Allele Dmel\zip1
| General Information | |||
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| Symbol | Dmel\zip1 | Species | D. melanogaster |
| Name | FlyBase ID | FBal0018862 | |
| Feature type | allele | Associated gene | Dmel\zip |
| Also Known As | zip1D16 | ||
| Allele class | amorphic allele - genetic evidence | ||
| Mutagen | ethyl methanesulfonate | ||
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| Description |
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| FB2013_03 | |||
| FB2013_02 | |||
| All updates | Click here to see a list of all updates to this record from FB2010_08 and on. | ||
Nature of the Allele
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| Allele class | |||
| Mutagen | |||
| Mutations Mapped to the Genome | |||
Type Location Additional Notes References | |||
| Associated Sequence Data | |||
| DDBJ
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EMBL / GenBank | DNA sequence Protein sequence Name | ||
| UniProtKB/Swiss-Prot | |||
| UniProtKB/TrEMBL | |||
| Progenitor genotype | |||
| Nature of the lesion | Statement Reference | ||
| Cytology | |||
Phenotypic Data
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Phenotypic Class
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Phenotype Manifest In
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amnioserosa (with zip2) filamentous actin & denticle field primordium filopodium (with zipIIX62) | |||
Detailed Description
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Statement Reference The mitochondria in the neurons of heterozygous zip[1] adult brains are markedly elongated compared to controls. Expression of a single copy of zip[FL.Scer\UAS.T:Avic\GFP] under the control of Scer\GAL4[en-e16E] results in a wing vein expansion phenotype in 82% of wings. The penetrance of this phenotype is slightly decreased (to 72%) in a zip[1]/+ background.
Expression of a single copy of zip[DN.Scer\UAS.T:Avic\GFP] under the control of Scer\GAL4[en-e16E] in a zip[1]/+ background results in lethality.
Expression of a single copy of zip[HMM.Scer\UAS.T:Avic\GFP] under the control of Scer\GAL4[en-e16E] in a zip[1]/+ background results in a wing vein expansion phenotype in 41% of wings.
Expression of a single copy of zip[Rod.Scer\UAS] under the control of Scer\GAL4[en-e16E] in a zip[1]/+ background results in loss of posterior compartment tissue in 100% of wings.
Expression of a single copy of zip[Rod.Scer\UAS.T:Avic\GFP] under the control of Scer\GAL4[en-e16E] in a zip[1]/+ 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). zip[3]/zip[1] 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.
zip[4]/zip[1] 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.
zip[2]/zip[1] 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. Single cell clones of zip[1] exhibit an increased apical cell area. Adherens junctions in multiple cell clones are intact. The eye phenotype of rok[cat.GMR] flies is suppressed in a zip[1]/+ background.
zip[1]/+ partially suppresses the wing phenotype of animals expressing rok[cat.Scer\UAS] under the control of Scer\GAL4[en-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. 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
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Interactions
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Phenotypic Class
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Enhancer of | |||
Statement Reference zip[+]/zip1 is an enhancer of neuroanatomy defective phenotype of Ppt1Scer\UAS.cKa, Scer\GAL4GMR.PF/Scer\GAL4GMR.PF zip1 is an enhancer of cytokinesis defective phenotype of Scer\GAL4Bx-MS1096, pblΔDH497-549.Scer\UAS | |||
Suppressor of | |||
Statement Reference zip[+]/zip1 is a suppressor | partially of cell polarity defective | recessive | somatic clone phenotype of flwFP41 | |||
Other | |||
Statement Reference | |||
Phenotype Manifest In
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Enhanced by | |||
Statement Reference | |||
Enhancer of | |||
Statement Reference zip[+]/zip1 is an enhancer of wing hair | supernumerary phenotype of Scer\GAL4hs.PB, towScer\UAS.cCa zip1 is an enhancer of wing hair | supernumerary phenotype of Scer\GAL4Bx-MS1096, pblΔDH497-549.Scer\UAS | |||
Suppressor of | |||
Statement Reference | |||
NOT Suppressor of | |||
Statement Reference zip1/zip1 is a non-suppressor of embryonic epidermis phenotype of Scer\GAL4en-e16E, diaCA.Scer\UAS.T:Ivir\HA1 | |||
Other | |||
Statement Reference | |||
Additional Comments
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Genetic Interactions
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Statement Reference 51.9% of gonads fail to compact properly in ena[C14-06]/+, zip[1]/+ transheterozygous embryos, compared to 33.3% in zip[1]/+ single heterozygotes. Expression of psidin[Scer\UAS.cKa] under the control of Scer\GAL4[slbo.2.6] in a zip[1] heterozygous background has little or no effect on border cell migration. A zip[1]/+ background enhances the visual system degeneration seen in Scer\GAL4[GMR.PF], Ppt1[Scer\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 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. 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
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Statement Reference One copy of zip[1] enhances the increase in mitochondria length seen when Hsap\MAPT[R406W.Scer\UAS] is expressed under the control of Scer\GAL4[elav.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 & Rescue Data
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| Rescued by | |||
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| Not rescued by | |||
| Comments | Expression of zip[FL.Scer\UAS.T:Avic\GFP] under the control of Scer\GAL4[sqh.PW] rescues the embryonic lethality of zip[1]/zip[2] animals. 86 +/- 2% of the rescued animals survive to the pupal stage, but only 6 +/- 7% eclose as adults.
Expression of zip[R1171C.Scer\UAS.T:Avic\GFP] under the control of Scer\GAL4[sqh.PW] rescues the embryonic lethality of zip[1]/zip[2] animals. 62 +/- 10% of the rescued animals survive to the pupal stage, but only 18 +/- 12% eclose as adults.
Expression of zip[D1430N.Scer\UAS.T:Avic\GFP] under the control of Scer\GAL4[sqh.PW] rescues the embryonic lethality of zip[1]/zip[2] animals. 72 +/- 5% of the rescued animals survive to the pupal stage, but no animals survive to the adult stage.
Expression of zip[D1847K.Scer\UAS.T:Avic\GFP] under the control of Scer\GAL4[sqh.PW] rescues the embryonic lethality of zip[1]/zip[2] animals. 85 +/- 12% of the rescued animals survive to the pupal stage, but no animals survive to the adult stage.
Expression of zip[R1933X.Scer\UAS.T:Avic\GFP] under the control of Scer\GAL4[sqh.PW] rescues the embryonic lethality of zip[1]/zip[2] 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. | ||
Stocks
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| Bloomington | |||
| Kyoto | 107626 | ||
Notes on Origin
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Comments
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External Crossreferences & Linkouts
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Synonyms & Secondary IDs
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| Reported As | |||
| Symbol Synonym | ID16 zip-1 zip1 (Franke et al., 2006, Brodu and Casanova, 2006, Christensen et al., 2008.9.3, Walters et al., 2006, Chung et al., 2007, Kirchner et al., 2007, Kirchner et al., 2007, Rodriguez-Diaz et al., 2008, Homem and Peifer, 2008, Warner and Longmore, 2009, Franke et al., 2010, Chung et al., 2009, Gettings et al., 2010, Monier et al., 2010, Djiane and Mlodzik, 2010, Verdier et al., 2006, Saja et al., 2010, Fiehler and Wolff, 2008, Okumura et al., 2010, Sun et al., 2011, Sano et al., 2012, Gault et al., 2012, Franke et al., 2007, Duboff et al., 2012) zip1D16 zipID16 zpr1D16 | ||
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References
( 51 ) | |||
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Recent research papers ( 5 ) | |||
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Recent Updates
External Crossreferences & Linkouts