Dmel\P{?'lacW}shg^R69 Insertion

General Information
Symbol	Dmel\P{?'lacW}shg^R69	Species	D. melanogaster
Name		FlyBase ID	FBti0012263
Feature type	transposable_element_insertion_site
Description
Inserted element	P{?'lacW}	Expression data
Affected gene(s)	Ecol\lacZ, shg	Viability / fertility
Causes allele(s)	Ecol\lacZ^shg-R69, shg^R69	Stock availability	none publicly available
LINE ID
Genomic Location
Chromosomal location	2R ( 57B15-57B16 )	Sequence location
Member of Large Scale Dataset(s)
Dataset
Recent Updates
Description	What does this section display? This section contains items that were added to this record for each release. It currently only tracks new links between this FlyBase report and other FlyBase data classes (e.g. genes, references, stocks) or controlled vocabulary terms (e.g. GO, anatomy terms). What does this section not display? This section does not currently display links that were removed or gene model changes.
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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.
Detailed Mapping Data
Chromosome (arm)
Sequence Location
Orientation
Cytological location (computed by FlyBase)	57B15-57B16 ( near gene of known cytology )
Cytological location (reported)
Comments concerning location
Sequence Data
Flanking sequence
Inserted Element
Construct	P{?'lacW}
Location-dependent role
Size
Associated alleles
Molecular map
Affected Gene(s)
Insertion may affect gene	Ecol\lacZ (Niewiadomska et al., 1999) shg (Godt and Tepass, 1998, Le Bras and Van Doren, 2006, Haruta et al., 2010)
Alleles and Phenotypes
Causes alleles	Ecol\lacZ^shg-R69 (Niewiadomska et al., 1999) shg^R69 (Godt and Tepass, 1998, Pacquelet et al., 2003, Geisbrecht and Montell, 2002, Le Bras and Van Doren, 2006, Haruta et al., 2010)

Lethality References lethal (Haruta et al., 2010) lethal \| embryonic stage \| recessive (Niewiadomska et al., 1999) lethal \| recessive (Myster et al., 2003)
Sterility References
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) 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 trachea (Haruta et al., 2010) embryonic head (Haruta et al., 2010) embryonic ventral epidermis (Myster et al., 2003, 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 (Haruta et al., 2010)
Detailed Description
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) 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) 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) 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) 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) 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) 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) Expression of the shg^αTub84B.PP transgene largely rescues the gonadal coalescence defects of shg^R69 embryos. (Mathews et al., 2006) shg^R69 embryos have gonadal coalescence defects. (Mathews et al., 2006) 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) shg^R69 homozygous germline clone cells do not survive in the testis. (Wang 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) 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) 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) 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 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) 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) In shg^-/shg⁺ the viability of p120ctn³⁰⁸ homozygotes is reduced to 20-60% of their shg⁺/shg⁺ siblings. (Myster et al., 2003) 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) 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) 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)
Expression Data
Reporter Expression

Additional Information
Statement Reference

Marker for
Reflects expression of
Reporter construct used in assay
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Data on Genetic Line
Line ID
Origin as a multiple insertion line
Progenitor(s) within the Genome

Related Aberration or Balancer
Aberration
Balancer
Stocks ( 0 )

Linkouts
Synonyms & Secondary IDs
Reported As
Symbol Synonym	P{?''lacW}shg^R69 (Godt and Tepass, 1998) P{?'lacW}shg^R69 (FlyBase, 1992-) shg^R69 (Le Bras and Van Doren, 2006)
Secondary FlyBase IDs

References ( 30 )

Generate a list of	All references relating to this insertion ( 30 )

List References by type	Research paper ( 28 ) Supplementary material ( 1 ) FlyBase analysis ( 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 ...

Dmel\P{?'lacW}shgR69 Insertion

Dmel\P{?'lacW}shg^R69 Insertion