Allele Dmel\shg^R69

General Information
Symbol	Dmel\shg^R69	Species	D. melanogaster
Name		FlyBase ID	FBal0092526
Feature type	allele	Associated gene	Dmel\shg

Allele class	loss of function allele
Mutagen	P-element activity
Recent Updates
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FB2013_03
FB2013_02
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Nature of the Allele
Allele class	loss of function allele (Godt and Tepass, 1998, Johnson et al., 2008)
Mutagen	P-element activity (Godt and Tepass, 1998)
Mutations Mapped to the Genome

Type Location Additional Notes References
Associated Sequence Data
DDBJ / EMBL / GenBank	DNA sequence Protein sequence Name

UniProtKB/Swiss-Prot
UniProtKB/TrEMBL

Progenitor genotype	shg^k03401 (Godt and Tepass, 1998)
Nature of the lesion	Statement Reference Deletion extending from the w gene in the P{lacW} element into the shg coding region, removing the translation start site, the signal peptide and all cadherin repeats. (Godt and Tepass, 1998)
Caused by insertion	P{?'lacW}shg^R69 (Godt and Tepass, 1998, Pacquelet et al., 2003, Geisbrecht and Montell, 2002, Le Bras and Van Doren, 2006, Haruta et al., 2010)
Cytology
Phenotypic Data
Phenotypic Class
	cell migration defective \| germline clone (Haruta et al., 2010) lethal (Haruta et al., 2010) lethal \| embryonic stage \| recessive (Niewiadomska et al., 1999) lethal \| recessive (Myster et al., 2003) size defective \| larval stage \| somatic clone (Haruta et al., 2010)
Phenotype Manifest In
	border follicle cell \| germline clone (Niewiadomska et al., 1999, Haruta et al., 2010) border follicle cell \| somatic clone (Niewiadomska et al., 1999) cell-cell adherens junction \| embryonic stage, with shg^{DEΔ734-1316.Ubi.T:Avic\GFP-EGFP} (Haruta et al., 2010) centripetally migrating follicle cell \| germline clone (Niewiadomska et al., 1999) centripetally migrating follicle cell \| somatic clone (Niewiadomska et al., 1999) cone cell \| somatic clone (Hayashi and Carthew, 2004) egg chamber \| somatic clone (Niewiadomska et al., 1999) embryonic/first instar larval cuticle (Fox et al., 2005, Sawyer et al., 2009) embryonic/larval hindgut (Taniguchi et al., 2011, Taniguchi et al., 2011) embryonic/larval hindgut (with shg^R758) (Taniguchi et al., 2011) embryonic/larval trachea (Haruta et al., 2010) embryonic head (Haruta et al., 2010) embryonic head, with shg^{DEΔ734-1316.Ubi.T:Avic\GFP-EGFP} (Haruta et al., 2010) embryonic head, with shg^{DEΔ833-1316.Ubi.T:Avic\GFP-EGFP} (Haruta et al., 2010) embryonic ventral epidermis (Myster et al., 2003, Haruta et al., 2010) embryonic ventral epidermis, with shg^{DEΔ833-1316.Ubi.T:Avic\GFP-EGFP} (Haruta et al., 2010) female germline stem cell \| somatic clone (Song et al., 2002) follicle stem cell \| somatic clone (Song and Xie, 2002) gonad \| embryonic stage (Mathews et al., 2006) imaginal disc \| somatic clone (Haruta et al., 2010) male germline stem cell \| germline clone (Wang et al., 2006) oocyte (Song and Xie, 2002) oocyte \| germline clone (Godt and Tepass, 1998, Haruta et al., 2010) oocyte \| somatic clone (Godt and Tepass, 1998) primary pigment cell \| somatic clone (Hayashi and Carthew, 2004) ventral furrow, with shg^{DEΔ734-1316.Ubi.T:Avic\GFP-EGFP} (Haruta et al., 2010)
Detailed Description
	Statement Reference Homozygous and shg[R758]/shg[R69] embryos show defects in the left-right asymmetry of the hindgut: left-right inversion and bilateralism phenotypes are seen at stage 14 in the mutant embryos. The mean length of the cell boundaries at the apical hindgut epithelium is greater than normal in mutant embryos at late stage 12, early stage 13 and late stage 13. (Taniguchi et al., 2011) Mutant hindgut epithelial cells do not show the left-right asymmetry in cell shape which is seen in wild-type hindgut epithelial cells at late stage 12 (before epithelial tube rotation). (Taniguchi et al., 2011) Zygotic mutant embryos of shg[R69] fail to maintain epithelial integrity in the ventral and head regions, and neighboring dorsal trunk branches of the trachea fail to fuse. shg[R69] mutant cell clones are not able to grow in size in the larval epithelia of imaginal discs and appear to be eliminated from the tissues. In egg chambers in which the germ-line is homozygous for shg[R69], the oocyte is misplaced, and the border cell cluster fails to migrate between the nurse cells. shg[DEΔ833-1316.Ubi.T:Avic\GFP-EGFP] is incapable of rescuing the zygotic shg[R69] defects in the head and ventral epidermis. However, the transgene exhibited some rescuing activity in helping form pinched fusions of the dorsal trunk branches of the trachea. The ventral epidermis and tracheal defects of shg[R69] are almost completely rescued by shg[DEΔ734-1316.Ubi.T:Avic\GFP-EGFP]. The head defects are not rescued by shg[DEΔ734-1316.Ubi.T:Avic\GFP-EGFP] and the primary defects appear to occur in the anterior terminal region before stage 11. Stage 12 and older embryos mutant for both maternal and zygotic shg[R69] that carry shg[DEΔ734-1316.Ubi.T:Avic\GFP-EGFP] show disorganized epidermal ectoderm, particularly in the head and ventral regions. These embryos also show defects in ventral furrow formation: the two lines of the ventral midline cells either fail to meet or only meet partially. Apical constrictions when cell shapes change are initiated relatively normally but subsequently decelerate in maternal and zygotic shg[R69] mutants carrying shg[DEΔ734-1316.Ubi.T:Avic\GFP-EGFP]. Catastrophic disruption of the junctional network follows the defective apical constriction in the mutant embryos. (Haruta et al., 2010) shg[R69] maternal and zygotic embryonic mutants retain only dorsal cuticle. (Sawyer et al., 2009) Septate junctions remain intact in pupal eye shg[R69] MARCM clones. (Warner and Longmore, 2009) shg^R69 embryos have gonadal coalescence defects. (Mathews et al., 2006) shg^R69 homozygous germline clone cells do not survive in the testis. (Wang et al., 2006) shg^R69 mutants lack head, ventral cuticle and, to some extent, dorsal cuticle. Approximately 6.6% of shg^R69 mutants are phenotypically wild-type. The majority of shg^R69 mutants (42.2%) exhibit holes in their embryonic/larval cuticle. Approximately 24.8% exhibit a dorsal cuticle only (i.e. lack ventral cuticle). Approximately 6.1% exhibit a ventral cuticle, although only in fragments. Finally, approximately 17.3% exhibit a U-shaped dorsal cuticle (a severe phenotype). (Fox et al., 2005) Primordial germ cells that are part of shg^R69 somatic clones induced in the first instar larva contribute approximately the proportions of cells to the 'germline stem cell niche' at late third instar as do wild-type. (Asaoka and Lin, 2004) When small clones of cells homozygous for shg^R69 are present in the pupal retina (40 hours after puparium formation), the membranes of mutant primary pigment cells do not adhere to neighbouring cells. However, mutant cone cells fail to adhere to primary pigment cells, but still adhere to each other. (Hayashi and Carthew, 2004) Homozygous mutant embryos secrete only a sheet or dorsal cuticle, as the ventral epidermis is so disrupted. (Myster et al., 2003) Mutant germline stem cells (GSCs) are lost very quickly (with a half-life of 0.8 weeks) after clone induction, so that mutant GSCs occur at a much lower frequency (10%) in germaria during the first week after clone induction compared to controls. More than 95% of mutant GSCs observed during the first week after clone induction are lost within 2 weeks. Homozygous primordial germ cells are only incorporated into 0.4% of niches in the ovary, compared to 17.3% incorporation in wild type. (Song et al., 2002) Marked shg^R69 somatic stem cell (SSC) clones are only induced in the adult ovary at 13% of the frequency of control clones. Two weeks after clone induction, no germaria have mutant SSC clones, but some ovarioles have mutant follicle cell patches on egg chambers. Mutant oocytes often fail to localise to the posterior end of the egg chamber. When marked shg^R69 SSC clones are induced in the third larval instar, only 0.8% of the resulting adult female germaria have marked mutant follicle cell patches, in contrast to marked wild-type clones induced in the third larval instar, where 34.3% of the resulting germaria have marked follicle cell patches. shg^R69 follicle cell clones are similar in size to control clones. (Song and Xie, 2002) Mosaic follicles in which the follicle cells are homozygous for shg^R69 show a variety of defects and eventually degenerate. Many of these follicles do not show defects in the integrity of the follicle until late oogenesis. Border follicle cell clusters in which all cells are homozygous for shg^R69 (in mosaic follicles) do not migrate between the nurse cells towards the oocyte. The clusters are located either near the anterior tip of the follicle or at the boundary between the first and second nurse cell. Mosaic border follicle cell clusters in which some cells are homozygous for shg^R69 (containing 3-5 shg⁺ and 2-4 shg^R69 cells) migrate between the nurse cells towards the oocyte. The shg⁺ cells are always found at the leading edge of the cluster. Centripetal cells show no or only rudimentary movement in stage 10b follicles that are homozygous for shg^R69 in the follicle cells (but shg⁺ in the germline). A few shg^R69 centripetal cells segregate from the follicular epithelium but remain at the periphery of the follicle. The cells do not elongate or form protrusive ends (as occurs in wild type) but take on a rounded shape. shg^R69 centripetal cells fail to migrate and have a rounded shape in mosaic follicles containing both shg^R69 homozygous and wild-type centripetal cells. The wild-type centripetal cells migrate between the nurse cells and oocyte in these mosaic follicles, but the cells have a shorter and bulkier morphology compared with wild-type follicles. Mosaic follicles in which the germline is homozygous for shg^R69 show a variety of defects and eventually degenerate. The border cell clusters remain attached to the follicular epithelium and do not penetrate between the nurse cells in follicles in which the oocyte is normally localised. They are typically found at the boundary between the first and second nurse cell. In mosaic follicles in which the germline is homozygous for shg^R69 and the oocyte is centrally localised, a border cell cluster forms at both poles of the follicle. Border cell clusters are never seen between nurse cells in these follicles, although 35% of the clusters reach the oocyte. Clusters that reach the oocyte are still in contact with the follicular epithelium. The centripetal cells fail to migrate in most mosaic follicles in which the germline is homozygous for shg^R69. In those follicles in which centripetal cells penetrate between the germline cells, the morphology of the invading cells is highly abnormal and they form irregular clusters. (Niewiadomska et al., 1999) The oocyte is positioned abnormally in 89% of stage 1 follicles with a homozygous germline and is positioned abnormally in 68% of stage 1 follicles with a homozygous follicular epithelium. Oocyte mislocalisation is also seen in follicles that are homozygous both in the germline and soma. In mosaic follicles in which 50% or more of the follicular epithelium is homozygous for shg^R69 and the oocyte is shg⁺, the oocyte attaches itself with high fidelity (98%) to the remaining shg⁺ cells. In contrast, in mosaic follicles in which 50% or more of the follicular epithelium is homozygous for shg^R69 and the oocyte is homozygous for shg^R69 only 39% of oocytes are attached to the shg⁺ follicle cells. (Godt and Tepass, 1998)
External Data
Linkouts
Interactions
	Show the genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhancer of
Statement Reference shg[+]/shg^R69 is an enhancer of increased cell death phenotype of Csk^{dsRNA.Scer\UAS}, Scer\GAL4^ptc-559.1 (Vidal et al., 2006) shg[+]/shg^R69 is an enhancer of increased cell number \| pupal stage phenotype of Scer\GAL4^GMR.PF, pyd^{3.dsRNA.Scer\UAS} (Seppa et al., 2008) shg[+]/shg^R69 is an enhancer of lethal phenotype of Patj^Δ1 (Sen et al., 2012) shg[+]/shg^R69 is an enhancer of neuroanatomy defective phenotype of p120ctn³⁰⁸ (Larson et al., 2008) shg[+]/shg^R69 is an enhancer of planar polarity defective phenotype of Scer\GAL4^GMR.PF/Scer\GAL4^GMR.PF, cindr^{dsRNA.PC.PD.Scer\UAS} (Johnson et al., 2008) shg[+]/shg^R69 is an enhancer of visible phenotype of RASSF8⁶ (Langton et al., 2009)
Other
Statement Reference Abl¹, shg[+]/shg^R69 has lethal \| embryonic stage phenotype (Grevengoed et al., 2001) Abl¹, shg^R69 has lethal \| embryonic stage phenotype (Grevengoed et al., 2001) p120ctn³⁰⁸, shg[+]/shg^R69 has partially lethal - majority die \| recessive phenotype (Myster et al., 2003) p120ctn³⁰⁸, shg^R69 has partially lethal - majority die phenotype (Myster et al., 2003) Patj^Δ1, shg[+]/shg^R69 has increased cell death \| embryonic stage phenotype (Sen et al., 2012)
Phenotype Manifest In
Enhanced by
Statement Reference shg^R69 has embryonic ventral epidermis phenotype, enhanceable by p120ctn³⁰⁸/p120ctn³⁰⁸ (Myster et al., 2003) shg^R69 has inter-ommatidial cell \| ectopic \| pupal stage P7 phenotype, enhanceable by Mad¹²/Mad[+] (Cordero et al., 2007) shg^R69 has inter-ommatidial cell \| ectopic \| pupal stage P7 phenotype, enhanceable by tkv⁸/tkv[+] (Cordero et al., 2007)
Suppressed by
Statement Reference shg^R69 has embryonic/first instar larval cuticle phenotype, suppressible by Rho1^rev220 (Fox et al., 2005)
Enhancer of
Statement Reference shg[+]/shg^R69 is an enhancer of embryonic/first instar larval cuticle phenotype of Patj^Δ1 (Sen et al., 2012) shg[+]/shg^R69 is an enhancer of embryonic/larval cuticle phenotype of baz⁴ (Shao et al., 2010) shg[+]/shg^R69 is an enhancer of eye phenotype of RASSF8⁶ (Langton et al., 2009) shg[+]/shg^R69 is an enhancer of inter-ommatidial cell \| ectopic \| pupal stage P7 phenotype of tkv⁸ (Cordero et al., 2007) shg[+]/shg^R69 is an enhancer of inter-ommatidial cell phenotype of p120ctn³⁰⁸ (Larson et al., 2008) shg[+]/shg^R69 is an enhancer of inter-ommatidial precursor cell \| supernumerary \| pupal stage phenotype of Scer\GAL4^GMR.PF, pyd^{3.dsRNA.Scer\UAS} (Seppa et al., 2008) shg[+]/shg^R69 is an enhancer of ommatidium phenotype of Scer\GAL4^GMR.PF/Scer\GAL4^GMR.PF, cindr^{dsRNA.PC.PD.Scer\UAS} (Johnson et al., 2008) shg[+]/shg^R69 is an enhancer of phenotype of p120ctn³⁰⁸ (Myster et al., 2003) shg[+]/shg^R69 is an enhancer of pigment cell phenotype of Scer\GAL4^GMR.PF/Scer\GAL4^GMR.PF, cindr^{dsRNA.PC.PD.Scer\UAS} (Johnson et al., 2008) shg[+]/shg^R69 is an enhancer of primary pigment cell phenotype of Scer\GAL4^GMR.PF/Scer\GAL4^GMR.PF, cindr^{dsRNA.PC.PD.Scer\UAS} (Johnson et al., 2008) shg[+]/shg^R69 is an enhancer of secondary pigment cell phenotype of Scer\GAL4^GMR.PF/Scer\GAL4^GMR.PF, cindr^{dsRNA.PC.PD.Scer\UAS} (Johnson et al., 2008) shg[+]/shg^R69 is an enhancer of tertiary pigment cell phenotype of Scer\GAL4^GMR.PF/Scer\GAL4^GMR.PF, cindr^{dsRNA.PC.PD.Scer\UAS} (Johnson et al., 2008) shg[+]/shg^R69 is an enhancer of wing vein phenotype of Scer\GAL4^sd-SG29.1, tkv^{dsRNA.IR2.Scer\UAS} (Cordero et al., 2007)
Suppressor of
Statement Reference shg[+]/shg^R69 is a suppressor of zonula adherens & disc epithelium proper phenotype of Csk^{dsRNA.Scer\UAS}, Scer\GAL4^ptc-559.1 (Vidal et al., 2006) shg^R69 is a suppressor of optic lobe \| somatic clone \| pupal stage phenotype of Scer\GAL4^ey-OK107, ey^{1-545.Scer\UAS.T:Hsap\MYC,T:Rep-en} (Morante et al., 2011)
Other
Statement Reference Abl⁴, shg^R69 has embryonic/first instar larval cuticle phenotype (Grevengoed et al., 2001, Grevengoed et al., 2001) Patj^Δ1, shg[+]/shg^R69 has embryonic epidermis phenotype (Sen et al., 2012)
Additional Comments
Genetic Interactions
Statement Reference shg[R69]/+ enhances the lethality of Patj[Δ1] homozygotes, with greater lethality at earlier stages. The frequency of cuticle defects seen in Patj[Δ1] embryos is also enhanced by shg[R69]/+. Late-stage shg[R69]/+ ; Patj[Δ1]/Patj[Δ1] embryos have a multilayered epidermis, many of the epidermal cells start to round up and many epidermal cells undergo apoptosis. (Sen et al., 2012) Clones in the developing optic lobe expressing ey[1-545.Scer\UAS.T:Hsap\MYC,T:en-Rep] under the control of Scer\GAL4[ey-OK107] which are also mutant for shg[R69] form clumps of cells at a much lower frequency than clones expressing ey[1-545.Scer\UAS.T:Hsap\MYC,T:en-Rep] under the control of Scer\GAL4[ey-OK107] in an otherwise wild-type background. (Morante et al., 2011) The cuticle phenotype of dead embryos derived from baz[4]/+ embryos derived from a cross of baz[4]/+ females to wild-type males is enhanced if the females also carry one copy of shg[R69]. (Shao et al., 2010) The enlarged eye phenotype seen in RASSF8[6] homozygotes is enhanced by shg[R69]/+. (Langton et al., 2009) The Scer\GAL4[GMR.PF]>cindr[dsRNA.PC.PD.Scer\UAS] mispatterning phenotype is enhanced in a heterozygous shg[R69] background. In addition, large patches of black tissue are observed in the eyes of 68.3% of these adult flies; this is a significant enhancement of the penetrance and extent of degenerative tissue that is observed in Scer\GAL4[GMR.PF]>cindr[dsRNA.PC.PD.Scer\UAS] mutant flies (12.6%). (Johnson et al., 2008) p120ctn[308], shg[R69]/+ mutant pupae exhibit disruption of the hexagonal inter-ommatidial precursor cell pattern with extra cells present in double layers around bristle cells in the retina. (Larson et al., 2008) One copy of shg[R69] strongly enhances the increase in inter-ommatidial precursor cell number seen when pyd[3.dsRNA.Scer\UAS] is expressed under the control of Scer\GAL4[GMR.PF]. (Seppa et al., 2008) shg[R69]/+ partially suppresses the abberant arangement of inter-ommatidial cells seen in the pupal and adult retinas of In(1)rst[3]/Y animals. The retinas of shg[R69]/+ animals at 42 hours APF have only very occasional inter-ommatidial patterning defects (the occasional extra or misplaced cell). This phenotype is dramatically enhanced in tkv[8]/shg[R69] or shg[R69]/shg[R69] transheterozygotes. The wing vein thickening phenotype seen in tkv[IR2.Scer\UAS]; Scer\GAL4[sd-SG29.1] adults is enhanced by shg[R69]/+. (Cordero et al., 2007) shg[R69]/+ suppresses the loss of apical profile, delamination and subsequent migration and cell death increase seen in cells at the posterior edge of theptc expression domain in Csk[IR.Scer\UAS] Scer\GAL4[ptc-559.1] third instar larvae. (Vidal et al., 2006) Follicle cells clones that are homozygous for both shg^R69 and Df(3L)79a do not cause oocyte mislocalisation, in contrast to the 75% mislocalisation induced by follicle cells mutant for Df(3L)79a alone. (Becam et al., 2005) Addition of Rho1^rev220 to shg^R69 suppresses the shg^R69 cuticular phenotype. A larger fraction of the double mutants exhibit less severe phenotypes compared to the shg<up>R69 single mutants. (Fox et al., 2005) When small clones of cells homozygous for shg^R69 are present in the retina of CadN^M19/CadN^M12 pupae (40 hours after puparium formation), cone cells in the mutant clones fail to adhere to their cone cell or primary pigment cell neighbours, and some lose all apical contact with other cells. The mutant cells round up, and the remaining wild-type cone cells in mosaic ommatidia pack into configurations typical for soap bubble aggregates. (Hayashi and Carthew, 2004) In shg^-/shg⁺ the viability of p120ctn³⁰⁸ homozygotes is reduced to 20-60% of their shg⁺/shg⁺ siblings. (Myster et al., 2003) Heterozygosity for shg^R69 results in lethality in Abl¹/+ embryos derived from homozygous Abl¹ female germline clones. 30% of the lethal progeny of females with homozygous Abl⁴ germline clones mated to shg^R69/+ ; Abl⁴/+ males have a prominent dorsal-anterior hole. (Grevengoed et al., 2001)
Xenogenetic Interactions
Statement Reference
Complementation & Rescue Data
Rescued by	Df(2R)E2/shg^R69 is rescued by shg^{Ubi-p63E.T:Avic\GFP-rs} (Oda and Tsukita, 2001) shg^R69 is rescued by shg^{mNcGSP.Ubi.T:Avic\GFP-EGFP} (Haruta et al., 2010) shg^R69 is rescued by shg^{Ubi-p63E.T:Avic\GFP-rs} (Haruta et al., 2010)
Partially rescued by	shg^R69 is partially rescued by shg^{DEΔ734-1316.Ubi.T:Avic\GFP-EGFP} (Haruta et al., 2010) shg^R69 is partially rescued by shg^{GGG-AAA.αTub84B} (Pacquelet et al., 2003) shg^R69 is partially rescued by shg^αTub84B.PP (Pacquelet et al., 2003, Mathews et al., 2006)
Not rescued by	shg^R69 is not rescued by shg^{DEΔ833-1316.Ubi.T:Avic\GFP-EGFP} (Haruta et al., 2010)
Comments	Expression of shg[Ubi-p63E.T:Avic\GFP-rs] rescues the lethality of shg[R69]. The head, ventral epidermis and tracheal defects of shg[R69] are almost completely rescued by shg[Ubi-p63E.T:Avic\GFP-rs]. When shg[Ubi-p63E.T:Avic\GFP-rs] is present, shg[R69] mutant cell clones are able to grow in size in the epithelia. These epithelia developed normally into adult tissues. When shg[Ubi-p63E.T:Avic\GFP-rs] is present in the background, egg chambers containing shg[R69] mutant germ-line clones show normal development. Cellularization occurs normally in embryos mutant for both maternal and zygotic shg[R69] that carry shg[Ubi-p63E.T:Avic\GFP-rs]. Similarly, in the presence of shg[Ubi-p63E.T:Avic\GFP-rs], posterior invagination occurs normally, and the ectoderm initiates extension and maintains epithelial integrity in embryos mutant for both maternal and zygotic shg[R69]. The ventral epidermis and tracheal defects of shg[R69] are almost completely rescued by shg[DEΔ734-1316.Ubi.T:Avic\GFP-EGFP]. The head defects are not rescued by shg[DEΔ734-1316.Ubi.T:Avic\GFP-EGFP] and the primary defects appear to occur in the anterior terminal region before stage 11. When shg[DEΔ734-1316.Ubi.T:Avic\GFP-EGFP] is present, shg[R69] mutant cell clones are able to grow in size in the epithelia. These epithelia developed normally into adult tissues. When shg[DEΔ734-1316.Ubi.T:Avic\GFP-EGFP] is present in the background, egg chambers containing shg[R69] mutant germ-line clones show normal development. Cellularization occurs normally in embryos mutant for both maternal and zygotic shg[R69] that carry shg[DEΔ734-1316.Ubi.T:Avic\GFP-EGFP]. Similarly, in the presence of shg[DEΔ734-1316.Ubi.T:Avic\GFP-EGFP], posterior invagination occurs normally, and the ectoderm initiates extension and maintains epithelial integrity in embryos mutant for both maternal and zygotic shg[R69]. However, ectopic furrows transiently appear and the extension is slightly affected, presumably because of failure in mesoderm invagination. shg[DEΔ833-1316.Ubi.T:Avic\GFP-EGFP] is incapable of rescuing the zygotic shg[R69] defects in the head and ventral epidermis. However, the transgene exhibited some rescuing activity in helping form pinched fusions of the dorsal trunk branches of the trachea. shg[mNcGSP.Ubi.T:Avic\GFP-EGFP] can rescue the lethality of of shg[R69]. The rescued embryos show normal ventral furrow and the ventral midline cells meet entirely. Stage 12 and older embryos mutant for both maternal and zygotic shg[R69] that carry shg[DEΔ734-1316.Ubi.T:Avic\GFP-EGFP] show disorganized epidermal ectoderm, particularly in the head and ventral regions. These embryos also show defects in ventral furrow formation: the two lines of the ventral midline cells either fail to meet or only meet partially. Apical constrictions when cell shapes change are initiated relatively normally but subsequently decelerate in maternal and zygotic shg[R69] mutants carrying shg[DEΔ734-1316.Ubi.T:Avic\GFP-EGFP]. Catastrophic disruption of the junctional network follows the defective apical constriction in the mutant embryos. (Haruta et al., 2010) Expression of the shg^αTub84B.PP transgene largely rescues the gonadal coalescence defects of shg^R69 embryos. (Mathews et al., 2006)
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Synonyms & Secondary IDs ( 3 )
Reported As
Symbol Synonym	DE-cadherin^shgR69 (Hayashi and Carthew, 2004) shg^R69 (Fox et al., 2005, Mathews et al., 2006, Taniguchi et al., 2011, Becam et al., 2005, Shao et al., 2010, Sen et al., 2012, Le Bras and Van Doren, 2006, Cordero et al., 2007, Warner and Longmore, 2009, Larson et al., 2008, Langton et al., 2009, Sawyer et al., 2009, Johnson et al., 2008, Morante et al., 2011, Martin et al., 2009, Taniguchi et al., 2011, Seppa et al., 2008, Haruta et al., 2010) Shg^R69 (Vidal et al., 2006)
Name Synonym
Secondary FlyBase IDs

References ( 32 )

Generate a list of	All references relating to this allele ( 32 )

List References by type	Research paper ( 31 ) Supplementary material ( 1 )
Recent research papers ( 3 )
	Sen et al., 2012, J. Cell Biol. 199(4): 685--698 Drosophila PATJ supports adherens junction stability by modulating Myosin light chain activity. [FBrf0219897] Morante et al., 2011, Development 138(4): 687--693 Cell migration in Drosophila optic lobe neurons is controlled by eyeless/Pax6. [FBrf0212874] Taniguchi et al., 2011, Science 333(6040): 339--341 Chirality in planar cell shape contributes to left-right asymmetric epithelial morphogenesis. [FBrf0214402] Show all research papers ...

Allele Dmel\shgR69

Allele Dmel\shg^R69