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General Information
Symbol
Dmel\hepr75
Species
D. melanogaster
Name
FlyBase ID
FBal0045852
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Nature of the Allele
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Cytology
Nature of the lesion
Statement
Reference

Excision of the P-element insertion.

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 ( 1 )
Disease
Interaction
References
ameliorates  cancer
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In

cuticle & abdomen

cuticle & abdomen | germ-line clone

cuticle & thorax

cuticle & thorax | germ-line clone

dorsal mesothoracic disc & cytoskeleton

embryonic leading edge cell & actin filament

embryonic leading edge cell & filopodium

peripodial epithelium & dorsal mesothoracic disc & prepupa

peripodial stalk & dorsal mesothoracic disc & prepupa

Detailed Description
Statement
Reference

hepr75 mutant clones in sensory neurons in adult wing do not display any defects in injury-induced axon degeneration (following an axotomy, the severed axons are cleared away normally).

hepr75 mutant clones do not affect photoreceptor differentiation or survival.

hepr75 neuroblast clones in mushroom bodies show axonal degeneration, though the main observable phenotype is overextension of axons.

Single cell hepr75 clones in mushroom bodies show a low frequency of axon breaks.

83.8% of hepr75 pupae show wing eversion defects 6 hours after puparium formation (eversion is complete at this time in wild-type animals); 31% have partially everted wings and 52.8% show a complete failure of disc eversion. 12.7% have leg eversion defects.

The basement membrane of wing discs is not degraded in hepr75 pupae which fail to evert their wing discs.

hepr75 follicle cell clones cease mitotic division too early, resulting in clones that contain a lower number of cells than their respective twin spots.

Homozygous hepr75 mutants exhibit a low level of ventral-to-dorsal R axon misrouting.

Wing disc fusion during thoracic closure is inhibited in hepr75 mutants, while dorsal closure is not affected. Wing discs of hepr75/+ females that are cut and left to regenerate are usually healed after 24 hours. In contrast, wounded wing discs of hepr75/Y males fail to heal, even after 7 days. In wild-type wing discs, wound healing is accomplished by the formation of an actin rich cable and filopodia for zipping epithelial edges together. In hepr75/Y mutants, wounds show an actin-rich area only at the wound vertex and not throughout the rest of the wound, and filpodial protrusions are much reduced compared to wild type. Additionally, peripodial epithelial cells do not elongate toward the wound edge, a process that occurs in wild-type wound healing.

Transplanted fragmented leg discs show a large reduction in transdetermination, compared to wild-type leg discs.

Mutant embryos show no defects in the initiation of mesoderm spreading.

Shortly after pupariation begins in wild-type flies, the wing discs move so that their peripodial side is in apposition with the larval epidermis. In 40% of hepr75 homozygotes, this apposition fails. In wild-type flies, appositions is proceeded by fusion of peripodial/stalk cells and larval epidermis, followed by eversion of the disc through a steadily enlarging hole in the fused peripodial epithelium / larval epidermis and then spread over the surrounding larval epidermis before fusing to adjacent discs. 50% of hepr75 homozygotes fail to complete this eversion and everted disc fails to spread. The remaining 10% of hepr75 homozygotes, the discs fail to fuse to adjacent discs.

During dorsal closure in hepr75 mutant embryos the embryonic leading edge cells lack filopodia and lamellipodia. Unlike wild-type no actin cable is visible in the leading edge cells of conventionally (formaldehyde/PBS) fixed embryos, although some evidence for a reduced actin cable can be seen in embryos fixed in the presence of phalloidin, and in live embryos. Very late in the process of closure, the epidermis and the amnioserosa detach from each other in these mutants.

The cuticles of embryos laid by hep1/hepr75 mothers crossed to hep1 hemizygous males display classic dorsal closure phenotypes (a large dorsal hole of variable size). The prominent actin cable seen in leading edge cells during dorsal closure in wild-type embryos is much reduced in these mutants.

Eggs derived from females with homozygous clones in the follicle cells show a strong reduction of the dorsal appendages (DA) with an accompanying expansion of their bases. The DA defects can either be partial or complete and symmetrical, depending on the size and location of the clones in the follicle cells. The micropyle is sometimes reduced in size with a more blunted aspect than normal. Abnormal stage 14 egg chambers with shortened anterior ends are seen in females with homozygous follicle cell clones. The centripetal and border follicle cells migrate normally in egg chambers that have either partially or completely mutant follicle cells. Homozygous germline clones do not produce (or only very rarely) dorsal appendage defects.

Embryos laid by hepr75/hep1 mothers (with hep1/Y fathers) abort dorsal closure early. The epithelium sweeps forward as normal and only fails at the onset of zippering. No signs of the normal actin based protrusions from leading edge cells at any stage during dorsal closure are seen. Fusion of opposing fronts also fails and segmental stripes are misaligned.

Wing discs of maternally recued homozygous hepr75 animals, unlike wild-type, remain in their initial position in the pre-pupa, they do not spread, and in many cases disc eversion does not take place. There is a compacting of the actin cytoskeleton at the leading edge. No filopodia appear to be generated from the imaginal epithelium, and imaginal cells are progressively pulled together, causing bunching of the epidermis.

hepr75/Y mutant eye discs show bristle mislocalisation and abnormal pigment cells shapes.

Discs dissected from L3 larvae are delayed in their development, reduced in size, and malformed or misfolded. Dissected pupae reveal one consistent and major defect: the absence or aberrant spreading and fusion of the two lateral wing discs. In some cases eversion does take place, in the absence of disc fusion. In viable hepr39/hepr75 transheterozygotes wing disc morphogenesis can proceed almost normally, with occasional unilateral defects. Gut and larval tissues are extruded on account of the failure of closure of the thorax in the mutant pupae. Eye antenna discs can fuse but the head does not form. Leg discs evert and fuse though their shape is abnormal. hepr75/hep1 adult females show mutant cleft thorax and bristle defects.

Transheterozygous embryos with hep1 display a dorsal open phenotype caused by lack of thoracic and abdominal cuticle. The head is very disorganised, the cephalopharyngeal skeleton is reduced to mouth hooks. Homozygous germline clones produce a similar dorsal open and head phenotype.

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

hepr75 has neuroanatomy defective phenotype, enhanceable by Wnt4[+]/Wnt4EMS23

hepr75 has neuroanatomy defective phenotype, enhanceable by Wnt4C1/Wnt4[+]

hepr75 has neuroanatomy defective phenotype, enhanceable by Wnt4[+]/Wnt4P23

Suppressed by
Statement
Reference

hepr75/hep1 has visible phenotype, suppressible by pucE69

NOT suppressed by
Statement
Reference

hepr75 has wound healing defective phenotype, non-suppressible by pucE69-A

hepr75 has lethal phenotype, non-suppressible by Mmus\Map2k7Ubi-p63E.PH

hepr75 has lethal phenotype, non-suppressible by Xlae\Mek2Ubi-p63E.PH

hepr75 has lethal phenotype, non-suppressible by Mmmm\Sek1Ubi-p63E.PH

Enhancer of
Statement
Reference

hepr75 is an enhancer of neuroanatomy defective phenotype of Wnt4C1

hepr75 is an enhancer of neuroanatomy defective phenotype of Wnt4P23

hep[+]/hepr75 is an enhancer of lethal | recessive phenotype of Src42AJp45

NOT Enhancer of
Statement
Reference
Suppressor of
Statement
Reference

hepr75 is a suppressor of hyperplasia phenotype of scrib1

hep[+]/hepr75 is a suppressor of planar polarity defective phenotype of dshhs.sev.B

NOT Suppressor of
Phenotype Manifest In
Enhanced by
Statement
Reference

hepr75 has axon | somatic clone phenotype, enhanceable by Mkk4e01485

hepr75 has neuron phenotype, enhanceable by Wnt4[+]/Wnt4EMS23

hepr75 has lamina phenotype, enhanceable by Wnt4[+]/Wnt4EMS23

hepr75 has eye photoreceptor cell phenotype, enhanceable by Wnt4[+]/Wnt4EMS23

hepr75 has neuron phenotype, enhanceable by Wnt4C1/Wnt4[+]

hepr75 has lamina phenotype, enhanceable by Wnt4C1/Wnt4[+]

hepr75 has eye photoreceptor cell phenotype, enhanceable by Wnt4C1/Wnt4[+]

hepr75 has neuron phenotype, enhanceable by Wnt4[+]/Wnt4P23

hepr75 has lamina phenotype, enhanceable by Wnt4[+]/Wnt4P23

hepr75 has eye photoreceptor cell phenotype, enhanceable by Wnt4[+]/Wnt4P23

Suppressed by
Statement
Reference

hepr75/hep1 has adult thorax phenotype, suppressible by pucE69

hepr75/hep1 has chaeta phenotype, suppressible by pucE69

hepr75 has imaginal disc phenotype, suppressible by pucE69

hepr75 has wing disc phenotype, suppressible by pucE69

NOT suppressed by
Statement
Reference
Enhancer of
Statement
Reference

hepr75 is an enhancer of axon | somatic clone phenotype of Mkk4e01485

hepr75 is an enhancer of neuron phenotype of Wnt4C1

hepr75 is an enhancer of lamina phenotype of Wnt4C1

hepr75 is an enhancer of eye photoreceptor cell phenotype of Wnt4C1

hepr75 is an enhancer of neuron phenotype of Wnt4EMS23

hepr75 is an enhancer of lamina phenotype of Wnt4EMS23

hepr75 is an enhancer of neuron phenotype of Wnt4P23

hepr75 is an enhancer of lamina phenotype of Wnt4P23

hepr75 is an enhancer of eye photoreceptor cell phenotype of Wnt4P23

hep[+]/hepr75 is an enhancer of adult thorax | dorsal phenotype of Src42AJp45

NOT Enhancer of
Statement
Reference

hep[+]/hepr75 is a non-enhancer of ommatidium phenotype of MtlUAS.cMa, Scer\GAL4hs.2sev

hepr75 is a non-enhancer of phenotype of Rho1rev220

Suppressor of
Statement
Reference

hepr75 is a suppressor | partially of wing phenotype of RbfUAS.cDa, Scer\GAL4vg.PM

hep[+]/hepr75 is a suppressor of eye phenotype of Mmus\Gria1Lc.UAS, Scer\GAL4hs.2sev

hep[+]/hepr75 is a suppressor of retina | progressive phenotype of ebi1-334.GMR

hep[+]/hepr75 is a suppressor of eye | somatic clone phenotype of ebik16213

hep[+]/hepr75 is a suppressor of eye phenotype of Scer\GAL4GMR.PS, TgA.UAS

hep[+]/hepr75 is a suppressor of ommatidium phenotype of Scer\GAL4GMR.PS, TgA.UAS

hepr75 is a suppressor of wing disc phenotype of scrib1

hep[+]/hepr75 is a suppressor of chorion phenotype of Gadd45UASp.cPa, Scer\GAL4VP16.nos.UTR

hep[+]/hepr75 is a suppressor | partially of eye disc | ventral phenotype of L2

hep[+]/hepr75 is a suppressor | partially of eye | ventral phenotype of L2

hepr75 is a suppressor of ommatidium phenotype of Rac1V12.hs.sev

hepr75 is a suppressor of wing disc phenotype of pucE69/puc[+], tkv7/tkv427

hepr75 is a suppressor of wing disc phenotype of pucE69, tkv7/tkv427

hep[+]/hepr75 is a suppressor of ommatidium phenotype of dshhs.sev.B

hep[+]/hepr75 is a suppressor of scutum & macrochaeta phenotype of RalaS25N.UAS, Scer\GAL4sca-537.4

hepr75 is a suppressor of phenotype of dshhs.sev.B

NOT Suppressor of
Statement
Reference

hep[+]/hepr75 is a non-suppressor of ommatidium phenotype of Scer\GAL4hs.2sev, nmoUAS.cUa

hepr75 is a non-suppressor of ommatidium phenotype of ecspok

hep[+]/hepr75 is a non-suppressor of ommatidium phenotype of MtlUAS.cMa, Scer\GAL4hs.2sev

hepr75 is a non-suppressor of phenotype of Rho1rev220

Other
Additional Comments
Genetic Interactions
Statement
Reference

The axon degeneration in sensory neurons clones in the adult wing expressing Ect4ΔARM.Scer\UAS.T:Hsap\MYC under the control of Scer\GAL4nSyb.PS can be suppressed by combination with hepr75.

hepr75 hemizygosity suppresses the tumor phenotype of scrib1 homozygous third instar larval wing discs.

hepr75 does not suppress the photoreceptor differentiation defects or increased cell death seen in Vps43B1 mutant eye disc clones.

A hepr75 mutant background partially suppresses the wing phenotypes seen when RbfScer\UAS.cDa is expressed under the control of Scer\GAL4vg.PM.

A hepr75 mutant background partially suppresses the ectopic wing tissue seen when RbfD253A.Scer\UAS is expressed under the control of Scer\GAL4vg.PM.

hepr75/+ suppresses the mild rough eye phenotype seen in eyes containing large ebik16213 clones.

hepr75/+ suppresses the late-onset retinal degeneration phenotype of ebi1-334.GMR/+ flies.

Single cell Mkk4e01485, hepr75 double mutant clones in mushroom bodies show a higher frequency of axon breaks than in clones of either single mutant.

A hepr75/+, background suppressed the rough eye phenotype found upon expression of TgA.Scer\UAS under the control of Scer\GAL4GMR.PS.

Hemizygous hepr75 suppresses the wing disc tumors seen in scrib1 mutant larvae.

hepr75/+ is unable to suppress the Scer\GAL4pnr-MD237>POSHScer\UAS.cSa lethality phenotype.

Expression of Axud1Scer\UAS.cGa with Scer\GAL4salm-EPv in a heterozygous hepr75 background results in a partial suppression of the ectopic Axud1Scer\UAS.cGa expression wing phenotype.

The cleft notum phenotype caused by expression of Nf-YAdsRNA.231-399.Scer\UAS.WIZ is only marginally enhanced by hepr75/+.

The ommatidial rotation defects observed in ecspok hemizygous adult eyes are not suppressed by hepr75/+.

The dorsalised eggshell phenotype caused by expression of Gadd45Scer\UAS.P\T.cPa under the control of Scer\GAL4nos.UTR.T:Hsim\VP16 is significantly suppressed by hepr75/+.

A hepr75 mutant background suppresses JNK pathway activation normally found when lkb1Scer\UAS.cLa is expressed by either Scer\GAL4GMR.PF or Scer\GAL4ap-md544. In addition, Scer\GAL4GMR.PF>lkb1Scer\UAS.cLa-induced apoptosis in eye imaginal discs is also completely suppressed.

A hepr75 background enhances the Wnt4EMS23/+ R axon misrouting phenotype.

A Wnt4EMS23/+ background enhances the hepr75 R axon misrouting phenotype.

A Wnt4C1/+ background enhances the hepr75 R axon misrouting phenotype. Along with ventral-to-dorsal misroutings, these mutants also show dorsal axons projecting to the medial region of the lamina.

A hepr75 background enhances the Wnt4C1/+ R axon misrouting phenotype. Along with ventral-to-dorsal misroutings, these mutants also show dorsal axons projecting to the medial region of the lamina.

A Wnt4P23/+ background enhances the hepr75 R axon misrouting phenotype.

A hepr75 background enhances the Wnt4P23/+ R axon misrouting phenotype.

32% of hepr75/+; L2/+ flies show a strong suppression of the ventral eye loss phenotype seen in L2/+ flies.

In flies carrying a pucE69-A transgene (with wild-type puc activity) in a hepr75 background, wounds in the wing discs do not heal after 24 hours, but are partially contracted. In contrast, in flies carrying a pucE69-F transgene (which inactivates puc) in a hepr75 background, wounds partially heal after 24 hours; wound edges become curled and peripodial epithelium cells elongate towards the wound.

The elimination of Ts(1Lt;2Lt)scS2/+ clones in wild-type wing discs is blocked if the wing discs are also mutant for hepr75.

Dominantly enhances the lethality and cleft thorax phenotypes of Src42AJp45 homozygotes.

Suppresses the cell death seen in the imaginal discs of lacek05305/lace2 animals.

The number of dying cells in the late third larval instar tkv7/tkv427 wing disc is increased compared to wild type; a cluster of dying cells appears in the primordial wing tip. The appearance of this apoptotic cluster is more apparent if the larvae are also heterozygous for pucE69. The appearance of the cluster of apoptotic cells is suppressed in hepr75/Y ; tkv7/tkv427; pucE69/+ larvae. Dying cells are distributed throughout the primordium of the proximal wing in wing discs expressing tkvCA.Scer\UAS under the control of Scer\GAL471B but are absent from the distal wing primordium. This cell death is suppressed if the larvae are also hemizygous for hepr75.

Double mutants with pucE69/+ show discs of uniform size intermediate between those of wild type and unsuppressed hep single mutants. In combination with pucE69 the hepr75/hep1 adult defects defects are strongly reduced.

hepr75, suppresses the ommatidial polarity defects seen in dshhs.sev.B flies grown at 29oC. About 85% of ommatidia are in their correct polarity compared to 55% in dshhs.sev.B alone. Dominantly suppresses the ommatidial polarity phenotype seen in flies with msnEP549 driven by Scer\GAL4hs.2sev, producing near wild-type ommatidial arrays.

hepr75/+ msn102/+ embryos have a dorsal open phenotype.

Xenogenetic Interactions
Statement
Reference

A hepr75/+ background rescues the reduced adult eye size phenotype found in Scer\GAL4hs.2sev->Mmus\Gria1Lc.Scer\UAS flies.

A hepr75 bsk1 background rescues the reduced adult eye size phenotype found in Scer\GAL4hs.2sev->Mmus\Gria1Lc.Scer\UAS flies. Quantification of the ommatidia density suggests that ~47% of spreading apoptosis in R cells can be rescued by a hepr75 bsk1 double mutant background.

The lethality of hemizygous males is not significantly rescued by Mmus\Prkmk7Ubi-p63E.PH, Xlae\Mek2Ubi-p63E.PH or Mmmm\Sek1Ubi-p63E.PH.

Complementation and Rescue Data
Comments

The lethality of hemizygous males is rescued by hepUbi-p63E.PG, giving rise to viable, fertile adults in 66% of cases.

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Mutant
Wild-type
Stocks (1)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (4)
References (67)