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General Information
Symbol
Dmel\Egfrf2
Species
D. melanogaster
Name
FlyBase ID
FBal0003530
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
flbIK35, flb1k35, Egfr1K35, EgfrIK35, flbf2, top1K35, topIK35
Nature of the Allele
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
point mutation
Nucleotide change:

C21555610T

Reported nucleotide change:

C1168T

Amino acid change:

Q267term | Egfr-PA; Q316term | Egfr-PB

Reported amino acid change:

Q267term

Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Cytology
Nature of the lesion
Statement
Reference

Amino acid replacement: Q267term.

Nucleotide substitution: C1168T.

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 )
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
Statement
Reference

Egfrf2 mutant embryos show severe cardioblast (CB) patterning defects, as well as a lower generic CBs:ostial CBs ratio than the typical 4:2 ratio.

Egfrf2 heterozygous embryos exhibit severe defects in morphogenesis. More than 95% of embryos exhibit a 'faint little ball' phenotype, with the posterior end of the embryo in close proximity to the head, indicating a defect in germband retraction. In less severely 'curled' embryos, holes are visible in the dorsal surface, that typically extend anteriorly into the head.

Prior to the initiation of germband retraction, the amnioserosa of Egfrf2 mutants begins to degrade, which in the most severe cases can lead to a complete and dramatic loss of the tissue. In some embryos the amnioserosa persists throughout germband retraction and dorsal closure, but has noticeably fewer cells than wild-type. Germband retraction appears abnormal in these mutants, as does the amnioserosa, with the tissue constricting perpendicularly to the normal anterior-posterior direction.

Egfrf2 mutants exhibit defects in terminal cell lumenogenesis, with terminal cells lacking a visible gas-filled lumen and exhibiting some branching defects. Only a small percentage (approximately 15%) of Egfrf2 mutant terminal cells exhibit defective lumen.

Blood cell progenitors, nephrocytes and cardioblasts are virtually absent in mutant embryos. Significant amounts of apoptotic cell death occur in the cardiogenic mesoderm of stage 11/12 mutant embryos.

Multiple photoreceptor-R8 cells are not observed in eye tissue from Egfrf2/+ animals.

Mutant stage 9 embryos show neuroblast hypoplasia and reduced mitotic activity in the developing neuroectoderm.

Egfrf2 mutant embryos exhibit a strong tracheal invagination phenotype, where the tight accumulation of actin around the invagination edge is disrupted.

Egfrf2 Minute clones in the eye disc fail to form the arcs and rosettes of cells in the morphogenetic furrow that are seen in wild-type eye discs.

The tracheal system of Egfrf2 embryos show branch interruptions and branches with cells only connected by cytoplasmic extensions.

Egfrf2 homozygous clones in the dorsal air sac primordium grow more slowly than wild-type clones, and are found at the tip of this primordium at a significantly lower frequency than wild-type clones.

No posterior spiracles are present in Egfrf2 larvae.

Egfrf2 clones generated in the wing, using the MARCM technique, that encompass a portion of the posterior crossvein (PCV) and a large portion of the adjacent fifth longitudinal vein cause disruption of the longitudinal vein and the posterior half of the PCV. Residual PCV development can be observed outside of the clone, nearest to the remaining longitudinal veins.

In stage 16 Egfract.B.Scer\UAS; Scer\GAL4en-e16E embryos, there are increased numbers of oenocytes per cluster. The number of oenocytes per cluster follows a multi-modal distribution, with peaks corresponding to multiples of 3 (12, 15, 18 and 21) suggesting that additional rounds of delamination, generally of 3 oeoncytes per round as in wild-type, are occurring. This multi-modal distribution and increased numbers of per cluster are partially suppressed by Egfrf2/+.

Egfrf2 embryos show a disorganization of and a significant loss of lateral ventral cluster sensory neurons in all hemisegments.

Heterozygous females lay eggs with fused or partially fused dorsal appendages (27.8% at 18oC, 24.6% at 25oC and 51.4% at 29oC).

In mutants the hindgut tube is much shortened due to a reduction of the cell number.

Homozygous mutant clones in the adult abdomen alter the distribution of bristles, but the polarity is normal.

Egfrf2 clones induced in the wing disc in a Minute background during the first or early second instar contribute only to the prospective wing blade, while clones induced in the Minute background during the late second and early third instar can also contribute to the wing hinge and medial notum. Egfrf2 clones are not found in the prospective lateral notum. Homozygous clones generated before the second larval instar (before dorsoventral compartmental segregation has occurred) show an extreme preference for the ventral compartment of the wing disc. Homozygous clones generated after dorsoventral compartmental segregation has occurred are restricted to either the dorsal or ventral compartment of the wing disc and survive equally well in either compartment. In rare cases dorsally situated clones in the wing disc from an ectopic ventral compartment.

Intermediate neuroblasts do not form in mutant embryos and medial and lateral neuroblasts lie next to each other.

Within homozygous somatic clones, the spacing of photoreceptor cell R8 cells is irregular. R8 cells usually form several cells away from their neighbours. The R8 cells are less apically restricted than wild type R8 cells.

Egfrf2 embryos have an average of 3.03 +/- 0.03 neurons per lch5 organ.

Heterozygotes show a quantitative effect on wing shape in intervein regions B and C compared to wild type.

Homozygous clones in the eye disc have contain excess R8 cell precursors which are in a less organised pattern than in wild-type discs. Excess cell death is associated with the clones, predominantly posterior to the morphogenetic furrow. Homozygous clones that extend to the margin of the eye disc cause impaired disc growth and excess cell death.

Homozygous embryos have a reduced number of cells in both the anterior and posterior Malpighian tubules compared to wild-type embryos. No BrdU incorporation occurs in the outbudding tubules at a time when cells divide in wild-type embryos.

All RP2 and RP2sib neurons are missing. Intermediate neuroblast column does not form. The development of neuroblast 2-5 is unaffected, neuroblast 1-1 is consistently mis-specified at a low frequency and the intermediate neuroblast 3-2 is absent. Neuroblast 5-2 and 7-1 are affected, with medial 7-1 acquiring characteristics of its lateral neighbor. A significant fraction of medial neuroblasts fail to activate their appropriate gene expression profile. The medial MP2 neuroblast is often incorrectly specified: 50% acquire traits characteristic of other neuroblasts.

The eg/en positive NB 7-3 cluster is missing in most hemineuromeres. In 10% of hemineuromeres neuroblast NB1-1 or NB7-1 are missing. In 97% of hemineuromeres the RP2/RP2sib neuroblasts are missing. GMC4-2a is also missing at earlier stages. 56% of hemineuromeres lack NB7-3. Cells from Egfrf2 mutant embryos have been used to demonstrate that Egfr is cell-autonomously required for the formation of intermediate NB lineages, is dispensable for the formation of lateral NB lineages, and is required for heterotopically transplanted dorsal NE cells to assume ventral NB identities, though not for assuming midline fate.

Germline clones reveal no requirement for Egfr in the oocyte in patterning the egg, or in the viability or patterning of the embryo.

Transheterozygous females with Egfrt1 or Egfrt2 display egg chambers with gaps in the follicular epithelium that uncover the nurse cells. Eggs derived from these females display weak or intermediate ventralised phenotypes.

Enhances the female sterility and adult morphological defects of Egfrt1. Rarely survives as transheterozygote with the semi-viable Egfrtop-CA allele.

Malpighian tubules in homozygous embryos are four tiny outpushings of the posterior hindgut. Reduction in size of the tubules is due to reduction in cell number, not cell death.

No changes in phenotype of tor13D embryos.

Homozygotes and hemizygotes display a severe 'flb' phenotype. Embryos produced from heteroallelic combination with Egfrt1 have a severe ventralised phenotype, reduction in size of their dorsal appendage.

severe allele

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

Egfr[+]/Egfrf2 is an enhancer of neuroanatomy defective | adult stage phenotype of atoSA-KI

Egfr[+]/Egfrf2 is an enhancer of size defective | adult stage phenotype of sl2

NOT Enhancer of
Statement
Reference

Egfr[+]/Egfrf2 is a non-enhancer of visible phenotype of Caf1-105NIG.12892R, Scer\GAL4ey.PH

Egfr[+]/Egfrf2 is a non-enhancer of size defective | adult stage phenotype of sl9

Egfrf2 is a non-enhancer of visible phenotype of Pp2B-14Dact.GMR

Suppressor of
Statement
Reference
NOT Suppressor of
Statement
Reference

Egfrf2 is a non-suppressor of decreased cell death phenotype of Ras85DR68Q

Egfrf2 is a non-suppressor of lethal | pupal stage phenotype of Cskj1D8/CskS030003

Egfrf2 is a non-suppressor of visible phenotype of Pp2B-14Dact.GMR

Other
Phenotype Manifest In
Enhanced by
Statement
Reference

Egfrf2 has dorsal appendage phenotype, enhanceable by CSN5L4032/CSN5[+]

Egfrf2 has phenotype, enhanceable by ebiunspecified/ebi[+]

Suppressed by
NOT suppressed by
Statement
Reference

Egfrf2 has phenotype, non-suppressible by eRF1[+]/eRF1F2

Enhancer of
Statement
Reference

Egfr[+]/Egfrf2 is an enhancer of eye photoreceptor cell phenotype of atoSA-KI

Egfr[+]/Egfrf2 is an enhancer of wing blade phenotype of sl2

Egfr[+]/Egfrf2 is an enhancer of eye phenotype of armS56F.GMR

Egfr[+]/Egfrf2 is an enhancer of ommatidium phenotype of SosJC2, sev6

Egfr[+]/Egfrf2 is an enhancer of photoreceptor cell R7 phenotype of SosJC2, sev6

Egfr[+]/Egfrf2 is an enhancer of ommatidium phenotype of SosJC2/Sos[+], sev6

Egfr[+]/Egfrf2 is an enhancer of photoreceptor cell R7 phenotype of SosJC2/Sos[+], sev6

Egfrf2 is an enhancer of eye phenotype of hidGMR.PG/WGMR.PG

Egfrf2 is an enhancer of ommatidium phenotype of hidGMR.PG/WGMR.PG

NOT Enhancer of
Statement
Reference

Egfr[+]/Egfrf2 is a non-enhancer of eye phenotype of Caf1-105NIG.12892R, Scer\GAL4ey.PH

Egfr[+]/Egfrf2 is a non-enhancer of wing blade phenotype of sl9

Egfr[+]/Egfrf2 is a non-enhancer of chemosensory ventral triple row & microchaeta | ectopic phenotype of ed4.12

Egfr[+]/Egfrf2 is a non-enhancer of dorsal triple row & microchaeta | ectopic phenotype of ed4.12

Egfr[+]/Egfrf2 is a non-enhancer of dorsocentral bristle | ectopic phenotype of ed4.12

Egfr[+]/Egfrf2 is a non-enhancer of scutellar bristle | ectopic phenotype of ed4.12

Egfrf2 is a non-enhancer of eye phenotype of Pp2B-14Dact.GMR

Egfrf2 is a non-enhancer of phenotype of Rho1rev220

Suppressor of
Statement
Reference

Egfr[+]/Egfrf2 is a suppressor | partially of wing vein | ectopic phenotype of sl2

Egfr[+]/Egfrf2 is a suppressor | partially of ommatidium phenotype of sl9

Egfr[+]/Egfrf2 is a suppressor of interommatidial bristle phenotype of sl9

Egfr[+]/Egfrf2 is a suppressor of photoreceptor cell R8 | supernumerary phenotype of ed4.12

Egfrf2 is a suppressor | partially of eye phenotype of sevS11.Tag:MYC

Egfr[+]/Egfrf2 is a suppressor of photoreceptor cell R7 | ectopic phenotype of sl1

Egfr[+]/Egfrf2 is a suppressor of photoreceptor cell R7 | ectopic phenotype of sl2

Egfrf2 is a suppressor of phenotype of rhohs.sev

Egfrf2 is a suppressor of phenotype of S218

NOT Suppressor of
Statement
Reference

Egfrf2 is a non-suppressor of wing vein | ectopic phenotype of Ras85DR68Q

Egfrf2 is a non-suppressor of eye phenotype of Ras85DR68Q

Egfrf2 is a non-suppressor of midline glial cell phenotype of Ras85DR68Q

Egfrf2 is a non-suppressor of ommatidium phenotype of Ras85DR68Q

Egfrf2 is a non-suppressor of wing phenotype of Ras85DR68Q

Egfrf2 is a non-suppressor of posterior crossvein phenotype of Ras85DR68Q

Egfrf2 is a non-suppressor of crossvein phenotype of Ras85DR68Q

Egfrf2 is a non-suppressor of wing vein L4 phenotype of Ras85DR68Q

Egfrf2 is a non-suppressor of wing vein L5 phenotype of Ras85DR68Q

Egfr[+]/Egfrf2 is a non-suppressor of chemosensory ventral triple row & microchaeta | ectopic phenotype of ed4.12

Egfr[+]/Egfrf2 is a non-suppressor of dorsal triple row & microchaeta | ectopic phenotype of ed4.12

Egfr[+]/Egfrf2 is a non-suppressor of dorsocentral bristle | ectopic phenotype of ed4.12

Egfr[+]/Egfrf2 is a non-suppressor of scutellar bristle | ectopic phenotype of ed4.12

Egfrf2 is a non-suppressor of eye phenotype of Pp2B-14Dact.GMR

Egfrf2 is a non-suppressor of phenotype of Rho1rev220

Other
Additional Comments
Genetic Interactions
Statement
Reference

Egfrf2 heterozygosity partially suppresses the highly prevalent duplication of mesanotum structures observed upon the expression of domeKK104700 under the control of Scer\GAL4sd.PU (and Dicer-2, for more efficient RNAi).

The reduced number of photoreceptor neurons per ommatidium characteristic for atoSA-KI mutants is further decreased by combination with a single copy of Egfrf2 and majority of the ommatidia contain only the R8 photoreceptor cell.

One copy of Egfrf2 does not enhance the small eye phenotype seen when Caf1-105NIG.12892R is expressed under the control of Scer\GAL4ey.PH.

One copy of Egfrf2 enhances the reduction in wing blade area seen in homozygous sl2 males.

One copy of Egfrf2 does not enhance the reduction in wing blade area seen in homozygous sl9 males.

One copy of Egfrf2 partially suppresses the ectopic wing vein phenotype seen in sl2 homozygotes.

One copy of Egfrf2 partially suppresses the percentage of sl2 mutant ommatidia that contain extra R7 photoreceptors.

The multiple photoreceptor-R8 phenotype seen in rno1 or rno1, Rbf15aΔ eye somatic mutant clones is not significantly affected by Egfrf2/+.

More than 90% of dm1/+ ; Egfrf2/+ embryos show severe defects in the nervous system at stage 17.

Expression of cv-cScer\UAS.cDa, under the control of Scer\GAL469B partially suppresses the Egfrf2 mutant invagination phenotype.

Df(3L)H99; Egfrf2 embryos, in which cell death is prevented, still show the same tracheal branch integrity phenotype as Egfrf2 single mutant embryos.

Border cells which are part of somatic clones of Pvr1; Egfrf2 double homozygous cells initiate migration, but fail to reach the oocyte.

The ed4.12 R8 cell twinning phenotype is strongly suppressed by Egfrf2/+. Egfrf2 clones in the eye disc induced in a homozygous ed4.12 background show abnormal spacing of R8 cells in the clone, but R8 cells rarely appear twinned. Twinned R8 cells can be observed in Egfrf2 scaBP2 double mutant clones in the eye disc.

The fused dorsal appendage phenotype of eggs laid by Egfrf2/+ females is weakly enhanced if the females are also heterozygous for CSN5L4032.

The photoreceptor cell R8 cells in Egfrf2, scaunspecified double mutant somatic clones are much closer to their neighbours than in Egfrf2 clones.

The rough eye phenotype caused by sevS11.T:Hsap\MYC is partially suppressed by one copy of Egfrf2.

In sev6 hemizygotes that are also heterozygous for SosJC2, 14.7% of ommatidia contain R7 cells. This phenotype is dominantly enhanced by Egfrf2.

The number of cells in the Malpighian tubules in Egfrf2 embryos is restored to a considerable extent by svpI.Scer\UAS or svpII.Scer\UAS expressed in the tubule primordium using Scer\GAL4unspecified.

Eye supernumerary R7 cell phenotype of sl1 and sl2 is almost completely suppressed by reducing the dosage of Egfr.

No effect on the faf eye phenotype.

Weak suppressor of the rough eye phenotype caused by two insertions of P{GMR-Rho1}.

Xenogenetic Interactions
Statement
Reference

The reduced growth and failure to localise to the primodium tip seen in Egfrf2 homozygous clones in the dorsal air sac primordium are both suppressed if the clone are also BacA\p35Scer\UAS.cHa; Scer\GAL4αTub84B.PL (Scer\GAL80/MARCM technique).

Complementation and Rescue Data
Fails to complement
Comments
Images (0)
Mutant
Wild-type
Stocks (2)
Notes on Origin
Discoverer

Selected as: Embryonic lethal.

Comments
Comments

Mutation of Egfr that coordinately affects all gene activities, a class I lesion. The allelic series for class I lesions: Egfrt2 = Egfrt1 < Egfrtop-EC20 < Egfrf7 = Egfrf1 = Egfrflb-2E07 < Egfrtop-EE39 = Egfrtop-ED26 = Egfrf5 < Egfrf9 = Egfrf10 = Egfrf2 = Egfrtop-EE42 = Egfrf11 = Egfrf24 = Egfrf3 = Df(2R)Egfr3.

Germline clone analysis indicates that there is very little, if any, requirement for Egfr in the germline.

Severe mutation.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (30)
Reported As
Symbol Synonym
flb
Name Synonyms
faint little ball
Secondary FlyBase IDs
    References (94)