FlyBase Allele Report: Dmel\Egfr[f2]

Egfr^f2 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 Egfr^f2 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.

(Shen et al., 2013)

Egfr^f2 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 Egfr^f2 mutant terminal cells exhibit defective lumen.

(Ruiz et al., 2012)

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.

(Grigorian et al., 2011)

Multiple photoreceptor-R8 cells are not observed in eye tissue from Egfr^f2/+ animals.

(Steele et al., 2009)

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

(Orian et al., 2007)

Egfr^f2 mutant embryos exhibit a strong tracheal invagination phenotype, where the tight accumulation of actin around the invagination edge is disrupted.

(Brodu and Casanova, 2006)

Egfr^f2 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.

(Brown et al., 2006)

The tracheal system of Egfr^f2 embryos show branch interruptions and branches with cells only connected by cytoplasmic extensions.

(Cela and Llimargas, 2006)

Egfr^f2 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.

(Cabernard and Affolter, 2005)

No posterior spiracles are present in Egfr^f2 larvae.

(Merabet et al., 2005)

Egfr^f2 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.

(Ralston and Blair, 2005)

In stage 16 Egfr^{act.B.Scer\UAS}; Scer\GAL4^en-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 Egfr^f2/+.

(Brodu et al., 2004)

Egfr^f2 embryos show a disorganization of and a significant loss of lateral ventral cluster sensory neurons in all hemisegments.

(Sepp and Auld, 2003)

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

(Doronkin et al., 2002)

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

(Fusse and Hoch, 2002)

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

(Lawrence et al., 2002)

Egfr^f2 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. Egfr^f2 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.

(Zecca and Struhl, 2002)

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

(Zhao and Skeath, 2002)

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.

(Baonza et al., 2001)

Egfr^f2 embryos have an average of 3.03 +/- 0.03 neurons per lch5 organ.

(Rusten et al., 2001)

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

(Palsson and Gibson, 2000)

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.

(Dominguez et al., 1998)

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.

(Kerber et al., 1998)

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.

(Skeath, 1998)

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 Egfr^f2 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.

(Udolph et al., 1998)

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

(Wasserman and Freeman, 1998)

Transheterozygous females with Egfr^t1 or Egfr^t2 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.

(Goode et al., 1996)

Enhances the female sterility and adult morphological defects of Egfr^t1. Rarely survives as transheterozygote with the semi-viable Egfr^top-CA allele.

(Clifford and Schupbach, 1994)

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.

(Baumann and Skaer, 1993)

No changes in phenotype of tor^13D embryos.

(Strecker et al., 1991)

Homozygotes and hemizygotes display a severe 'flb' phenotype. Embryos produced from heteroallelic combination with Egfr^t1 have a severe ventralised phenotype, reduction in size of their dorsal appendage.

(Clifford and Schupbach, 1989)

severe allele

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Suppressed by

Statement

Reference

Egfr^f2 has decreased cell number | somatic clone phenotype, suppressible by Scer\GAL4^αTub84B.PL/BacA\p35^UAS.cHa

(Cabernard and Affolter, 2005)

Egfr^f2 has decreased cell number | embryonic stage phenotype, suppressible by Scer\GAL4^unspecified/svp^II.UAS

(Kerber et al., 1998)

Egfr^f2 has decreased occurrence of cell division | embryonic stage phenotype, suppressible by Scer\GAL4^unspecified/svp^II.UAS

(Kerber et al., 1998)

Egfr^f2 has decreased cell number | embryonic stage phenotype, suppressible by svp^I.UAS/Scer\GAL4^unspecified

(Kerber et al., 1998)

Egfr^f2 has decreased occurrence of cell division | embryonic stage phenotype, suppressible by svp^I.UAS/Scer\GAL4^unspecified

(Kerber et al., 1998)

Enhancer of

Statement

Reference

Egfr[+]/Egfr^f2 is an enhancer of visible | adult stage phenotype of Scer\GAL4^lz-gal4, Shrm^A.UAS

(Hildebrand et al., 2021)

Egfr[+]/Egfr^f2 is an enhancer of neoplasia | spermatogenesis phenotype of E(Pc)^JF03101, Scer\GAL4^NP1624

(Feng et al., 2017)

Egfr[+]/Egfr^f2 is an enhancer of abnormal neuroanatomy | adult stage phenotype of ato^SA-KI

(Quan et al., 2016)

Egfr[+]/Egfr^f2 is an enhancer of abnormal size | adult stage phenotype of sl²

(Murillo-Maldonado et al., 2011)

Egfr^f2 is an enhancer of visible phenotype of CanB^GMR.PS, Pp2B-14D^act.GMR

(Sullivan and Rubin, 2002)

NOT Enhancer of

Statement

Reference

Egfr[+]/Egfr^f2 is a non-enhancer of visible phenotype of Caf1-105^NIG.12892R, Scer\GAL4^ey.PH

(Yu et al., 2013)

Egfr[+]/Egfr^f2 is a non-enhancer of abnormal size | adult stage phenotype of sl⁹

(Murillo-Maldonado et al., 2011)

Egfr[+]/Egfr^f2 is a non-enhancer of increased cell number | third instar larval stage | somatic clone phenotype of rno¹

(Steele et al., 2009)

Egfr[+]/Egfr^f2 is a non-enhancer of increased cell number | third instar larval stage | somatic clone phenotype of Rbf^15aΔ, rno¹

(Steele et al., 2009)

Egfr^f2 is a non-enhancer of visible phenotype of Pp2B-14D^act.GMR

(Sullivan and Rubin, 2002)

Suppressor of

Statement

Reference

Egfr[+]/Egfr^f2 is a suppressor | partially of visible | adult stage phenotype of Scer\GAL4^sd.PU, dome^KK104700

(Recasens-Alvarez et al., 2017)

Egfr^f2 is a suppressor of increased cell number | male | heat sensitive phenotype of E(z)⁷³¹/E(z)⁶¹

(Eun et al., 2014)

Egfr[+]/Egfr^f2 is a suppressor of increased cell number | adult stage phenotype of sl²

(Murillo-Maldonado et al., 2011)

Egfr[+]/Egfr^f2 is a suppressor | partially of abnormal planar polarity | recessive phenotype of sl⁹

(Schlesinger et al., 2004)

Egfr^f2 is a suppressor of visible phenotype of sev^S11.Tag:MYC

(Luschnig et al., 2000)

NOT Suppressor of

Statement

Reference

Egfr^f2 is a non-suppressor of decreased cell death phenotype of Ras85D^R68Q

(Gafuik and Steller, 2011)

Egfr^f2 is a non-suppressor of lethal | pupal stage phenotype of Csk^j1D8/Csk^S030003

(Read et al., 2004)

Egfr^f2 is a non-suppressor of visible phenotype of Pp2B-14D^act.GMR

(Sullivan and Rubin, 2002)

Other

Statement

Reference

Egfr^f2, Myc^dm-1/dm[+] has lethal | dominant | maternal effect | embryonic stage phenotype

(Orian et al., 2007)

Egfr^f2, Myc^dm-1/dm[+] has abnormal neuroanatomy | dominant | embryonic stage phenotype

(Orian et al., 2007)

Egfr^f2, Myc²/dm[+] has lethal | dominant | maternal effect | embryonic stage phenotype

(Orian et al., 2007)

Egfr^f2, brm[+]/brm² has visible phenotype

(Armstrong et al., 2005)

Egfr[+]/Egfr^f2, brm² has visible | dominant phenotype

(Armstrong et al., 2005)

Phenotype Manifest In

Enhanced by

Statement

Reference

Egfr^f2 has dorsal appendage phenotype, enhanceable by CSN5^L4032/CSN5[+]

(Doronkin et al., 2002)

Egfr^f2 has phenotype, enhanceable by ebi^unspecified/ebi[+]

(Dong et al., 1999)

Suppressed by

Statement

Reference

Egfr^f2 has tracheal primordium phenotype, suppressible by cv-c^UAS.cDa/Scer\GAL4^69B

(Brodu and Casanova, 2006)

Egfr^f2 has presumptive embryonic/larval tracheal system phenotype, suppressible by cv-c^UAS.cDa/Scer\GAL4^69B

(Brodu and Casanova, 2006)

Egfr^f2 has dorsal air sac primordium | somatic clone phenotype, suppressible by Scer\GAL4^αTub84B.PL/BacA\p35^UAS.cHa

(Cabernard and Affolter, 2005)

Egfr^f2 has embryonic Malpighian tubule phenotype, suppressible by svp^I.UAS/Scer\GAL4^unspecified

(Kerber et al., 1998)

Egfr^f2 has embryonic Malpighian tubule phenotype, suppressible by Scer\GAL4^unspecified/svp^II.UAS

(Kerber et al., 1998)

NOT suppressed by

Statement

Reference

Egfr^f2 has tracheal branch primordium phenotype, non-suppressible by Df(3L)H99

(Cela and Llimargas, 2006)

Egfr^f2 has phenotype, non-suppressible by eRF1[+]/eRF1^F2

(Chao et al., 2003)

Enhancer of

Statement

Reference

Egfr[+]/Egfr^f2 is an enhancer of wing phenotype of Scer\GAL4^lz-gal4, Shrm^A.UAS

(Hildebrand et al., 2021)

Egfr[+]/Egfr^f2 is an enhancer of male germline stem cell | increased number phenotype of E(Pc)^GL00169, Scer\GAL4^NP1624

(Feng et al., 2017)

Egfr[+]/Egfr^f2 is an enhancer of eye photoreceptor cell phenotype of ato^SA-KI

(Quan et al., 2016)

Egfr[+]/Egfr^f2 is an enhancer of wing blade phenotype of sl²

(Murillo-Maldonado et al., 2011)

Egfr^f2 is an enhancer of eye phenotype of CanB^GMR.PS, Pp2B-14D^act.GMR

(Sullivan and Rubin, 2002)

Egfr[+]/Egfr^f2 is an enhancer of eye phenotype of arm^S56F.GMR

(Freeman and Bienz, 2001)

Egfr[+]/Egfr^f2 is an enhancer of ommatidium phenotype of Sos^JC2, sev⁶

(Dong et al., 1999)

Egfr[+]/Egfr^f2 is an enhancer of photoreceptor cell R7 phenotype of Sos^JC2, sev⁶

(Dong et al., 1999)

Egfr[+]/Egfr^f2 is an enhancer of ommatidium phenotype of Sos^JC2/Sos[+], sev⁶

(Dong et al., 1999)

Egfr[+]/Egfr^f2 is an enhancer of photoreceptor cell R7 phenotype of Sos^JC2/Sos[+], sev⁶

(Dong et al., 1999)

Egfr^f2 is an enhancer of eye phenotype of hid^GMR.PG

(Bergmann et al., 1998)

Egfr^f2 is an enhancer of ommatidium phenotype of hid^GMR.PG

(Bergmann et al., 1998)

NOT Enhancer of

Statement

Reference

Egfr[+]/Egfr^f2 is a non-enhancer of eye phenotype of Caf1-105^NIG.12892R, Scer\GAL4^ey.PH

(Yu et al., 2013)

Egfr[+]/Egfr^f2 is a non-enhancer of wing blade phenotype of sl⁹

(Murillo-Maldonado et al., 2011)

Egfr[+]/Egfr^f2 is a non-enhancer of photoreceptor cell R8 | third instar larval stage | somatic clone phenotype of rno¹

(Steele et al., 2009)

Egfr[+]/Egfr^f2 is a non-enhancer of photoreceptor cell R8 | third instar larval stage | somatic clone phenotype of Rbf^15aΔ, rno¹

(Steele et al., 2009)

Egfr[+]/Egfr^f2 is a non-enhancer of chemosensory ventral triple row & microchaeta | ectopic phenotype of ed^4.12

(Rawlins et al., 2003)

Egfr[+]/Egfr^f2 is a non-enhancer of dorsal triple row & microchaeta | ectopic phenotype of ed^4.12

(Rawlins et al., 2003)

Egfr[+]/Egfr^f2 is a non-enhancer of dorsocentral bristle | ectopic phenotype of ed^4.12

(Rawlins et al., 2003)

Egfr[+]/Egfr^f2 is a non-enhancer of scutellar bristle | ectopic phenotype of ed^4.12

(Rawlins et al., 2003)

Egfr^f2 is a non-enhancer of eye phenotype of Pp2B-14D^act.GMR

(Sullivan and Rubin, 2002)

Egfr^f2 is a non-enhancer of phenotype of Rho1^rev220

(Magie et al., 1999)

Suppressor of

Statement

Reference

Egfr[+]/Egfr^f2 is a suppressor | partially of mesonotum | ectopic | adult stage phenotype of Scer\GAL4^sd.PU, dome^KK104700

(Recasens-Alvarez et al., 2017)

Egfr^f2 is a suppressor of cyst progenitor cell | increased number | heat sensitive phenotype of E(z)⁷³¹/E(z)⁶¹

(Eun et al., 2014)

Egfr^f2 is a suppressor of testis | heat sensitive phenotype of E(z)⁷³¹/E(z)⁶¹

(Eun et al., 2014)

Egfr[+]/Egfr^f2 is a suppressor of wing vein | ectopic phenotype of sl²

(Murillo-Maldonado et al., 2011)

Egfr[+]/Egfr^f2 is a suppressor of photoreceptor cell R7 | adult stage phenotype of sl²

(Murillo-Maldonado et al., 2011)

Egfr[+]/Egfr^f2 is a suppressor | partially of photoreceptor cell R7 | increased number phenotype of sl⁹

(Schlesinger et al., 2004)

Egfr[+]/Egfr^f2 is a suppressor | partially of ommatidium phenotype of sl⁹

(Schlesinger et al., 2004)

Egfr[+]/Egfr^f2 is a suppressor of interommatidial bristle phenotype of sl⁹

(Schlesinger et al., 2004)

Egfr[+]/Egfr^f2 is a suppressor of photoreceptor cell R8 | increased number phenotype of ed^4.12

(Rawlins et al., 2003)

Egfr^f2/Egfr^f2 is a suppressor of photoreceptor cell R8 | increased number phenotype of ed^4.12

(Rawlins et al., 2003)

Egfr^f2 is a suppressor of ommatidium phenotype of sev^S11.Tag:MYC

(Luschnig et al., 2000)

Egfr^f2 is a suppressor of eye phenotype of sev^S11.Tag:MYC

(Luschnig et al., 2000)

Egfr[+]/Egfr^f2 is a suppressor of photoreceptor cell R7 | ectopic phenotype of sl¹

(Thackeray et al., 1998)

Egfr[+]/Egfr^f2 is a suppressor of photoreceptor cell R7 | ectopic phenotype of sl²

(Thackeray et al., 1998)

Egfr^f2 is a suppressor of phenotype of S²¹⁸

(Freeman, 1994)

Egfr^f2 is a suppressor of phenotype of rho^hs.sev

(Freeman, 1994)

NOT Suppressor of

Statement

Reference

Egfr^f2 is a non-suppressor of photoreceptor cell R7 phenotype of Ras85D^R68Q

(Gafuik and Steller, 2011)

Egfr^f2 is a non-suppressor of wing vein L5 phenotype of Ras85D^R68Q

(Gafuik and Steller, 2011)

Egfr^f2 is a non-suppressor of wing vein | ectopic phenotype of Ras85D^R68Q

(Gafuik and Steller, 2011)

Egfr^f2 is a non-suppressor of eye phenotype of Ras85D^R68Q

(Gafuik and Steller, 2011)

Egfr^f2 is a non-suppressor of midline glial cell phenotype of Ras85D^R68Q

(Gafuik and Steller, 2011)

Egfr^f2 is a non-suppressor of ommatidium phenotype of Ras85D^R68Q

(Gafuik and Steller, 2011)

Egfr^f2 is a non-suppressor of wing phenotype of Ras85D^R68Q

(Gafuik and Steller, 2011)

Egfr^f2 is a non-suppressor of posterior crossvein phenotype of Ras85D^R68Q

(Gafuik and Steller, 2011)

Egfr^f2 is a non-suppressor of crossvein phenotype of Ras85D^R68Q

(Gafuik and Steller, 2011)

Egfr^f2 is a non-suppressor of wing vein L4 phenotype of Ras85D^R68Q

(Gafuik and Steller, 2011)

Egfr^f2 is a non-suppressor of photoreceptor cell R8 | increased number phenotype of sca^BP2

(Rawlins et al., 2003)

Egfr[+]/Egfr^f2 is a non-suppressor of chemosensory ventral triple row & microchaeta | ectopic phenotype of ed^4.12

(Rawlins et al., 2003)

Egfr[+]/Egfr^f2 is a non-suppressor of dorsal triple row & microchaeta | ectopic phenotype of ed^4.12

(Rawlins et al., 2003)

Egfr[+]/Egfr^f2 is a non-suppressor of dorsocentral bristle | ectopic phenotype of ed^4.12

(Rawlins et al., 2003)

Egfr[+]/Egfr^f2 is a non-suppressor of scutellar bristle | ectopic phenotype of ed^4.12

(Rawlins et al., 2003)

Egfr^f2 is a non-suppressor of eye phenotype of Pp2B-14D^act.GMR

(Sullivan and Rubin, 2002)

Egfr^f2 is a non-suppressor of phenotype of Rho1^rev220

(Magie et al., 1999)

Other

Statement

Reference

Egfr^f2, brm² has humeral bristle phenotype

(Armstrong et al., 2005)

Egfr[+]/Egfr^f2, brm² has humeral bristle phenotype

(Armstrong et al., 2005)

Egfr^f2, Pvr¹ has border follicle cell | somatic clone phenotype

(Jekely et al., 2005)

Egfr^f2, sca^unspecified has photoreceptor cell R8 | somatic clone phenotype

(Baonza et al., 2001)

Additional Comments

Genetic Interactions

Statement

Reference

Egfr^f2 heterozygosity partially suppresses the highly prevalent duplication of mesanotum structures observed upon the expression of dome^KK104700 under the control of Scer\GAL4^sd.PU (and Dicer-2, for more efficient RNAi).

(Recasens-Alvarez et al., 2017)

The reduced number of photoreceptor neurons per ommatidium characteristic for ato^SA-KI mutants is further decreased by combination with a single copy of Egfr^f2 and majority of the ommatidia contain only the R8 photoreceptor cell.

(Quan et al., 2016)

One copy of Egfr^f2 does not enhance the small eye phenotype seen when Caf1-105^NIG.12892R is expressed under the control of Scer\GAL4^ey.PH.

(Yu et al., 2013)

One copy of Egfr^f2 enhances the reduction in wing blade area seen in homozygous sl² males.

One copy of Egfr^f2 does not enhance the reduction in wing blade area seen in homozygous sl⁹ males.

One copy of Egfr^f2 partially suppresses the ectopic wing vein phenotype seen in sl² homozygotes.

One copy of Egfr^f2 partially suppresses the percentage of sl² mutant ommatidia that contain extra R7 photoreceptors.

(Murillo-Maldonado et al., 2011)

The multiple photoreceptor-R8 phenotype seen in rno¹ or rno¹, Rbf^15aΔ eye somatic mutant clones is not significantly affected by Egfr^f2/+.

(Steele et al., 2009)

More than 90% of dm¹/+ ; Egfr^f2/+ embryos show severe defects in the nervous system at stage 17.

(Orian et al., 2007)

Expression of cv-c^Scer\UAS.cDa, under the control of Scer\GAL4^69B partially suppresses the Egfr^f2 mutant invagination phenotype.

(Brodu and Casanova, 2006)

Df(3L)H99; Egfr^f2 embryos, in which cell death is prevented, still show the same tracheal branch integrity phenotype as Egfr^f2 single mutant embryos.

(Cela and Llimargas, 2006)

Border cells which are part of somatic clones of Pvr¹; Egfr^f2 double homozygous cells initiate migration, but fail to reach the oocyte.

(Jekely et al., 2005)

The ed^4.12 R8 cell twinning phenotype is strongly suppressed by Egfr^f2/+. Egfr^f2 clones in the eye disc induced in a homozygous ed^4.12 background show abnormal spacing of R8 cells in the clone, but R8 cells rarely appear twinned. Twinned R8 cells can be observed in Egfr^f2 sca^BP2 double mutant clones in the eye disc.

(Rawlins et al., 2003)

The fused dorsal appendage phenotype of eggs laid by Egfr^f2/+ females is weakly enhanced if the females are also heterozygous for CSN5^L4032.

(Doronkin et al., 2002)

The photoreceptor cell R8 cells in Egfr^f2, sca^unspecified double mutant somatic clones are much closer to their neighbours than in Egfr^f2 clones.

(Baonza et al., 2001)

The rough eye phenotype caused by sev^{S11.T:Hsap\MYC} is partially suppressed by one copy of Egfr^f2.

(Luschnig et al., 2000)

In sev⁶ hemizygotes that are also heterozygous for Sos^JC2, 14.7% of ommatidia contain R7 cells. This phenotype is dominantly enhanced by Egfr^f2.

(Dong et al., 1999)

The number of cells in the Malpighian tubules in Egfr^f2 embryos is restored to a considerable extent by svp^I.Scer\UAS or svp^II.Scer\UAS expressed in the tubule primordium using Scer\GAL4^unspecified.

(Kerber et al., 1998)

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

(Thackeray et al., 1998)

No effect on the faf eye phenotype.

(Huang and Fischer-Vize, 1996)

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

(Hariharan et al., 1995)

Xenogenetic Interactions

Statement

Reference

The reduced growth and failure to localise to the primodium tip seen in Egfr^f2 homozygous clones in the dorsal air sac primordium are both suppressed if the clone are also BacA\p35^Scer\UAS.cHa; Scer\GAL4^αTub84B.PL (Scer\GAL80/MARCM technique).

(Cabernard and Affolter, 2005)

Complementation and Rescue Data

Fails to complement

Egfr^k05115

(Liu et al., 1999)

Comments

Images (0)

Mutant

Wild-type

Stocks (1)

Bloomington

2768

cn¹ Egfr^f2 bw¹ speck¹/CyO

Notes on Origin

Discoverer

Selected as: Embryonic lethal.

Comments

Mutation of Egfr that coordinately affects all gene activities, a class I lesion. The allelic series for class I lesions: Egfr^t2 = Egfr^t1 < Egfr^top-EC20 < Egfr^f7 = Egfr^f1 = Egfr^flb-2E07 < Egfr^top-EE39 = Egfr^top-ED26 = Egfr^f5 < Egfr^f9 = Egfr^f10 = Egfr^f2 = Egfr^top-EE42 = Egfr^f11 = Egfr^f24 = Egfr^f3 = Df(2R)Egfr3.

(Clifford and Schupbach, 1989)

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

(Clifford and Schupbach, 1992)

Severe mutation.

(Baumann and Skaer, 1993)

Class I allele.

(Clifford and Schupbach, 1994)

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (30)

Reported As

Symbol Synonym

DER^IK35

(Huang and Fischer-Vize, 1996)

EGF^F2

(Moses et al., 2011)

EGFR^1K35

(Dominguez et al., 1998)

EGFR^f2

(Tian et al., 2023, Jussen et al., 2016, Ruiz et al., 2012, Grigorian et al., 2011, Helman et al., 2011, Doronkin et al., 2002)

EGFR^fb2

(Ruiz et al., 2012)

EGFR^flb1K35

(Freeman and Bienz, 2001)

Egfr^-

(Lawrence et al., 2002)

Egfr^1K35

(Levings and Nakato, 2018, Xu et al., 2011, de Navascués and Modolell, 2007, Brown et al., 2006, Baonza and Freeman, 2005, Baonza et al., 2001, Wasserman and Freeman, 1998)

Egfr^F2

(Sepp and Auld, 2003, Magie et al., 1999)

Egfr^IK35

(Hasson et al., 2005, Rawlins et al., 2003, Rawlins et al., 2003, Zecca and Struhl, 2002)

Egfr^Ik35

(Goering and Gibson, 2005)

Egfr^flb-IK35

(von Ohlen and Doe, 2000)

der^f2

(Luschnig et al., 2000)

egfr^F2

(Recasens-Alvarez et al., 2017)

egfr^K35

(Cabernard and Affolter, 2005)

egfr^f2

(Bandyopadhyay et al., 2016, Quan et al., 2016, Grigorian et al., 2013, Moses et al., 2011, Pilgram et al., 2011)

flb

flb^1K35

(Schlesinger et al., 2004, Szuts et al., 1998, zur Lage et al., 1997, Schweitzer et al., 1995, Baumann and Skaer, 1993, Raz et al., 1991, Schejter and Shilo, 1989)

flb^1k35

(Thackeray et al., 1998)

flb^IK-35

(Hariharan et al., 1995)

flb^IK35

(Fusse and Hoch, 2002, Zhao and Skeath, 2002, Liu et al., 1999, Kerber et al., 1998, Skeath, 1998, Udolph et al., 1998, Yagi et al., 1998, Luer et al., 1997, D'Alessio and Frasch, 1996, Raz et al., 1991, Strecker et al., 1991)

flb^IK

(Tearle and Nusslein-Volhard, 1987)

flb^f2

(Gafuik and Steller, 2011, Bergmann et al., 2002, Bergmann et al., 1998)

flb^ik35

(Maybeck and Röper, 2009)

flbIK³⁵

(Rusten et al., 2001)

top^1K35

(Clifford and Schupbach, 1994, Clifford and Schupbach, 1989, Price et al., 1989)

top^IK35

(Goode et al., 1996, Clifford and Schupbach, 1992)

top^f2

(Jekely et al., 2005)

Name Synonyms

faint little ball

Secondary FlyBase IDs

References (103)

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