mutants show a more regular arrangement of ommatidia. The extra crossvein phenotype seen in the wings of EgfrE3/+ flies is partially suppressed in Cct1EP831/+, EgfrE3/+ double mutants, with the majority of these flies exhibiting two, rather than several, extra crossveins. This phenotype is further suppressed in Cct116919/+, EgfrE3/+ double mutants, with the majority of these flies exhibiting no, or only one, extra crossvein in the wing. Further, the expression of Cct1Ala.Scer\UAS under the control of Scer\GAL4sd-SG29.1 also partially suppresses the EgfrE3 wing phenotype. The EgfrE3 allele dominantly enhances the notched wing phenotype seen in N55e11/+ flies.
The number of ommatidia in the eyes of EgfrE1/EgfrE3 adults is not altered if the flies are also expressing BacA\p35GMR.PH, but the number of pigment cells is increased in these animals.
The addition of SelDk11320/+ to EgfrE3/+ animals leads to a complete suppression of the ectopic wing phenotype in 66% of wings and a partial suppression in the rest.
Heterozygous mutants do not cause any defects in the ocellar sensory system (OSS) neurogenesis or axon guidance.
25 minutes of heat induced stghs.PE3 expression causes mitotic cell appearance in the eye and wing discs. Induction of mitosis in the eye discs leads to a marked reduction of pyknotic bodies that were normally present on the basal side of the discs. Cellular progression into and through apoptosis is disrupted by ectopic stg expression. Heat induced stg expression does not affect the mutant eye phenotype: adults exhibit small elliptical and rough eyes as seen in EgfrE3 homozygotes.
Reduction of the dose of spi causes some suppression of the EgfrE3 phenotype; more ommatidia and increase in the size of the eye. S218 EgfrE3 double heterozygous adults exhibit severely reduced and rough eyes. Most ommatidia have a reduced number of photoreceptor cells, there are also defects in orientation, spacing and pigment cell and bristle numbers. This phenotype is more severe than a simple addition of the dominant effects of Egfr and S. Mutation has no effect on rhohs.sev rough eye phenotype.
Enhances the wing phenotype of Df(1)N-54l9, N264-39, Dl9P, and DlKX6 mutations, and the eye phenotype of Nspl-1.
Double mutant combinations of EgfrE3/EgfrE3 with netunspecified/netunspecified or px1/px1 have a superadditive phenotype. EgfrE3/EgfrE3 shows a negative interaction in combination with either rhounspecified/rhounspecified or kniunspecified/kniunspecified. EgfrE3/+ shows a negative interaction in combination with either H2/+ or Vnounspecified/+. EgfrE3/EgfrE3 shows a simple additive phenotype with tt1/tt1 and NAx-M1/+. EgfrE3/+ shows a simple additive phenotype with N55e11/+ and DlM1/+. E(spl)rv1 grounspecified EgfrE3/EgfrE3 flies show a simple additive phenotype. The lack of vein phenotype of rhounspecified vnunspecified flies is partially rescued by EgfrE3/EgfrE3.
Expression of Hsap\CDKN1AGMR.PH in homozygous EgfrE3 mutants does not prevent the apoptosis of undifferentiated cells in the eye disc that is seen in the EgfrE3 mutant background.
Expression of Egfr1.Scer\UAS under the control of Scer\GAL4GMR.PF in EgfrE3 flies results in mitosis in all cells in the eye disc. Expression of stghs.PE3 using heat shock in EgfrE3 discs causes all G2-arrested cells to enter mitosis. This mitosis is abnormal, with the cells remaining in mitosis for 4 hours (mitosis normally lasts about 15 minutes). Extensive cell death occurs amongst the mitotically arrested cells from 2-4 hours, so that some of the disc epithelium is lost.
Clonal analysis shows that normal ommatidia are less likely to develop if precluster cells R2, R3, R4, R5 or R8 are EgfrE3/EgfrE3.
Egfr protein expression in the eye imaginal discs of EgfrE3 homozygous third instar larvae has been compared with wild-type expression. The pattern of cell divisions posterior to the morphogenetic furrow is altered in EgfrE3 homozygotes.
No interaction with P{sev-svp1} or P{sev-svp2} exists.