FlyBase Allele Report: Dmel\shg[R69]

General Information

Symbol

Dmel\shg^R69

Species

D. melanogaster

Name

FlyBase ID

FBal0092526

Feature type

allele

Associated gene

Dmel\shg

Associated Insertion(s)

P{?'lacW}shg^R69

Carried in Construct

Key Links

Allele class

loss of function allele

Mutagen

P-element activity

Nature of the Allele

Allele class

loss of function allele

(Johnson et al., 2008, Godt and Tepass, 1998)

Mutagen

P-element activity

(Godt and Tepass, 1998)

Progenitor genotype

shg^k03401

(Godt and Tepass, 1998)

Associated Insertion(s)

P{?'lacW}shg^R69

Cytology

Description

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)

Mutations Mapped to the Genome

Curation Data

Type

Location

Additional Notes

References

Variant Molecular Consequences

Associated Sequence Data

DDBJ / EMBL / GenBank

DNA sequence

Protein sequence

UniProtKB/Swiss-Prot

UniProtKB/TrEMBL

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 ( 0 )

Disease

Interaction

References

Comments on Models/Modifiers Based on Experimental Evidence ( 0 )

Disease-implicated variant(s)

Phenotypic Data

Phenotypic Class

Phenotype Manifest In

adherens junction | embryonic stage, with shg^{DEΔ734-1316.Ubi.EGFP}

(Haruta et al., 2010)

border follicle cell | germline clone

(Haruta et al., 2010, Niewiadomska et al., 1999)

border follicle cell | somatic clone

(Pacquelet and Rorth, 2005, Niewiadomska et al., 1999)

centripetal follicle cell | germline clone

(Niewiadomska et al., 1999)

centripetal follicle cell | somatic clone

(Pacquelet and Rorth, 2005, Niewiadomska et al., 1999)

cone cell | somatic clone

(Hayashi and Carthew, 2004)

egg chamber | somatic clone

(Pacquelet and Rorth, 2005, Niewiadomska et al., 1999)

embryonic/first instar larval cuticle

(Sawyer et al., 2009, Fox et al., 2005)

embryonic/larval hindgut

(Taniguchi et al., 2011, Taniguchi et al., 2011)

embryonic/larval hindgut (with shg^R758)

(Taniguchi et al., 2011)

embryonic/larval hindgut epithelium | embryonic stage

(Inaki et al., 2024)

embryonic/larval tracheal section

(Haruta et al., 2010)

embryonic head

(Haruta et al., 2010)

embryonic head, with shg^{DEΔ734-1316.Ubi.EGFP}

(Haruta et al., 2010)

embryonic head, with shg^{DEΔ833-1316.Ubi.EGFP}

(Haruta et al., 2010)

embryonic hindgut

(Inaki et al., 2024)

embryonic ventral epidermis

(Haruta et al., 2010, Myster et al., 2003)

embryonic ventral epidermis, with shg^{DEΔ833-1316.Ubi.EGFP}

(Haruta et al., 2010)

epithelial cell | somatic clone

(Pacquelet and Rorth, 2005)

female germline cyst | progressive

(Pan et al., 2007)

female germline stem cell | germline clone

(Jin et al., 2008)

female germline stem cell | progressive

(Pan et al., 2007)

female germline stem cell | somatic clone

(Song et al., 2002)

follicle stem cell | somatic clone

(Song and Xie, 2002)

germarium | progressive

(Pan et al., 2007)

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

(Haruta et al., 2010, Godt and Tepass, 1998)

oocyte | somatic clone

(Godt and Tepass, 1998)

primary pigment cell | somatic clone

(Hayashi and Carthew, 2004)

ventral furrow, with shg^{DEΔ734-1316.Ubi.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 germline stem cell (GSC) clones show less contact with the germarium cap cells than wild type clones, which leads the mutant cells to be out-competed from the niche.

(Jin et al., 2008)

7-day old shg^R69/+ germaria have normal numbers of germline stem cells (GSCs), but at 63-days old, these germaria have significantly lower GSC numbers and contain significantly fewer cysts than controls, while cap cells are maintained at normal numbers.

(Pan et al., 2007)

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)

shg^R69 mixed border cell clones exhibit migration defects, where border cell clusters are split; wild-type border cells migrate normally, whereas shg^R69 border cells are left behind.

shg^R69 mutant centripetal cells fail to migrate and eventually round up.

(Pacquelet and Rorth, 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)

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)

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)

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 genetic interaction network for Enhancers & Suppressors

Phenotypic Class

NOT Enhanced by

Statement

Reference

α-Cat::shg^Δβ.UASp, Scer\GAL4^{FRT.Rnor\Cd2.αTub84B}, shg^R69 has abnormal cell migration | somatic clone phenotype, non-enhanceable by p120ctn^RNAi.700.UAS, Scer\GAL4^{FRT.Rnor\Cd2.αTub84B}

(Pacquelet and Rorth, 2005)

Suppressed by

Statement

Reference

shg^R69 has abnormal cell migration | somatic clone phenotype, suppressible by α-Cat::shg^{shg.ΔCyt.UASp}/Scer\GAL4^{FRT.Rnor\Cd2.αTub84B}

(Pacquelet and Rorth, 2005)

shg^R69 has abnormal cell migration | somatic clone phenotype, suppressible by shg::Rnor\Cd2::α-Cat^{shg.ΔCyt.UASp}/Scer\GAL4^{FRT.Rnor\Cd2.αTub84B}

(Pacquelet and Rorth, 2005)

shg^R69 has abnormal cell migration | somatic clone phenotype, suppressible by Scer\GAL4^{FRT.Rnor\Cd2.αTub84B}/α-Cat::shg^UASp.fl

(Pacquelet and Rorth, 2005)

shg^R69 has abnormal cell migration | somatic clone phenotype, suppressible by Scer\GAL4^{FRT.Rnor\Cd2.αTub84B}/α-Cat::shg^Δβ.UASp

(Pacquelet and Rorth, 2005)

shg^R69 has abnormal cell migration | somatic clone phenotype, suppressible by Scer\GAL4^{FRT.Rnor\Cd2.αTub84B}/shg::Mmus\Cdh1^{shg.ΔCyt.UASp}

(Pacquelet and Rorth, 2005)

Enhancer of

Statement

Reference

shg[+]/shg^R69 is an enhancer of abnormal cell migration phenotype of Csk^GD9345, Scer\GAL4^ptc-559.1

(Rudrapatna et al., 2014)

shg[+]/shg^R69 is an enhancer of lethal phenotype of Patj^Δ1

(Sen et al., 2012)

shg[+]/shg^R69 is an enhancer of visible phenotype of RASSF8⁶

(Langton et al., 2009)

shg[+]/shg^R69 is an enhancer of abnormal planar polarity phenotype of Scer\GAL4^GMR.PF, cindr^{RNAi.PC.PD.UAS}

(Johnson et al., 2008)

shg[+]/shg^R69 is an enhancer of abnormal neuroanatomy phenotype of p120ctn³⁰⁸

(Larson et al., 2008)

shg[+]/shg^R69 is an enhancer of increased cell number | pupal stage phenotype of Scer\GAL4^GMR.PF, pyd^RNAi.3.UAS

(Seppa et al., 2008)

shg[+]/shg^R69 is an enhancer of increased cell death phenotype of Csk^RNAi.UAS, Scer\GAL4^ptc-559.1

(Vidal et al., 2006)

Suppressor of

Statement

Reference

shg[+]/shg^R69 is a suppressor of abnormal cell migration phenotype of Scer\GAL4^ptc-559.1, Sin3A^KK100700

(Das et al., 2013)

NOT Suppressor of

Statement

Reference

shg[+]/shg^R69 is a non-suppressor of abnormal neuroanatomy | third instar larval stage phenotype of AdamTS-A^rnwy2/AdamTS-A^rnwy1

(Skeath et al., 2017)

Other

Statement

Reference

Patj^Δ1, shg[+]/shg^R69 has increased cell death | embryonic stage phenotype

(Sen et al., 2012)

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)

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)

Phenotype Manifest In

Enhanced by

Statement

Reference

shg^R69 has interommatidial cell | pupal stage P7 | ectopic phenotype, enhanceable by tkv⁸/tkv[+]

(Cordero et al., 2007)

shg^R69 has interommatidial cell | pupal stage P7 | ectopic phenotype, enhanceable by Mad¹²/Mad[+]

(Cordero et al., 2007)

shg^R69 has embryonic ventral epidermis phenotype, enhanceable by p120ctn³⁰⁸/p120ctn³⁰⁸

(Myster et al., 2003)

Suppressed by

Statement

Reference

shg^R69 has embryonic/first instar larval cuticle phenotype, suppressible by Rho1^rev220

(Fox et al., 2005)

shg^R69 has border follicle cell | somatic clone phenotype, suppressible by shg::Rnor\Cd2::α-Cat^{shg.ΔCyt.UASp}/Scer\GAL4^{FRT.Rnor\Cd2.αTub84B}

(Pacquelet and Rorth, 2005)

shg^R69 has epithelial cell | somatic clone phenotype, suppressible by shg::Rnor\Cd2::α-Cat^{shg.ΔCyt.UASp}/Scer\GAL4^{FRT.Rnor\Cd2.αTub84B}

(Pacquelet and Rorth, 2005)

shg^R69 has egg chamber | somatic clone phenotype, suppressible by shg::Rnor\Cd2::α-Cat^{shg.ΔCyt.UASp}/Scer\GAL4^{FRT.Rnor\Cd2.αTub84B}

(Pacquelet and Rorth, 2005)

shg^R69 has centripetal follicle cell | somatic clone phenotype, suppressible by shg::Rnor\Cd2::α-Cat^{shg.ΔCyt.UASp}/Scer\GAL4^{FRT.Rnor\Cd2.αTub84B}

(Pacquelet and Rorth, 2005)

shg^R69 has border follicle cell | somatic clone phenotype, suppressible by Scer\GAL4^{FRT.Rnor\Cd2.αTub84B}/α-Cat::shg^UASp.fl

(Pacquelet and Rorth, 2005)

shg^R69 has epithelial cell | somatic clone phenotype, suppressible by Scer\GAL4^{FRT.Rnor\Cd2.αTub84B}/α-Cat::shg^UASp.fl

(Pacquelet and Rorth, 2005)

shg^R69 has egg chamber | somatic clone phenotype, suppressible by Scer\GAL4^{FRT.Rnor\Cd2.αTub84B}/α-Cat::shg^UASp.fl

(Pacquelet and Rorth, 2005)

shg^R69 has border follicle cell | somatic clone phenotype, suppressible by Scer\GAL4^{FRT.Rnor\Cd2.αTub84B}/α-Cat::shg^Δβ.UASp

(Pacquelet and Rorth, 2005)

shg^R69 has epithelial cell | somatic clone phenotype, suppressible by Scer\GAL4^{FRT.Rnor\Cd2.αTub84B}/α-Cat::shg^Δβ.UASp

(Pacquelet and Rorth, 2005)

shg^R69 has egg chamber | somatic clone phenotype, suppressible by Scer\GAL4^{FRT.Rnor\Cd2.αTub84B}/α-Cat::shg^Δβ.UASp

(Pacquelet and Rorth, 2005)

shg^R69 has border follicle cell | somatic clone phenotype, suppressible by Scer\GAL4^{FRT.Rnor\Cd2.αTub84B}/shg::Mmus\Cdh1^{shg.ΔCyt.UASp}

(Pacquelet and Rorth, 2005)

shg^R69 has epithelial cell | somatic clone phenotype, suppressible by Scer\GAL4^{FRT.Rnor\Cd2.αTub84B}/shg::Mmus\Cdh1^{shg.ΔCyt.UASp}

(Pacquelet and Rorth, 2005)

shg^R69 has egg chamber | somatic clone phenotype, suppressible by Scer\GAL4^{FRT.Rnor\Cd2.αTub84B}/shg::Mmus\Cdh1^{shg.ΔCyt.UASp}

(Pacquelet and Rorth, 2005)

shg^R69 has border follicle cell | somatic clone phenotype, suppressible by α-Cat::shg^{shg.ΔCyt.UASp}/Scer\GAL4^{FRT.Rnor\Cd2.αTub84B}

(Pacquelet and Rorth, 2005)

shg^R69 has epithelial cell | somatic clone phenotype, suppressible by α-Cat::shg^{shg.ΔCyt.UASp}/Scer\GAL4^{FRT.Rnor\Cd2.αTub84B}

(Pacquelet and Rorth, 2005)

shg^R69 has egg chamber | somatic clone phenotype, suppressible by α-Cat::shg^{shg.ΔCyt.UASp}/Scer\GAL4^{FRT.Rnor\Cd2.αTub84B}

(Pacquelet and Rorth, 2005)

shg^R69 has centripetal follicle cell | somatic clone phenotype, suppressible by α-Cat::shg^{shg.ΔCyt.UASp}/Scer\GAL4^{FRT.Rnor\Cd2.αTub84B}

(Pacquelet and Rorth, 2005)

Enhancer of

Statement

Reference

shg[+]/shg^R69 is an enhancer of embryonic epidermis phenotype of step^KG09493/step^k08110

(West et al., 2017)

shg[+]/shg^R69 is an enhancer of head | embryonic stage phenotype of step^KG09493/step^k08110

(West et al., 2017)

shg[+]/shg^R69 is an enhancer of wing disc phenotype of Csk^GD9345, Scer\GAL4^ptc-559.1

(Rudrapatna et al., 2014)

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 primary pigment cell phenotype of Scer\GAL4^GMR.PF, cindr^{RNAi.PC.PD.UAS}

(Johnson et al., 2008)

shg[+]/shg^R69 is an enhancer of ommatidium phenotype of Scer\GAL4^GMR.PF, cindr^{RNAi.PC.PD.UAS}

(Johnson et al., 2008)

shg[+]/shg^R69 is an enhancer of pigment cell phenotype of Scer\GAL4^GMR.PF, cindr^{RNAi.PC.PD.UAS}

(Johnson et al., 2008)

shg[+]/shg^R69 is an enhancer of secondary pigment cell phenotype of Scer\GAL4^GMR.PF, cindr^{RNAi.PC.PD.UAS}

(Johnson et al., 2008)

shg[+]/shg^R69 is an enhancer of tertiary pigment cell phenotype of Scer\GAL4^GMR.PF, cindr^{RNAi.PC.PD.UAS}

(Johnson et al., 2008)

shg[+]/shg^R69 is an enhancer of interommatidial cell phenotype of p120ctn³⁰⁸

(Larson et al., 2008)

shg[+]/shg^R69 is an enhancer of interommatidial precursor cell | pupal stage | increased number phenotype of Scer\GAL4^GMR.PF, pyd^RNAi.3.UAS

(Seppa et al., 2008)

shg[+]/shg^R69 is an enhancer of interommatidial cell | pupal stage P7 | ectopic phenotype of tkv⁸

(Cordero et al., 2007)

shg[+]/shg^R69 is an enhancer of wing vein phenotype of Scer\GAL4^sd-SG29.1, tkv^RNAi.IR2.UAS

(Cordero et al., 2007)

shg[+]/shg^R69 is an enhancer of phenotype of p120ctn³⁰⁸

(Myster et al., 2003)

Suppressor of

Statement

Reference

shg[+]/shg^R69 is a suppressor of wing disc phenotype of Scer\GAL4^ptc-559.1, Sin3A^KK100700

(Das et al., 2013)

shg^R69 is a suppressor of adult optic lobe | somatic clone | pupal stage phenotype of Scer\GAL4^ey-OK107, ey^{1-545.enRD.UAS.Tag:MYC}

(Morante et al., 2011)

shg^R69 is a suppressor of female germline stem cell | germline clone phenotype of bgcn²⁰⁰⁹³

(Jin et al., 2008)

shg[+]/shg^R69 is a suppressor of zonula adherens & disc epithelium proper phenotype of Csk^RNAi.UAS, Scer\GAL4^ptc-559.1

(Vidal et al., 2006)

NOT Suppressor of

Statement

Reference

shg[+]/shg^R69 is a non-suppressor of larval brain | third instar larval stage phenotype of AdamTS-A^rnwy2/AdamTS-A^rnwy1

(Skeath et al., 2017)

Other

Statement

Reference

Patj^Δ1, shg[+]/shg^R69 has embryonic epidermis phenotype

(Sen et al., 2012)

Abl⁴, shg^R69 has embryonic/first instar larval cuticle phenotype

(Grevengoed et al., 2001)

Additional Comments

Genetic Interactions

Statement

Reference

The neural invasion phenotype (neural cells from the brain invade adjacent peripheral structures such as imaginal discs) observed in AdamTS-A^rnwy1/AdamTS-A^rnwy2 mutant third instar larvae is not suppressed by combination with a single copy of shg^R69.

(Skeath et al., 2017)

Heterozygosity for shg^R69 severely enhances the "head hole" phenotype of step^KG09493/step^k08110 transheterozygotes, as it results in more frequent and wider head holes, often involving merged head and dorsal holes.

(West et al., 2017)

A shg^R69 heterozygous mutant background enhances the actin remodelling and subsequent basolateral invasion of epithelial cells seen in flies expressing Csk^GD9345 in a stripe of cells at the anterior/posterior boundary of the larval wing disc under the control of Scer\GAL4^ptc-559.1.

(Rudrapatna et al., 2014)

The cell invasion phenotype seen when Sin3A^KK100700 is strongly expressed (using a line in which the transgene has been mobilised to the third chromosome) under the control of Scer\GAL4^ptc-559.1 is suppressed in a shg^R69/+ background.

(Das et al., 2013)

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 baz⁴/+ embryos derived from a cross of baz⁴/+ 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 RASSF8⁶ homozygotes is enhanced by shg^R69/+.

(Langton et al., 2009)

Unlike bgcn²⁰⁰⁹³ germline stem cell (GSC) clones, clones carrying both bgcn²⁰⁰⁹³ and shg^R69 do not outcompete wild type GSCs.

(Jin et al., 2008)

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)

p120ctn³⁰⁸, 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)rst³/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 tkv⁸/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

Expression of shg::α-Cat^{shg.ΔCyt.Scer\UAS} in follicle cells using the MARCM system and Scer\GAL4^{Scer\FRT.Rnor\CD2.αTub84B} fails to suppress the follicle cell sorting, loss of epithelial integrity and oocyte mispositioning phenotypes seen in shg^R69/+ mutant follicle cell clones.

Expression of shg::α-Cat^{shg.ΔCyt.Scer\UAS} in wild-type egg chambers using the MARCM system and Scer\GAL4^{Scer\FRT.Rnor\CD2.αTub84B} leads to a very mild cell migration defect. In mixed border cell clusters, in which half of the cells are wild-type and the other half are shg^R69 mutant cells expressing shg::α-Cat^{shg.ΔCyt.Scer\UAS}, mild delays in migration are seen. This is similar to the phenotype seen in border cells that are half wild-type and half shg^R69 mutant. Interestingly, in the presence of shg::α-Cat^{shg.ΔCyt.Scer\UAS}, mixed shg^R69/wild-type border cell clusters are never split, and all possible ratios of wild-type to mutant cells are observed.

Expression of shg::α-Cat^{shg.ΔCyt.Scer\UAS} using the MARCM system and Scer\GAL4^{Scer\FRT.Rnor\CD2.αTub84B} suppresses the migration defects seen in shg^R69 mutant centripetal cells.

Expression of shg::Rnor\CD2::α-Cat^{shg.ΔCyt.Scer\UAS} in follicle cells using the MARCM system and Scer\GAL4^{Scer\FRT.Rnor\CD2.αTub84B} suppresses the follicle cell sorting, loss of epithelial integrity and oocyte mispositioning phenotypes seen in shg^R69/+ mutant follicle cell clones. However, expression of shg::Rnor\CD2::α-Cat^{shg.ΔCyt.Scer\UAS} fails to fully suppress the migration defects of shg mutant border cells.

Expression of shg::α-Cat^Scer\UAS.fl in follicle cells using the MARCM system and Scer\GAL4^{Scer\FRT.Rnor\CD2.αTub84B} suppresses the follicle cell sorting, loss of epithelial integrity and oocyte mispositioning phenotypes seen in shg^R69/+ mutant follicle cell clones. shg::α-Cat^Scer\UAS.fl also fully rescues the migration defects of shg mutant border cells.

Expression of shg::α-Cat^{Δβ.Scer\UAS} in follicle cells using the MARCM system and Scer\GAL4^{Scer\FRT.Rnor\CD2.αTub84B} suppresses the follicle cell sorting, loss of epithelial integrity and oocyte mispositioning phenotypes seen in shg^R69/+ mutant follicle cell clones. In border cells, shg::α-Cat^{Δβ.Scer\UAS} expression partially rescues shg migration defects.

Knockdown of p120ctn through expression of p120ctn^{dsRNA.700.Scer\UAS} in shg::α-Cat^{Δβ.Scer\UAS} mutant border cells, under the control of Scer\GAL4^{Scer\FRT.Rnor\CD2.αTub84B}, does not increase the migration defects observed in shg::α-Cat^{Δβ.Scer\UAS} shg^R69/+ mutant cells.

Expression of shg::Mmus\cdh1^{shgΔC.Scer\UAS.cPa} in follicle cells using the MARCM system and Scer\GAL4^{Scer\FRT.Rnor\CD2.αTub84B} suppresses the follicle cell sorting, loss of epithelial integrity and oocyte mispositioning phenotypes seen in shg^R69/+ mutant follicle cell clones. In border cells, shg::Mmus\cdh1^{shgΔC.Scer\UAS.cPa} expression rescues shg migration defects.

(Pacquelet and Rorth, 2005)

Complementation and Rescue Data

Rescued by

shg^R69 is rescued by shg^{Ubi-p63E.sgGFP}

(Haruta et al., 2010)

shg^R69 is rescued by shg^{mNcGSP.Ubi.EGFP}

(Haruta et al., 2010)

shg^R69 is rescued by shg^UAS.cSa/Scer\GAL4^{FRT.Rnor\Cd2.αTub84B}

(Pacquelet and Rorth, 2005)

shg^R69 is rescued by shg^{ΔJM.αTub84B.PP}

(Pacquelet and Rorth, 2005)

shg^R69 is rescued by shg^{4YF.Tub84B.PP}

(Pacquelet and Rorth, 2005)

Df(2R)E2/shg^R69 is rescued by shg^{Ubi-p63E.sgGFP}

(Oda and Tsukita, 2001)

Partially rescued by

shg^R69 is partially rescued by shg^αTub84B.PP

(Mathews et al., 2006)

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)

Not rescued by

shg^R69 is not rescued by shg^{DEΔ833-1316.Ubi.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.

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^{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.

(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)

Expression of shg^Scer\UAS.cSa under the control of Scer\GAL4^{Scer\FRT.Rnor\CD2.αTub84B} suppresses the follicle cell sorting, loss of epithelial integrity and oocyte mis-positioning phenotypes seen in shg^R69 mutant follicle cell clones.

The presence of shg^{ΔJM.αTub84B.PP} fully rescues the border cell migration defects found in shg^R69 mutants. shg^{ΔJM.αTub84B.PP} also rescues all other shg^R69 phenotypes during oogenesis as well as lethality caused by the absence of endogenous shg in the embryo.

(Pacquelet and Rorth, 2005)

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Synonyms and Secondary IDs (4)

Reported As

Symbol Synonym

DE-cadherin^shgR69

(Hayashi and Carthew, 2004)

Shg^R69

(Vidal et al., 2006)

shg^null

(Hall et al., 2019)

Name Synonyms

Secondary FlyBase IDs

References (46)

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