FlyBase Allele Report: Dmel\Egfr[f24]

Df(2R)Egfr3/Egfr^f24 mutant embryos exhibit severe defects in ventral patterning. The embryos are very short with no denticle belts and a large anterior hole.

(Austin et al., 2014)

Egfr^f24 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^f24 mutant terminal cells exhibit defective lumen.

(Ruiz et al., 2012)

Although the initial growth of Egfr^f24 mutant intestinal stem cell clones is normal, their long-term proliferation is severely compromised. These clones do not grow even after the flies have recovered from Pseudomonas entomophila infection.

(Jiang et al., 2011)

In contrast to wild-type, supplementing Apis mellifera royal jelly to food does not influence body size or developmental time in Egfr^tsla/Egfr^f24 mutants. When wild-type flies are reared on medium containing royal jelly, they show increased body size (body weight and body length) and fecundity, and have extended lifespan and shortened developmental time compared with flies reared on control medium.

(Kamakura, 2011)

In stage 16 Egfr^tsla/Egfr^f24 embryos the two neurons that normally arise closest to the midline are lost, vdaB (in 79% of cases) and the class III neurons (in 76% of cases). Loss of these neurons are preceded by the loss of SOPs 1a (73%() and 1 (69%).

(Karim and Moore, 2011)

Egfr^f24/Egfr^T1 flies have severe rough eyes which have a reduced number of photoreceptor cells per ommatidium. Most of vein L4 is lost in the wing.

(Rendina et al., 2010)

The cardiac function of Egfr^f24/Egfr^tsla flies is similar to that of wild-type controls at 18[o]C. The cardiac function of Egfr^f24/Egfr^tsla flies deteriorates after 24 h at 25[o]C.

(Yu et al., 2010)

Marker expression analysis shows that in Egfr^tsla/Egfr^f24 flies heat shocked for 24 hours at the beginning of pupariation, the proportion of pale-ommatidia is reduced and hybrid ommatidia are present with a yellow-type R8 and a pale-type R7. These animals have very rough eyes.

(Birkholz et al., 2009)

Homozygous Egfr^f24 mutant adult midgut progenitor cells fail to proliferate during larval development.

(Jiang and Edgar, 2009)

Egfr^f24/+ flies show rotation defects in 26% of ommatidia.

(Weber et al., 2008)

Primordial germ cells overproliferate in Egfr^tsla/Egfr^f24 larvae grown at a restrictive temperature. Fewer intermingled cells (somatic cells adjacent to primordial germ cells) are present in Egfr^tsla/Egfr^f24 gonads compared to wild-type.

(Gilboa and Lehmann, 2006)

Oocyte polarity is disrupted when the posterior follicle cell layer contains Egfr^f24 mutant clones.

(Poulton and Deng, 2006)

Egfr^t1/Egfr^f24 animals show loss of the anterior crossvein (100% penetrance) and partial loss of vein L4 in the wing (169% penetrance).

(Alvarado et al., 2004)

Egfr^tsla/Egfr^f24 animals shifted to restrictive temperatures for 24 hours during the first half of the third larval instar have leg truncations, with the size of the truncation increasing with temperature. At lower restrictive temperatures (28.7^oC) only the most distal structures (the claws) are missing but at high temperatures (33^oC) structures tarsal segments 2-5 are absent. At 33^oC development of regions more proximal to the tarsal segments is occasionally disrupted. Egfr^tsla/Egfr^f24 clones do not survive in distal regions of the leg disc at temperatures above 31^oC. Egfr^tsla/Egfr^f24 animals shifted to 33^oC for 12 hours during the first quarter of the third larval instar show truncations of the tarsus. However, a 12 hour shift during the second quarter of the third larval instar results in legs with normal distal elements (claw and tarsal segment 5) but fusions or deletions of the intermediate tarsal segments 2-4.

(Campbell, 2002)

When Egfr^tsla/Egfr^f24 mutants are grown at the permissive temperature (18^oC) throughout larval development, and then shifted to the non-permissive temperature (29^oC) between 0 and 10 hours after puparium formation (APF) recognizable transverse rows (t-rows) of bristles are seen on the basitarsus and distal tibia are seen, but bristles within each row are jumbled in irregular groups. (bristles line up, with sockets touching in wild-type). Up shifts after 10h APF have little effect. When these mutants are grown at 18^oC throughout larval development, shifted up to 29^oCat pupariation and shifted back down between 0 and 14 hours APF, little effect is seen. Down shifts after 21h APF cause disruption of the organisation of the t-rows. When downshifts occur between 14 and 20h APF, other phenotypes emerge. In a minority of legs (13%) adjacent rows bend toward one another and join at Y or X shaped intersections.

(Held, 2002)

When Egfr^tsla/Egfr^f24 animals are raised at the permissive temperature (of 18^oC) they have a wild-type pattern of bracts. Those raised at 29^oC lack all bracts. The sensitive period for tibial and basitarsal bracts are 17-28h and 13-28h AP respectively.

(Held, 2002)

Only 2% of egg chambers contain homozygous follicle cell clones 5 days after clone induction. Homozygous follicle cell clones are detected 3 days after clone induction, but they are smaller and less frequent than control clones.

(James et al., 2002)

In Egfr^f24 embryos division cycles 14 to 16 in the Malpighian tubules occur normally. But arrest occurs from Cycle 17. The number of Malpighian tubule is about 39 after 8 hours, but is eventually reduced to about about 26 by cell death (wild type Malpighian tubules have about 125 cells).

(Sudarsan et al., 2002)

Homozygous clones in the eye disc lack mitosis completely. Posterior to the morphogenetic furrow, mutant clones undergo S phase, as shown by BrdU incorporation.

(Baker and Yu, 2001)

Egfr^tsla/Egfr^f24 flies at 18^oC frequently lack the anterior supraalar bristle, posterior supraalar bristle and posterior postalar bristle, and the anterior postalar bristle and anterior dorsocentral bristle are frequently duplicated. When late LIII larvae are shifted to 30^oC for 15 hours, all notum macrochaetae show reduced liklihood to develop except the scutellar bristles.

(Culi et al., 2001)

When all outer border cells are mutant for Egfr^f24 in egg chambers containing homozygous clones, the cluster remains in the centre of the egg chamber at stage 10, whereas 90% of wild-type clusters are found dorsally. When mixed clusters with both wild-type and mutant cells move dorsally, the wild-type cells are in front. When patches of border cells are mutant for Egfr^f24 in egg chambers containing homozygous clones, the border cells still migrate dorsally.

(Duchek and Rorth, 2001)

Egfr^f24/Egfr^tsla embryos raised at 18^oC until approximately stage 12, and then shifted to 29^oC for the remainder of development exhibit reduced numbers and increased apoptosis of longitudinal (interface) glial cells.

(Hidalgo et al., 2001)

Egfr^f24/Egfr^tsla animals kept at the restrictive temperature between 168-180 hours after egg deposition (AED) develop an adult eye that lacks ommatidia. Imaginal discs from these animals examined at either 192 or 204 hours AED lack both the ommatidia and the morphogenetic furrow. Egfr^f24/Egfr^tsla animals kept at the restrictive temperature between 192-204 hours AED develop an eye with severe structural defects along the posterior-lateral margins (ommatidia at the intersection of the equator and posterior margin appear not to be affected). The morphogenetic furrow has clearly initiated at the posterior margin in imaginal discs from these animals examined at 204 hours AED, but its continued re-initiation along the lateral margins is inhibited.

(Kumar and Moses, 2001)

If Egfr^tsla/Egfr^f24 flies are raised at 17^oC, transferred to 25^oC for 24 hours at second instar larval stages, and then returned to 17^oC leads to a mirror image duplication of the wing.

(Baonza et al., 2000)

When Egfr^tsla/Egfr^f24 mutant males are raised at the permissive temperature (18^oC), and then shifted to the restrictive temperature (29^oC), a spermatogenesis phenotype is seen. Although all stages of spermatogenesis are initially present, by one week of at non-permissive temperature, testes are filled with massive numbers of early germ cells with small nuclei. The early germ cells appear to proliferate at the expense of differentiation, as spermatocytes and spermatids are absent or markedly reduced in numbers. Many early germ cells displayed expression marker, subcellular structures and cell division behaviour characteristic of stem cells and gonialblasts. Mutants have many more cells with ball shaped or dumbbell-shaped spectrosomes, both near the tip and displaced down the testis. In Egfr^tsla/Egfr^f24 mutant males, early cyst cells often form improper associations with early germ cells. In general accumulation of early germ cells is not associated with a corresponding increase in the total number of cyst progenitor or early cyst cells. Homozygous Egfr^f24 germline clones produce cysts with the normal number of differentiating spermatocytes. No overproliferation of early germ cells is seen.

(Kiger et al., 2000)

When Egfr^tsla/Egfr^f24 flies are grown at the restrictive temperature for Egfr^tsla during the second instar, the notum is lost, the wings are present but have pattern abnormalities and fail to inflate.

(Wang et al., 2000)

Suppresses the dominant Egfr^E1 phenotype towards wild-type in transheterozygotes.

(Kumar et al., 1998)

Homozygotes have mutant egg chambers.

(Gonzalez-Reyes et al., 1995)

orb^F343 interact genetically with Egfr, double heterozygote embryos display fused dorsal appendages.

(Christerson and McKearin, 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)

Homozygous embryos fail to complete germ band retraction, lack most anterior, posterior and ventral cuticle, and have reduced or no denticles. Cell death is seen in the head, amnioserosa and germband at stage 10, and abnormally deep segmental grooves are seen on the outside of the germband. By stage 12, large patches of dead cells are seen in the amnioserosa, the brain and cephalic epidermis, and clumps of necrotic cells appear in what may be a segmentally repeated pattern in the epidermal tissues of the germ band.

(Clifford and Schupbach, 1992)

The viability of homozygous clones in the wing is very low. Homozygous clones in the legs, notum and head seem to be inviable. Homozygous clones in the abdominal tergites are viable. Wild-type chaetae are clustered immediately adjacent to or included within these clones and there is a depletion of chaetae around the clones for several cell diameters.

(Diaz-Benjumea and Garcia-Bellido, 1990)

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)

Embryonic head appears to be abnormal at the time of stomodeal invagination: clumps of cells fall away.

(Price et al., 1989)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Enhanced by

Statement

Reference

Egfr^T1/Egfr^f24 has visible phenotype, enhanceable by Bap170^C1.UAS/Scer\GAL4^Bx-MS1096

(Rendina et al., 2010)

Suppressed by

Statement

Reference

Egfr^T1/Egfr^f24 has visible phenotype, suppressible | partially by Bap170^hfl1/Bap170[+]

(Rendina et al., 2010)

Egfr^f24 has abnormal planar polarity | dominant phenotype, suppressible by fz[+]/fz²¹

(Weber et al., 2008)

Egfr^f24 has abnormal planar polarity | dominant phenotype, suppressible by fz²³/fz[+]

(Weber et al., 2008)

Egfr^t1/Egfr^f24 has visible phenotype, suppressible by kek1^RA5/kek1^RM2

(Alvarado et al., 2004)

NOT Enhancer of

Statement

Reference

Egfr^f24 is a non-enhancer of visible phenotype of upd1^GMR.PB

(Bach et al., 2003)

Suppressor of

Statement

Reference

Egfr[+]/Egfr^f24 is a suppressor of abnormal neuroanatomy | adult stage phenotype of Graf¹

(Kim et al., 2021)

Egfr[+]/Egfr^f24 is a suppressor of increased cell number | third instar larval stage phenotype of Graf¹

(Kim et al., 2017)

NOT Suppressor of

Statement

Reference

Egfr^f24 is a non-suppressor of increased occurrence of cell division | adult stage phenotype of Scer\GAL4^NP7397, Src42A^UAS.cPa

(Kohlmaier et al., 2015)

Egfr^f24 is a non-suppressor of visible phenotype of upd1^GMR.PB

(Bach et al., 2003)

Other

Statement

Reference

Egfr^f24, pnt^p2, rl^S-135 has visible | adult stage phenotype

(Wu et al., 2020)

Egfr^f24, pnt^p3/pnt^p2, rl^S-135 has decreased cell number phenotype

(Wu et al., 2020)

Egfr^f24, pnt^p3/pnt^p2, rl^S-135 has visible | adult stage phenotype

(Wu et al., 2020)

Egfr^f24, pnt^p3, rl^S-135 has visible | adult stage phenotype

(Wu et al., 2020)

Egfr^f24, pnt^p3, rl^S-135 has lethal - all die before end of P-stage | temperature conditional phenotype

(Wu et al., 2020)

Phenotype Manifest In

Enhanced by

Statement

Reference

Egfr^T1/Egfr^f24 has wing vein L4 phenotype, enhanceable by Bap170^C1.UAS/Scer\GAL4^Bx-MS1096

(Rendina et al., 2010)

Suppressed by

Statement

Reference

Egfr^T1/Egfr^f24 has eye phenotype, suppressible | partially by Bap170^hfl1/Bap170[+]

(Rendina et al., 2010)

Egfr^T1/Egfr^f24 has eye photoreceptor cell phenotype, suppressible | partially by Bap170^hfl1/Bap170[+]

(Rendina et al., 2010)

Egfr^T1/Egfr^f24 has wing vein L4 phenotype, suppressible by Bap170^hfl1/Bap170[+]

(Rendina et al., 2010)

Egfr^f24 has ommatidium phenotype, suppressible by fz[+]/fz²¹

(Weber et al., 2008)

Egfr^f24 has ommatidium phenotype, suppressible by fz²³/fz[+]

(Weber et al., 2008)

Egfr^t1/Egfr^f24 has eye phenotype, suppressible | partially by kek1^RA5/kek1[+]

(Alvarado et al., 2004)

Egfr^t1/Egfr^f24 has wing vein L4 phenotype, suppressible by kek1^RA5/kek1^RM2

(Alvarado et al., 2004)

Egfr^f24 has Malpighian tubule phenotype, suppressible by hid^unspecified

(Sudarsan et al., 2002)

Enhancer of

Statement

Reference

Egfr^f24 is an enhancer of dorsal appendage phenotype of Lis-1^k11702

(Lei and Warrior, 2000)

NOT Enhancer of

Statement

Reference

Egfr^f24 is a non-enhancer of eye phenotype of upd1^GMR.PB

(Bach et al., 2003)

Egfr[+]/Egfr^f24 is a non-enhancer of phenotype of ct^L188

(Jackson and Berg, 1999)

Egfr[+]/Egfr^f24 is a non-enhancer of phenotype of ct^C145

(Jackson and Berg, 1999)

Egfr^f24 is a non-enhancer of phenotype of ct^C145

(Jackson and Berg, 1999)

Suppressor of

Statement

Reference

Egfr[+]/Egfr^f24 is a suppressor of adult mushroom body beta-lobe phenotype of Graf¹

(Kim et al., 2021)

Egfr[+]/Egfr^f24 is a suppressor of axon | adult stage phenotype of Graf¹

(Kim et al., 2021)

Egfr[+]/Egfr^f24 is a suppressor of midline | adult stage phenotype of Graf¹

(Kim et al., 2021)

Egfr[+]/Egfr^f24 is a suppressor of hemocyte | increased number | third instar larval stage phenotype of Graf¹

(Kim et al., 2017)

Egfr^f24 is a suppressor of eye phenotype of Scer\GAL4^GMR.PU, miple1^UAS.Tag:HA

(Muñoz-Soriano et al., 2013)

Egfr^f24 is a suppressor of eye phenotype of Scer\GAL4^hs.2sev, miple1^UAS.Tag:HA

(Muñoz-Soriano et al., 2013)

Egfr[+]/Egfr^f24 is a suppressor of denticle | ectopic phenotype of fng¹³

(Walters et al., 2005)

Egfr[+]/Egfr^f24 is a suppressor of phenotype of Src42A^Su(Raf)1-1

(Zhang et al., 1999)

NOT Suppressor of

Statement

Reference

Egfr^f24 is a non-suppressor of adult midgut phenotype of Scer\GAL4^NP7397, Src42A^UAS.cPa

(Kohlmaier et al., 2015)

Egfr^f24 is a non-suppressor of eye phenotype of upd1^GMR.PB

(Bach et al., 2003)

Other

Statement

Reference

Egfr^f24, pnt^p2, rl^S-135 has wing margin phenotype

(Wu et al., 2020)

Egfr^f24, pnt^p3/pnt^p2, rl^S-135 has wing margin phenotype

(Wu et al., 2020)

Egfr^f24, pnt^p3/pnt^p2, rl^S-135 has eye photoreceptor cell | decreased number phenotype

(Wu et al., 2020)

Egfr^f24, pnt^p3, rl^S-135 has wing margin phenotype

(Wu et al., 2020)

Bap170^C1.UAS, Egfr^T1/Egfr^f24, Scer\GAL4^Bx-MS1096 has wing vein L3 phenotype

(Rendina et al., 2010)

Additional Comments

Genetic Interactions

Statement

Reference

The increased concentration of circulating hemocytes characteristic for Graf¹/Y mutant third instar larvae is suppressible by combination with a single copy of Egfr^f24.

(Kim et al., 2017)

Downregulation of Egfr, through a Egfr^f24 mutant background, suppresses the Scer\GAL4^GMR.PU>miple1^{Scer\UAS.T:Ivir\HA1} eye phenotype.

Downregulation of Egfr, through a Egfr^f24 mutant background, does not alter the ommatidial rotation phenotype seen in flies expressing miple1^{Scer\UAS.T:Ivir\HA1} under the control of Scer\GAL4^hs.2sev.

(Muñoz-Soriano et al., 2013)

Bap170^hfl1/+ partially suppresses the rough eye phenotype and loss of photoreceptor cells which is seen in Egfr^f24/Egfr^T1 flies. The loss of wing vein L4 which is seen in Egfr^f24/Egfr^T1 flies is rescued by Bap170^hfl1/+ in 85% of cases.

Expression of Bap170^C1.Scer\UAS under the control of Scer\GAL4^Bx-MS1096 enhances the loss of wing vein L4 that is seen in Egfr^f24/Egfr^T1 flies, such that there is a loss of the entire L4 vein. In addition the central region of wing vein L3 does not form.

(Rendina et al., 2010)

The frequency of rotation defects in the ommatidia of Egfr^f24/+ flies is reduced to 12% or 18% respectively if they are also carrying fz²¹/+ or fz²³/+.

(Weber et al., 2008)

The reduction in germline stem cells seen in the testes of Gef26³/Gef26⁴ animals is significantly suppressed by Egfr^f24/+.

(Wang et al., 2006)

fng¹³; Egfr^f24/+ double mutant larvae have a lower penetrance of the extra denticle phenotype seen in fng¹³ single mutants.

(Walters et al., 2005)

Heterozygous kek1^RA5 partially suppresses the rough eye phenotype seen Egfr^f24/Egfr^t1 animals.

(Alvarado et al., 2004)

The loss of wing vein L4 seen in Egfr^t1/Egfr^f24 animals is suppressed if they are also mutant for kek1 (kek1^RA5/kek1^RM2).

(Alvarado et al., 2004)

The addition of W^unspecified suppresses the Malpighian tubule phenotype seen in Egfr^f24 animals suggesting that it is at least partly caused by cell death.

(Sudarsan et al., 2002)

Dominantly suppresses the ability of Src42A^Su(phl)1-1 to suppress the lethality of phl¹/Y flies.

(Zhang et al., 1999)

Xenogenetic Interactions

Statement

Reference

Complementation and Rescue Data

Comments

Images (0)

Mutant

Wild-type

Stocks (3)

Bloomington

51293

w^*; P{neoFRT}42D mam¹⁰ Egfr^f24/CyO, P{ActGFP}JMR1

51291

w^*; smo^D16 P{neoFRT}42D mam¹⁰ Egfr^f24/CyO, P{ActGFP}JMR1

51296

P{hsFLP}12, y¹ w^*; P{neoFRT}42D Egfr^f24/CyO; ci⁹⁴/Dp(1;4)1021, y⁺, sv^spa-pol

Notes on Origin

Discoverer

Selected as: Failure to complement the female sterile effect of "Egfr^t" alleles.

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)

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (28)

Reported As

Symbol Synonym

(Weber et al., 2012)

DER^co

(Baonza et al., 2000)

DER^topco

(Hidalgo et al., 2001)

EGFR^24f

(Yu et al., 2010)

EGFR^f24

(Tian et al., 2023, Jia et al., 2014, Wildonger et al., 2005)

EGFR^top-co

(Ruiz et al., 2012, Walters et al., 2005)

Egfr²⁴

(Karim and Moore, 2011)

Egfr^<up>CO</up>

(Jiang and Edgar, 2009)

Egfr^CO

(Kohlmaier et al., 2015, Muñoz-Soriano et al., 2013, Jiang et al., 2011, Birkholz et al., 2009, Weber et al., 2008, Chen and Schupbach, 2006, Wang et al., 2006, Galindo et al., 2002, Held, 2002, Held, 2002, James et al., 2002, Culi et al., 2001, Kiger et al., 2000, Kumar et al., 1998, Neuman-Silberberg and Schupbach, 1996)

Egfr^F24

(Austin et al., 2014)

Egfr^co

(Zhang et al., 1999)

Egfr^f24

(Kim et al., 2021, Duan et al., 2018, Newcomb et al., 2018, Kim et al., 2017, Martin et al., 2017, Li et al., 2015, Kondo and Hayashi, 2013, Hwang and Rulifson, 2011, Kamakura, 2011, Rendina et al., 2010, Birkholz et al., 2009, Christensen et al., 2008.12.28, Wang et al., 2006)

Egfr^null

(Tsuda et al., 2002)

Egfr^topC0

(Jackson and Berg, 1999)

Egfr^topCO

(Kumar and Moses, 2001)

(Shamloula et al., 2002)

egfr^CO

(Fregoso Lomas et al., 2013, Bernardi et al., 2007, Umetsu et al., 2006, Alvarado et al., 2004, Alvarado et al., 2004, Lim and Choi, 2004)

egfr^F24

(Deignan et al., 2016)

egfr^co

(Wu et al., 2020)

egfr^f24

(Ogura et al., 2018, Bandyopadhyay et al., 2016, Liu et al., 2010, Baker et al., 2009, Gilboa and Lehmann, 2006, Yu et al., 2002)

egfr^top-co

(Hatini and DiNardo, 2001)

egfr^ts

(Gilboa and Lehmann, 2006)

f24

(Weber et al., 2012)

flb

flb^CO

(Bach et al., 2003)

top^CO

(Chang et al., 2008, Poulton and Deng, 2006, Galindo et al., 2005, Meignin et al., 2004, Sudarsan et al., 2002, Baker and Yu, 2001, Duchek and Rorth, 2001, Lei and Warrior, 2000, Lesokhin et al., 1999, Gonzalez-Reyes and St. Johnston, 1998, Gonzalez-Reyes et al., 1995, Christerson and McKearin, 1994, Baumann and Skaer, 1993, Clifford and Schupbach, 1992, Diaz-Benjumea and Garcia-Bellido, 1990, Clifford and Schupbach, 1989, Price et al., 1989)

top^f24

(Matsuda et al., 2015)

Name Synonyms

faint little ball

Secondary FlyBase IDs

References (82)

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