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General Information
Symbol
Dmel\hep1
Species
D. melanogaster
Name
FlyBase ID
FBal0005438
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

P{SDFL} insertion 179bp upstream of the ATG codon in the longest cDNA.

Insertion components
P{SDFL}hep1
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
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In

axon & dorsal cluster neuron

embryonic leading edge cell & actin filament

Detailed Description
Statement
Reference

Hemizygous males show significantly reduced energy stores (lipids and carbohydrates) in ad libitum conditions compared to control flies. The mutant flies show rapid depletion of nutrient stores (lipids and carbohydrates) upon wet starvation compared to control flies.

Hemizygous males are significantly more sensitive to dry starvation than wild-type controls.

Wild-type flies show a reduction in wing area when shifted from 25[o]C to 29[o]C. This reduction is less pronounced in hep1 flies subjected to the same experimental conditions. hep1 flies do not show a significant reduction in the number of cells per wing when shifted from 25[o]C to 29[o]C, in contrast to wild-type flies, which show a significant reduction in the number of cells per wing under these experimental conditions. hep1 flies do not show a significant reduction in weight after being shifted from 25[o]C to 29[o]C, in contrast to wild-type flies, which show a significant reduction in weight under these conditions.

5% of hep1 homozygotes have a failure in thorax closure and hence a cleft thorax phenotype.

23% of hep1/hep699 adults have terminalia defects; females show truncation of structures posterior to tergite 7 and are unable to defecate or lay eggs. 2% of the hep1/hep699 adults have maxillary palp defects.

An average of only 7.3 dorsal cluster neuron axons cross the second optic chiasm to innervate the medulla in hep1 flies, while the wild-type number is 11 to 12.

hep1 heterozygous mutants do not have a thoracic cleft phenotype.

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

A greater number of hep1/Y mutant flies die after feeding with paraquat than wild-type flies. However, the sensitivity of these flies to G148 is similar to wild-type flies.

100% (n=70) of hep1 mutant embryo cuticles have a dorsal hole. During dorsal closure leading edge cells in these embryos lack an actin cable and there is a loss of adhesion between the amnioserosa and the dorsal epidermis.

No epidermal defects are seen in mutant animals.

Male progeny hemizygous for hep1 from hep1 homozygous mothers die as embryos with mild dorsal closure defects. All of these cuticles are 'anterior open', but only 30% fail to close the four posterior segments. 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.

Mutant adults display a mild thorax closure defect.

Eggs derived from homozygous females show an occasional reduction of the dorsal appendages.

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.

Hemizygous adults have a cleft in the dorsal midline of the thorax.

Causes poorly penetrant adult head and thoracic abnormalities. Phenotypes range from slight to strong unilateral deletions of imaginal disc-derived adult structures such as the wings, legs and eyes. A cleft runs along the dorsal midline of the thorax. In severe cases the wing disc is improperly located in the abdominal cavity with well differentiated wing tissues. hepr39/hep1 and hepr75/hep1 adult females show mutant cleft thorax and bristle defects.

Mutant embryos show a dorsal hole.

Homozygous and hemizygous adults have a cleft in the thorax at the dorsal midline, which causes a gap in the bristle pattern.

Hemizygous embryos have a dorsal open phenotype.

Homozygous adults show slight widening of the dorsal thorax.

Embryos exhibit a dorsal open phenotype.

Homozygotes often have a cleft along the dorsal midline of the thorax.

Homozygous females mated to hep1 males lay eggs that do not hatch. Homozygous females mated to wild type males yield solely female progeny. The cuticle of dead embryos from both crosses show a large gap in the dorsal structures. A few survivors also show unilateral deletions of head structures, wing, dorsal mesothorax, eye or metathoracic leg. Transheterozygous embryos with hepr75 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 females lay female progeny, any dead embryos display a strong dorsal open phenotype.

Partial deletion of eye, wing, thorax and leg. Deletions concern mostly one side of the adult body.

Partial deletions of adult structures, often unilaterally. Imprecise excision alleles cause pupal lethality.

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

hep1 has visible | recessive phenotype, enhanceable by pydtam

Suppressed by
Statement
Reference

hep1 has abnormal neuroanatomy phenotype, suppressible by Rac1J10/Rac1[+]

hep1 has chemical sensitive phenotype, suppressible by pucE69/puc[+]

hepr39/hep1 has visible phenotype, suppressible by pucE69

hepr75/hep1 has visible phenotype, suppressible by pucE69

Enhancer of
Statement
Reference

hep[+]/hep1 is an enhancer of visible phenotype of by2

NOT Enhancer of
Statement
Reference

hep[+]/hep1 is a non-enhancer of visible phenotype of Scer\GAL4en-e16E, kermitGS2053

Suppressor of
Statement
Reference

hep[+]/hep1 is a suppressor | partially of neoplasia phenotype of Sox21a6

hep1 is a suppressor of visible | adult stage phenotype of PGRP-LF200

hep[+]/hep1 is a suppressor | partially of visible phenotype of Scer\GAL4hs.2sev, Tak1UAS.cMa

hep1 is a suppressor of long lived | dominant phenotype of pucE69

hep1 is a suppressor of chemical resistant | dominant phenotype of pucE69

hep[+]/hep1 is a suppressor of visible phenotype of Rac1GMR.PN

hep1 is a suppressor | partially of lethal | recessive phenotype of pucE69

hep1/hep1 is a suppressor of lethal | recessive phenotype of pucE69

NOT Suppressor of
Statement
Reference
Other
Phenotype Manifest In
Enhanced by
Statement
Reference

hep1 has adult thorax | dorsal phenotype, enhanceable by pydtam

hep1 has adult thorax & adult cuticle | dorsal phenotype, enhanceable by pydtam

Suppressed by
Statement
Reference

hep1 has axon & dorsal cluster neuron phenotype, suppressible by Rac1J10/Rac1[+]

hep1 has axon & dorsal cluster neuron phenotype, suppressible by btlH852-3

hep1 has embryonic leading edge cell & actin filament phenotype, suppressible | partially by dshΔDEP+.UAS/Scer\GAL469B

hep1 has embryonic leading edge cell & actin filament phenotype, suppressible | partially by dshΔDIX.UAS/Scer\GAL469B

hep1 has embryonic leading edge cell & actin filament phenotype, suppressible | partially by dshUAS.cAa/Scer\GAL469B

hep1 has embryonic leading edge cell & actin filament phenotype, suppressible | partially by wgUAS.cGa/Scer\GAL469B

hep1 has wing phenotype, suppressible by pucE69

hep1 has leg phenotype, suppressible by pucE69

hep1 has eye phenotype, suppressible by pucE69

hep1 has wing disc phenotype, suppressible by pucE69

hepr39/hep1 has adult thorax phenotype, suppressible by pucE69

hepr39/hep1 has chaeta phenotype, suppressible by pucE69

hepr75/hep1 has adult thorax phenotype, suppressible by pucE69

hepr75/hep1 has chaeta phenotype, suppressible by pucE69

NOT suppressed by
Statement
Reference

hep1 has embryonic leading edge cell & actin filament phenotype, non-suppressible by armS10.UAS.Tag:MYC/Scer\GAL469B

Enhancer of
Statement
Reference

hep[+]/hep1 is an enhancer of adult thorax phenotype of Scer\GAL4ap-md544, parkUAS.Tag:MYC

hep[+]/hep1 is an enhancer of wing phenotype of by2

NOT Enhancer of
Statement
Reference
Suppressor of
Statement
Reference

hep[+]/hep1 is a suppressor | partially of adult anterior midgut epithelium phenotype of Sox21a6

hep1 is a suppressor of wing phenotype of DaxxEY09290, Scer\GAL4Bx-MS1096

hep1 is a suppressor of eye phenotype of Mmus\Gria1Lc.UAS, Scer\GAL4hs.2sev

hep[+]/hep1 is a suppressor of eye phenotype of Scer\GAL4GMR.PS, TgA.UAS

hep[+]/hep1 is a suppressor of ommatidium phenotype of Scer\GAL4GMR.PS, TgA.UAS

hep1 is a suppressor of wing phenotype of PGRP-LF200

hep[+]/hep1 is a suppressor | partially of eye phenotype of Scer\GAL4hs.2sev, Tak1UAS.cMa

hep[+]/hep1 is a suppressor | partially of eye phenotype of rprGMR.PW

hep[+]/hep1 is a suppressor | partially of ommatidium phenotype of rprGMR.PW

hep[+]/hep1 is a suppressor of eye phenotype of Rac1GMR.PN

hep[+]/hep1 is a suppressor of ommatidium phenotype of Rac1GMR.PN

hep1 is a suppressor of ommatidium phenotype of Rac1V12.hs.sev

hep[+]/hep1 is a suppressor of scutum & macrochaeta phenotype of RalaS25N.UAS, Scer\GAL4sca-537.4

NOT Suppressor of
Statement
Reference
Other
Additional Comments
Genetic Interactions
Statement
Reference

One copy of hep1 reduces tumor formation in the anterior midgut of Sox21a6 mutant flies.

The reduced wing phenotype caused by expression of DLPEY09290 under the control of Scer\GAL4Bx-MS1096 is suppressed by hep1.

Hemizygosity for hep1 does not suppress the thorax pigmentation defects seen in Pk92BΔN.Scer\UAS.T:Zzzz\FLAG, Scer\GAL4pnr-MD237 flies.

A hep1/+ background suppressed the rough eye phenotype found upon expression of TgA.Scer\UAS under the control of Scer\GAL4GMR.PS.

Males hemizygous for hep1 strongly suppress the small eye phenotype seen when egrScer\UAS.cMa is expressed under the control of Scer\GAL4GMR.PF.

The increased sensitivity of hep1/Y animals to dry starvation is suppressed by expression of NLazScer\UAS.cHTa under the control of Scer\GAL4ppl.PP.

The depletion of nutrient stores (lipids and carbohydrates) seen in hep1/Y animals upon wet starvation is suppressed by expression of NLazScer\UAS.cHTa under the control of Scer\GAL4ppl.PP.

The mild cleft thorax phenotype produced by Scer\GAL4pnr-MD237-mediated expression of Rab30dsRNA.Scer\UAS (without Dcr-2Scer\UAS.cDa) is enhanced in a background of hep1 heterozygosity or hemizygosity.

hep1 suppresses the notching phenotypes and low adult viability seen in homozygous PGRP-LF200 mutants.

The cleft notum phenotype caused by expression of Nf-YAdsRNA.231-399.Scer\UAS.WIZ under the control of Scer\GAL4pnr-MD237 is not affected by hep1/+.

Heterozygosity for hep1 partially suppresses the mutant eye phenotype caused by expression of Tak1Scer\UAS.cMa under the control of Scer\GAL4hs.2sev.

The eye ablation phenotype seen in adults expressing egrGS9830 under the control of Scer\GAL4GMR.PF is partially suppressed by hep1/+.

Rac1J10/+ suppresses the decrease in dorsal cluster neuron axon extension of hep1 mutants.

The dorsal cluster neuron axon extension phenotype of hep1 mutants is suppressed by btlH852-3.

Ectopic expression of bskK53R.Scer\UAS, under the regulatory control of Scer\GAL4Ddc.PL in hep1 mutants restores the morphology of dorsomedial dopaminergic neuron. Expression of parkScer\UAS.T:Hsap\MYC in the notum of the wing imaginal discs, under the regulation of Scer\GAL4ap-md544, in hep1/+ mutants enhances the thoracic cleft phenotype observed in parkScer\UAS.T:Hsap\MYC/Scer\GAL4ap-md544 mutants alone.

Expression of Traf1EP578, under the control of Scer\GAL4GMR.PF, in a hep1/Y background, results in the recovery of an eye of wild-type appearance.

pucE69/+, hep1/Y mutant flies have a decreased mortality rate in response to paraquat compared to hep1/Y single mutants, but an increased mortality rate compared to pucE69/+ single mutants. pucE69/+ flies with a hep1/Y background have a less pronounced extension of lifespan than pucE69/+ single mutant flies.

The addition of hep1/+ to egrGS9830, Scer\GAL4GMR.PF animals leads to a suppression of the eye phenotype. The addition of hep1/Y leads to an almost complete suppression of the eye phenotype.

The dorsal hole phenotype, loss of leading edge actin cable, and loss of adhesion between the amnioserosa and dorsal epidermis of hep1 mutant embryos are all partially suppressed by Scer\GAL469B with dshΔDEP+.Scer\UAS, wgScer\UAS.cGa, dshScer\UAS.cAa, or dshΔDIX.Scer\UAS (in decreasing order of strength of suppression). armS10.Scer\UAS.T:Hsap\MYC with Scer\GAL469B weakly suppresses the dorsal hole phenotype as well as suppressing the adhesion phenotype, but fails to rescue the formation of an actin cable. panScer\UAS.cWa with Scer\GAL469B fails to significantly suppress the dorsal hole phenotype.

The small rough eye of Traf1Scer\UAS.T:Ivir\HA1; Scer\GAL4GMR.PF animals is markedly suppressed in a hep1 heterozygous background. The rprGMR.PW eye phenotypes are significantly suppressed by heterozygosity for hep1.

The severity of the dorsal closure phenotype of male hep1 hemizygotes from hep1 homozygous mothers is enhanced by heterozygosity for chic221 : 65% of dead embryos show failure to close the four posterior segments, compared to 30% in chic+.

In combination with pucE69 the hepr39/hep1 and hepr75/hep1 adult defects are strongly reduced.

The dorsal hole phenotype is ameliorated by mutation at the N locus.

The lethality of embryos which are maternally and zygotically hep1 is rescued by one copy of pucE69. The lethality of pucE69 homozygotes is rescued if the flies are also homozygous or hemizygous for hep1. The rescued flies look remarkably normal, except some females have macrochaetae with a kink.

The dorsal open phenotype of hemizygous embryos is partially suppressed by one copy of either pucE69 or pucA251.1F3.

hep1/+ msn102/+ embryos have a dorsal open phenotype.

cnomis1/cno3 embryos have no apparent defects in dorsal closure. hep1 dominantly enhances the cnomis1/cno3 phenotype; hep1/+ ; cnomis1/cno3 embryos have a dorsal open phenotype. The dorsal thoracic cuticle of hep1 homozygous adults is severely disrupted in a pydtam homozygous background.

The hep1 dorsal open phenotype can be significantly rescued by heat induced expression of JraAsp.hs.sev.

Xenogenetic Interactions
Statement
Reference

A hep1/Y background rescues the reduced adult eye size phenotype found in Scer\GAL4hs.2sev->Mmus\Gria1Lc.Scer\UAS flies.

Complementation and Rescue Data
Comments
Images (0)
Mutant
Wild-type
Stocks (1)
Notes on Origin
Discoverer
Comments
Comments

JNK activity is reduced threefold compared to wild-type and ERK activity is similar to wild-type in extracts of homozygous embryos.

Imprecise excision by Δ2-3 gives rise to recessive pupal lethality in 10% of revertants and the lethality is associated with defects in imaginal defects.

Hybrid dysgenic excision of the P-element results in wild type and recessive revertants establishing that hep1 mutant phenotype is due to the P-element insertion.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (4)
References (70)