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General Information
Symbol
Dmel\zip1
Species
D. melanogaster
Name
FlyBase ID
FBal0018862
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
zip1D16
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
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
filamentous actin & denticle field primordium
Detailed Description
Statement
Reference
zip1 heterozygotes do not show significant differences in wing size, as compared to controls.
No myoblast fusion defects are observed in zip1 zygotic mutants.
Mutant embryos show alterations in epithelial wound repair compared to wild type. An actomyosin purse string is not assembled at the leading edge of the wound. The edges of the wound are irregular, with actin accumulated in patches that extend over a few cells and particularly at cell-cell junctions, but never forming the thick continuous cable that encircles wounds in wild-type embryos. The wounds heal, but with a severe delay, especially in the contraction phase. Wound closure is achieved by actin-rich cellular protrusions, which are increased in number in the mutant embryos compared to wild type. The reduction of the wound area occurs in jumps, as protrusions pull the wound closed by capturing protrusions from adjacent or opposing cells.
The mitochondria in the neurons of heterozygous zip1 adult brains are markedly elongated compared to controls.
Zygotic mutants for zip1 are embryonic lethal and display a prominent dorsal hole due to failed dorsal closure.
Expression of a single copy of zipFL.Scer\UAS.T:Avic\GFP under the control of Scer\GAL4en-e16E results in a wing vein expansion phenotype in 82% of wings. The penetrance of this phenotype is slightly decreased (to 72%) in a zip1/+ background. Expression of a single copy of zipDN.Scer\UAS.T:Avic\GFP under the control of Scer\GAL4en-e16E in a zip1/+ background results in lethality. Expression of a single copy of zipHMM.Scer\UAS.T:Avic\GFP under the control of Scer\GAL4en-e16E in a zip1/+ background results in a wing vein expansion phenotype in 41% of wings. Expression of a single copy of zipRod.Scer\UAS under the control of Scer\GAL4en-e16E in a zip1/+ background results in loss of posterior compartment tissue in 100% of wings. Expression of a single copy of zipRod.Scer\UAS.T:Avic\GFP under the control of Scer\GAL4en-e16E in a zip1/+ background results in a more severe phenotype than expression in a wild-type background.
Mutant embryos show a reduced level of cell intercalation at the segment boundary during dorsal closure (in the abdominal segments of wild-type embryos at the end of dorsal closure, a mixer cell moves across the segment boundary from the anterior compartment to the posterior compartment and two cells from the ventral ectoderm intercalate into the leading edge, posterior to the mixer cell).
zip3/zip1 embryos show laterality defects in the proventriculus and anterior midgut. The laterality of the other parts of the embryonic gut, including the hindgut and the posterior part of the midgut is normal in these mutants. The proventriculus and the anterior midgut do not rotate (as in wild-type) in these mutants at stages 15 to 17. zip4/zip1 embryos show laterality defects in the proventriculus and anterior midgut. The laterality of the other parts of the embryonic gut, including the hindgut and the posterior part of the midgut is normal in these mutants. The proventriculus and the anterior midgut do not rotate (as in wild-type) in these mutants at stages 15 to 17. zip2/zip1 embryos show laterality defects in the proventriculus and anterior midgut. The laterality of the other parts of the embryonic gut, including the hindgut and the posterior part of the midgut is normal in these mutants. The proventriculus and the anterior midgut do not rotate (as in wild-type) in these mutants at stages 15 to 17.
zip1/zip2 stage 16 embryos have longer dorsal trunks than normal.
Single cell clones of zip1 exhibit an increased apical cell area. Adherens junctions in multiple cell clones are intact.
zip1 mutant embryos, neither myosin nor actin accumulates tightly around the invagination edge; instead they form aggregates. In zip1 mutants, the small group of cells that initiate apical constriction is not observed, and tracheal cells form a large cavity during invagination.
The eye phenotype of rokcat.GMR flies is suppressed in a zip1/+ background. zip1/+ partially suppresses the wing phenotype of animals expressing rokcat.Scer\UAS under the control of Scer\GAL4en-e16E.
zip1 stage 15 larvae show a range of denticle phenotypes. In the mildest phenotype, larvae show cuticle shaping defects and have slightly misaligned denticle rows. The moderate phenotype, which has the highest penetrance, consists of a reduced denticle field that is ovoid in shape, misaligned denticle rows and shortened denticles. In the most severe phenotype, denticles are missing altogether. The ventral epidermis of stage 15 zip1 embryos show shaping defects of the actin protrusions that precede the formation of denticles. These protrusions are broad at the base, and are more elongated and wavy than those in wild-type embryos. Additionally, the protrusions are often not positioned at the posterior edge of denticle field primordium cells.
zip1/zip2 embryos show a dorsal closure phenotype with low penetrance. In transgenic mosaic embryos in which some cells express zipFL.Scer\UAS.T:Avic\GFP under the control of Scer\GAL4e22c in a zip1/zip2 background, leading-edge cells that do not express zipFL.Scer\UAS.T:Avic\GFP cannot maintain tension and are stretched by neighbouring zipFL.Scer\UAS.T:Avic\GFP expressing cells. The length of contiguous regions of Scer\GAL4e22c>zipFL.Scer\UAS.T:Avic\GFP expressing leading-edge cells along the supracellular purse string decrease in length over time, indicative of contraction. In contrast, non zipFL.Scer\UAS.T:Avic\GFP-expressing contiguous regions fail to contract, increasing in length over time. In transgenic mosaic embryos in which some cells express zipFL.Scer\UAS.T:Avic\GFP under the control of Scer\GAL4sqh.PW in a zip1/zip2 background, Scer\GAL4sqh.PW>zipFL.Scer\UAS.T:Avic\GFP expressing leading-edge cells that contact Scer\GAL4sqh.PW>zipFL.Scer\UAS.T:Avic\GFP expressing amnioserosa cells are severely contracted, and the scalloped morphology of the early leading edge is enhanced. In contrast, when non-expressing leading-edge cells contact non-expressing amnioserosa cells the leading edge cells fail to contract and become stretched. When non-expressing leading-edge cells contact Scer\GAL4sqh.PW>zipFL.Scer\UAS.T:Avic\GFP-expressing amnioserosa cells, leading-edge cells show some contraction. Finally, Scer\GAL4sqh.PW>zipFL.Scer\UAS.T:Avic\GFP-expressing cells show some contraction when they contact non-expressing amnioserosa cells, although this is to a lesser extent than when both cell types express zipFL.Scer\UAS.T:Avic\GFP. Nonexpressing leading-edge cells fail to incorporate into the canthus and cause inward progression of the canthus to stall. These nonexpressors never get fully incorporated into the seam - instead, a small gap is formed when zipping fails and closure bypasses the nonexpressing cells to initiate a new seam. In contrast, Scer\GAL4sqh.PW>zipFL.Scer\UAS.T:Avic\GFP-expressing cells are incorporated into each canthus at a similar and nearly constant rate. In transgenic mosaic embryos in which some amnioserosa cells express zipFL.Scer\UAS.T:Avic\GFP under the control of Scer\GAL4c381 in a zip1/zip2 background, nonexpressing amnioserosa cells fail to contract apically and remain rounded. These cells do show an apical shape change at later stages but this may be due to forces generated by surrounding Scer\GAL4c381>zipFL.Scer\UAS.T:Avic\GFP-expressing amnioserosa cells and the approaching lateral-epidermis sheet. Embryos that express zipFL.Scer\UAS.T:Avic\GFP under the control of Scer\GAL4en-e16E in a zip1/zip2 background display stripe-alignment defects in 65% of cases. Expression of zipDN.Scer\UAS.T:Avic\GFP, under the control of Scer\GAL4en-e16E, in a zip1/+ background causes stripe misalignments in 52% of embryos, while only 4% of zip1/+ embryos show this phenotype without transgene expression.
Mutant embryos exhibit defects in germ band elongation.
Unlike in wild-type, deep metameric furrow persist ventrally in zip1 embryos until well into stage 15.
zip1 homozygous and zip1/zipIIX62 embryos exhibit dramatic defects in head involution. 8% of zip1 homozygous embryos and 58% of zip1/zipIIX62 embryos have a clear dorsal hole. The remaining embryos complete dorsal closure, although they frequently show puckering or segment misalignments along the closed midline seam. During dorsal closure the leading edge in zip1/zipIIX62 embryos is very disporganized and extends a broader extent of lamellipodial and filopodial protrusions per unit length of leading edge than wild-type. The total protrusive area of leading edge cells in zip1/zip1 embryos is up to 300% greater than wild-type. Filopodia extended by these cells often coalesce into lamellipodia. The cytoskeletal architecture typical of the leading edge during dorsal clonsure in wild-type embryos is lost in zip1 homozygotes.
zip1/Df(2R)ES1 transheterozygous mutant embryos the muscle VA3 is missing from each segment and VA1 and VA2 are often both not present in each segment.
Homozygous embryos do not complete head involution. The salivary glands appear wild-type. Malpighian tubules are abnormal, remaining coiled near their juncture with the hindgut rather than extending anteriorly as in the wild-type. The diameter of the Malpighian tubules is similar to wild-type. The hindgut appears normal and the midgut constrictions appear substantially similar to wild-type. Abnormalities in the peripheral nervous system cannot be detected.
Embryos exhibit defects in dorsal closure and head involution. Labial lobes fail to migrate or fuse ventrally. Labial sensory organs remain external and become ectopic external sensory organs.
Embryos fail to complete dorsal closure as the mutant myosin fails to contribute sufficient myosin to drive dorsal closure to completion.
The nervous system develops abnormally in homozygotes, with brain tissue located more anteriorly and being larger than normal in the fully developed embryo. It is partially surrounded by the cuticle which never encloses the brain completely. The lateral fascicles of different abdominal segments do not respect segment boundaries in a variable manner. Sensory neurons of the gnathal sensory organs remain in the position of the progenitor cells, and their axons fasiculate in a single, thick axon bundle. Homozygous embryos also have an abnormal cuticle pattern.
strong allele showing severe cuticular and neurological defects
External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhancer of
Statement
Reference
zip[+]/zip1 is an enhancer of visible phenotype of Scer\GAL4en-e16E, kermitGS2053
zip[+]/zip1 is an enhancer of visible phenotype of Scer\GAL4hs.PB, towUAS.cCa
zip[+]/zip1 is an enhancer of visible | heat sensitive phenotype of fzI.hs
zip[+]/zip1 is an enhancer of visible | recessive phenotype of dsh1
Suppressor of
Statement
Reference
NOT Suppressor of
Statement
Reference
Other
Phenotype Manifest In
Enhanced by
NOT Enhanced by
Enhancer of
Statement
Reference
zip1 is an enhancer of myoblast phenotype of kirrerP298-G4
zip[+]/zip1 is an enhancer of embryonic/first instar larval cuticle phenotype of baz4
zip[+]/zip1 is an enhancer of wing hair phenotype of Scer\GAL4en-e16E, kermitGS2053
zip[+]/zip1 is an enhancer of eye phenotype of Ppt1UAS.cKa, Scer\GAL4GMR.PF/Scer\GAL4GMR.PF
zip[+]/zip1 is an enhancer of wing hair | supernumerary phenotype of Scer\GAL4hs.PB, towUAS.cCa
zip1 is an enhancer of ommatidium phenotype of S48-5
zip[+]/zip1 is an enhancer of wing hair | supernumerary phenotype of fzI.hs
zip[+]/zip1 is an enhancer of wing hair | supernumerary phenotype of dsh1
Suppressor of
Statement
Reference
zip[+]/zip1 is a suppressor | partially of head | embryonic stage phenotype of stepKG09493/stepk08110
zip[+]/zip1 is a suppressor | partially of embryonic epidermis phenotype of stepKG09493/stepk08110
zip[+]/zip1 is a suppressor of wing disc phenotype of CskGD9345, Scer\GAL4ptc-559.1
dia[+], zip[+], dia5, zip1 is a suppressor of furrow canal phenotype of Scer\GAL4VP16.mat.αTub67C, stepHMS00365
zip[+]/zip1 is a suppressor | partially of eye phenotype of Scer\GAL4arm.PS, aurAIM, aurAUAS.cWa
zip[+]/zip1 is a suppressor of eye phenotype of Scer\GAL4GMR.PU, RokUAS.cMa
zip[+]/zip1 is a suppressor of eye phenotype of Scer\GAL4GMR.PU, RokS753A.S908A.UAS
zip[+]/zip1 is a suppressor | partially of oocyte | somatic clone phenotype of flwFP41
zip[+]/zip1 is a suppressor of ommatidium phenotype of Scer\GAL4hs.2sev, nmoUAS.cUa
zip[+]/zip1 is a suppressor of wing phenotype of flw1, pucA251.1F3/puc[+]
zip[+]/zip1 is a suppressor of eye phenotype of Rokcat.GMR
zip[+]/zip1 is a suppressor | partially of crossvein phenotype of Scer\GAL4en-e16E, Rokcat.UAS
zip[+]/zip1 is a suppressor of eye disc | somatic clone phenotype of MbsT541
zip[+]/zip1 is a suppressor | partially of eye phenotype of Rac1GMR.PN
zip[+]/zip1 is a suppressor of mitotic domain 1 | embryonic cycle 14 phenotype of CycB+t10
NOT Suppressor of
Statement
Reference
zip[+]/zip1 is a non-suppressor of wing phenotype of Scer\GAL4nub-AC-62, ykiUAS.cXa.Tag:FLAG
zip[+]/zip1 is a non-suppressor of aster | embryonic cycle 5 phenotype of CycB+t10
zip[+]/zip1 is a non-suppressor of aster | embryonic cycle 6 phenotype of CycB+t10
zip[+]/zip1 is a non-suppressor of aster | embryonic cycle 7 phenotype of CycB+t10
zip[+]/zip1 is a non-suppressor of mitotic domain 1 | embryonic cycle 10 phenotype of CycB+t10
Other
Statement
Reference
Additional Comments
Genetic Interactions
Statement
Reference
Heterozygosity for zip1 partially suppresses the increased lethality, "head hole" phenotype and epidermal rosette-like structures during germband retraction, observed in stepKG09493/stepk08110 transheterozygous embryos.
zip1 enhances the myoblast fusion defects seen in kirrerP298 mutant embryos. zip1 enhances the myoblast fusion defects seen in kirrerP298 mutant embryos. In contrast to the round and dense morphology seen in wild type, the F-actin enriched-structures between unfused fusion-competent myoblasts and miniature myotubes are irregularly shaped and exhibit abnormally long protrusions.
A zip1 heterozygous mutant background suppresses the actin remodelling and subsequent basolateral invasion of epithelial cells seen in flies expressing CskGD9345 in a stripe of cells at the anterior/posterior boundary of the larval wing disc under the control of Scer\GAL4ptc-559.1.
Maternal heterozygosity for zip1 does not suppress the furrow canal expansion phenotype seen in embryos derived from mothers expressing stepHMS00365 under the control of Scer\GAL4mat.αTub67C.T:Hsim\VP16. Maternal heterozygosity for both dia5 and zip1 suppresses the furrow canal expansion phenotype seen in embryos derived from mothers expressing stepHMS00365 under the control of Scer\GAL4mat.αTub67C.T:Hsim\VP16.
A zip1 heterozygous background suppresses the small, rough eye phenotype found upon expression of rokScer\UAS.cMa under the control of Scer\GAL4GMR.PU. A zip1 heterozygous background suppresses the small, rough eye phenotype found upon expression of rokS119A.S129A.S307A.Scer\UAS under the control of Scer\GAL4GMR.PU. A zip1 heterozygous background suppresses the small, rough eye phenotype found upon expression of rokS753A.S908A.Scer\UAS under the control of Scer\GAL4GMR.PU.
51.9% of gonads fail to compact properly in enaC14-06/+, zip1/+ transheterozygous embryos, compared to 33.3% in zip1/+ single heterozygotes.
Expression of psidinScer\UAS.cKa under the control of Scer\GAL4slbo.2.6 in a zip1 heterozygous background has little or no effect on border cell migration.
One copy of zip1 partially suppresses the oocyte polarity defects seen when the posterior follicle cells are mutant for flwFP41.
aPKCk06403, zip1 double mutants display a prominent dorsal hoe merged with a large head hole indicating enhancement of the zip1 embryonic phenotype. par-6Δ226, zip1, aPKCk06403 triple mutants show similar enhancement. par-6Δ226, zip1 double mutants display a prominent dorsal hoe merged with a large head hole indicating enhancement of the zip1 embryonic phenotype. par-6Δ226, zip1, aPKCk06403 triple mutants show similar enhancement. zip1/+ enhances the baz4 embryonic phenotype, generating merged dorsal head holes and ventral holes.
A zip1/+ background enhances the visual system degeneration seen in Scer\GAL4GMR.PF, Ppt1Scer\UAS.cKa flies.
The multiple wing hair phenotype caused by expression of towScer\UAS.cCa under the control of Scer\GAL4hs.PB using heat shock at 24 hours after puparium formation is enhanced if the flies are also carrying one copy of zip1.
The wing defects seen in flw1/Y ; pucA251.1F3/+ flies are suppressed to wild type by zip1/+.
The mislocalization of photoreceptors in MbsT541 clones is suppressed when eye discs have a zip1/+ background.
The amount of blistering and crumpling of wings in flies expressing MYPT-75DF117A.Scer\UAS under the control of Scer\GAL4Bx-MS1096 is suppressed by zip1.
S48-5/zip1 mutants show 19.34%+-7.06 misrotated ommatidia compared to 9.55%+-1.43 seen in S48-5 mutants alone.
The small, rough eye phenotype of Rac1GMR.PN flies is partially suppressed by heterozygosity for zip1.
The fraction of flies showing a malformed leg phenotype in at least one leg, for zip1 in double heterozygous combination with one of the following alleles is - SbEbr20 : 0%, SbEbr48 : 0%, SbEbr228 : 0%, SbEbr448 : 1%, SbEbr536 : 0%, SbEbr623 : 0%, Rho1Ebr233 : 2%, Rho1Ebr246 : 6%, bsEbr292 : 0%, E(br)24Ebr24 : 11%, E(br)65Ebr65 : 2%, E(br)155Ebr155 : 1%, E(br)165Ebr165 : 6%, E(br)333Ebr333 : 3%, E(br)72Ebr72 : 1%, E(br)121Ebr121 : 32%, E(br)160Ebr160 : 1%, E(br)187Ebr187 : 0%, E(br)420Ebr420 : 2% and E(br)444Ebr444 : 1%.
Xenogenetic Interactions
Statement
Reference
One copy of zip1 enhances the increase in mitochondria length seen when Hsap\MAPTR406W.Scer\UAS is expressed under the control of Scer\GAL4elav.PU.
Expression of two copies of Dpse\l(2)gl+t12.2 raises the penetrance of the zip1/zip2 failed dorsal closure phenotype to 100%. Ubiquitous overexpression of zipFL.Scer\UAS.T:Avic\GFP, under the control of the Scer\GAL4sqh.PW, rescues dorsal closure in more than 84% of zip1/zip2; Dpse\l(2)gl+t12.2/Dpse\l(2)gl+t12.2 embryos. 61% of these rescued flies survive to hatch as larvae, 41% survive to pupal stages and 2.8% eclose as adults. Expression of zipFL.Scer\UAS.T:Avic\GFP in the epidermis and a few amnioserosa cells, driven by Scer\GAL4e22c, rescues the zip1/zip2; Dpse\l(2)gl+t12.2/Dpse\l(2)gl+t12.2 dorsal closure phenotype in 88% of embryos. Rescued flies survive to larval stages in 60% of cases and to pupal stages in 21% of cases, although no flies eclose. Expression of zipFL.Scer\UAS.T:Avic\GFP in the amnioserosa, driven by Scer\GAL4c381, rescues the dorsal closure phenotype of Dpse\l(2)gl+t12.2/Dpse\l(2)gl+t12.2 mutants in 82% of embryos. However, none of the rescued embryos survive to larval stages. Similarly, when zipFL.Scer\UAS.T:Avic\GFP expression is driven in the leading edge by Scer\GAL4LE, dorsal closure is rescued in 87% of embryos, but only 1% of flies survive to larval stages. zipFL.Scer\UAS.T:Avic\GFP expression in epidermal stripes, driven by Scer\GAL4en-e16E, rescues dorsal closure in only half of embryos and does not rescue lethality.
Complementation and Rescue Data
Comments
Expression of zipFL.Scer\UAS.T:Avic\GFP under the control of Scer\GAL4sqh.PW rescues the embryonic lethality of zip1/zip2 animals. 86 +/- 2% of the rescued animals survive to the pupal stage, but only 6 +/- 7% eclose as adults. Expression of zipR1171C.Scer\UAS.T:Avic\GFP under the control of Scer\GAL4sqh.PW rescues the embryonic lethality of zip1/zip2 animals. 62 +/- 10% of the rescued animals survive to the pupal stage, but only 18 +/- 12% eclose as adults. Expression of zipD1430N.Scer\UAS.T:Avic\GFP under the control of Scer\GAL4sqh.PW rescues the embryonic lethality of zip1/zip2 animals. 72 +/- 5% of the rescued animals survive to the pupal stage, but no animals survive to the adult stage. Expression of zipD1847K.Scer\UAS.T:Avic\GFP under the control of Scer\GAL4sqh.PW rescues the embryonic lethality of zip1/zip2 animals. 85 +/- 12% of the rescued animals survive to the pupal stage, but no animals survive to the adult stage. Expression of zipR1933X.Scer\UAS.T:Avic\GFP under the control of Scer\GAL4sqh.PW rescues the embryonic lethality of zip1/zip2 animals. 85 +/- 4% of the rescued animals survive to the pupal stage, but no animals survive to the adult stage.
Expression of zipScer\UAS.T:Avic\GFP, driven by Scer\GAL4mat.αTub67C.T:Hsim\VP16, allows 34% of zip1 mutants to hatch and undergo larval development, instead of dying as embryos.
Images (0)
Mutant
Wild-type
Stocks (2)
Notes on Origin
Discoverer
Comments
Comments
zip1 homozygous embryos show a more severe phenotype than zip2 homozygous embryos.
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (8)
References (62)