Excision of the P-element insertion.
adult thorax (with hep1)
cuticle & abdomen
cuticle & abdomen | germ-line clone
cuticle & thorax
cuticle & thorax | germ-line clone
cuticle | dorsal | rescuable maternal effect (with hep1)
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
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.
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.
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.
hepr75 has abnormal neuroanatomy | somatic clone phenotype, enhanceable by Mkk4e01485
hepr75 has abnormal neuroanatomy phenotype, enhanceable by Wnt4[+]/Wnt4EMS23
hepr75 has abnormal neuroanatomy phenotype, enhanceable by Wnt4C1/Wnt4[+]
hepr75 has abnormal neuroanatomy phenotype, enhanceable by Wnt4[+]/Wnt4P23
hepr75 has abnormal wound healing phenotype, suppressible | partially by pucE69-F
hepr75 has abnormal wound healing 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
hepr75 is an enhancer of abnormal neuroanatomy | somatic clone phenotype of Mkk4e01485
hepr75 is an enhancer of abnormal neuroanatomy phenotype of Wnt4C1
hepr75 is an enhancer of abnormal neuroanatomy phenotype of Wnt4EMS23
hepr75 is an enhancer of abnormal neuroanatomy phenotype of Wnt4P23
hep[+]/hepr75 is an enhancer of lethal | recessive phenotype of Src42AJp45
hep[+]/hepr75 is a non-enhancer of abnormal planar polarity phenotype of MtlUAS.cMa, Scer\GAL4hs.2sev
hep[+]/hepr75 is a suppressor | partially of increased cell death | larval stage phenotype of RpS3Plac92, ykiB5
hep[+]/hepr75 is a suppressor | partially of visible | adult stage phenotype of RpS3Plac92, ykiB5
hep[+]/hepr75 is a suppressor | partially of decreased size | adult stage phenotype of RpS3Plac92, ykiB5
hep[+]/hepr75 is a suppressor | partially of visible | adult stage phenotype of CtBP334Δ4, Scer\GAL4rn-GAL4-5, egrUAS.cUa
hepr75 is a suppressor of neoplasia | third instar larval stage phenotype of scrib1
hepr75 is a suppressor | partially of visible phenotype of RbfUAS.cDa, Scer\GAL4vg.PM
hep[+]/hepr75 is a suppressor of increased cell death phenotype of Mmus\Gria1Lc.UAS, Scer\GAL4hs.2sev
bsk1/hepr75 is a suppressor of increased cell death phenotype of Mmus\Gria1Lc.UAS, Scer\GAL4hs.2sev
hep[+]/hepr75 is a suppressor of abnormal neuroanatomy | adult stage | progressive phenotype of ebi1-334.GMR
hepr75 is a suppressor of hyperplasia phenotype of scrib1
hep[+]/hepr75, Scer\GAL4salm.EPv is a suppressor | partially of visible phenotype of Axud1UAS.cGa, Scer\GAL4salm.EPv
hep[+], Scer\GAL4GMR.PF, hepr75, Scer\GAL4GMR.PF is a suppressor of increased cell death phenotype of Scer\GAL4GMR.PF/Scer\GAL4GMR.PF, Lkb1UAS.cLa
hepr75 is a suppressor | partially of increased cell death | cell non-autonomous phenotype of Scer\GAL4dpp.blk1, MycUAS.cZa
hepr75 is a suppressor | partially of increased cell death | somatic clone phenotype of Slik1
hepr75 is a suppressor | partially of abnormal planar polarity phenotype of Scer\GAL4hs.2sev, Tak1UAS.cMa
hep[+]/hepr75 is a suppressor of abnormal planar polarity phenotype of dshhs.sev.B
hep[+]/hepr75 is a suppressor of abnormal planar polarity phenotype of Scer\GAL4hs.2sev, msnEP549
hepr75 is a non-suppressor of abnormal neuroanatomy | somatic clone | adult stage phenotype of SarmΔARM.UAS.Tag:MYC, Scer\GAL4nSyb.PS
hepr75 is a non-suppressor of increased cell death | somatic clone | third instar larval stage phenotype of Vps43B1
hep[+]/hepr75 is a non-suppressor of lethal - all die during embryonic stage phenotype of POSHUAS.cSa, Scer\GAL4pnr-MD237
hep[+]/hepr75 is a non-suppressor of abnormal planar polarity phenotype of MtlUAS.cMa, Scer\GAL4hs.2sev
hepr75 has Kenyon cell | somatic clone phenotype, enhanceable by Mkk4e01485
hepr75 has axon | somatic clone phenotype, enhanceable by Mkk4e01485
hepr75 has eye photoreceptor cell phenotype, enhanceable by Wnt4[+]/Wnt4EMS23
hepr75 has eye photoreceptor cell phenotype, enhanceable by Wnt4C1/Wnt4[+]
hepr75 has eye photoreceptor cell phenotype, enhanceable by Wnt4[+]/Wnt4P23
hepr75/hep1 has adult thorax phenotype, suppressible by pucE69
hepr75 has imaginal disc phenotype, suppressible by pucE69
hepr75 has micropyle | somatic clone | maternal effect phenotype, non-suppressible by licUbi-p63E.PS
hepr75 has dorsal appendage | somatic clone | maternal effect phenotype, non-suppressible by licUbi-p63E.PS
hepr75 is an enhancer of Kenyon cell | somatic clone phenotype of Mkk4e01485
hepr75 is an enhancer of axon | somatic clone phenotype of Mkk4e01485
hepr75 is an enhancer of eye photoreceptor cell phenotype of Wnt4C1
hepr75 is an enhancer of embryonic/larval optic stalk phenotype of Wnt4C1
hepr75 is an enhancer of eye photoreceptor cell phenotype of Wnt4EMS23
hepr75 is an enhancer of embryonic/larval optic stalk phenotype of Wnt4EMS23
hepr75 is an enhancer of eye photoreceptor cell phenotype of Wnt4P23
hepr75 is an enhancer of embryonic/larval optic stalk phenotype of Wnt4P23
hepr75 is an enhancer of mesothoracic tergum phenotype of PvrdsRNA.UAS, Scer\GAL4pnr-MD237
hepr75 is an enhancer of thorax phenotype of PvrdsRNA.UAS, Scer\GAL4pnr-MD237
hep[+]/hepr75 is an enhancer of adult thorax | dorsal phenotype of Src42AJp45
hep[+]/hepr75 is a non-enhancer of ommatidium phenotype of MtlUAS.cMa, Scer\GAL4hs.2sev
hepr75 is a non-enhancer of phenotype of Rho1rev220
hep[+]/hepr75 is a suppressor | partially of wing phenotype of RpS3Plac92, ykiB5
hep[+]/hepr75 is a suppressor | partially of wing disc | larval stage phenotype of RpS3Plac92, ykiB5
hep[+]/hepr75 is a suppressor | partially of wing | ectopic phenotype of CtBP334Δ4, Scer\GAL4rn-GAL4-5, egrUAS.cUa
hepr75 is a suppressor of wing disc | third instar larval stage phenotype of scrib1
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
bsk1/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
hep[+]/hepr75 is a suppressor of interommatidial bristle phenotype of Scer\GAL4GMR.PS, TgA.UAS
hep[+]/hepr75, Scer\GAL4salm.EPv is a suppressor | partially of wing blade phenotype of Axud1UAS.cGa, Scer\GAL4salm.EPv
hep[+]/hepr75, Scer\GAL4salm.EPv is a suppressor | partially of wing phenotype of Axud1UAS.cGa, Scer\GAL4salm.EPv
hep[+]/hepr75 is a suppressor of dorsal appendage phenotype of Gadd45UASp.cPa, Scer\GAL4VP16.nos.UTR
hep[+]/hepr75 is a suppressor of egg chorion phenotype of Gadd45UASp.cPa, Scer\GAL4VP16.nos.UTR
hepr75 is a suppressor | partially of eye phenotype of Scer\GAL4hs.2sev, Tak1UAS.cMa
hepr75 is a suppressor | partially of eye photoreceptor cell phenotype of Scer\GAL4hs.2sev, Tak1UAS.cMa
hepr75 is a suppressor of ommatidium phenotype of Rac1V12.hs.sev
hepr75 is a suppressor of wing disc phenotype of lace2/lacek05305
hepr75 is a suppressor of wing disc phenotype of Scer\GAL471B, tkvCA.UAS
hep[+]/hepr75 is a suppressor of ommatidium phenotype of dshhs.sev.B
hepr75 is a suppressor of ommatidium phenotype of Scer\GAL4hs.2sev, msnEP549
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
hepr75 is a non-suppressor of sensory neuron | somatic clone | adult stage phenotype of SarmΔARM.UAS.Tag:MYC, Scer\GAL4nSyb.PS
hepr75 is a non-suppressor of axon | somatic clone | adult stage phenotype of SarmΔARM.UAS.Tag:MYC, Scer\GAL4nSyb.PS
hepr75 is a non-suppressor of eye disc | somatic clone | third instar larval stage phenotype of Vps43B1
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
hep[+]/hepr75, msn102 has embryonic/first instar larval cuticle | dorsal phenotype
hepr75, msn[+]/msn102 has embryonic/first instar larval cuticle | dorsal phenotype
Expression of egrUAS.cUa under the control of Scer\GAL4rn-GAL4-5 (with tub-Gal80[ts] restricting expression to third instar larvae) in hepr75/+ background does not lead to ectopic wings compared to controls.
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.
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.
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 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.
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.
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.
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.
hepr75 is rescued by hepUbi-p63E.PG
hepr75 is rescued by hepUbi-p63E.PG
The lethality of hemizygous males is rescued by hepUbi-p63E.PG, giving rise to viable, fertile adults in 66% of cases.