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General Information
D. melanogaster
FlyBase ID
Feature type
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
shgIG29, shgIG
Key Links
Nature of the Allele
Mutations Mapped to the Genome
Additional Notes
Associated Sequence Data
DNA sequence
Protein sequence
Progenitor genotype
Nature of the lesion
Expression Data
Reporter Expression
Additional Information
Marker for
Reflects expression of
Reporter construct used in assay
Human Disease Associations
Disease Ontology (DO) Annotations
Models Based on Experimental Evidence ( 0 )
Modifiers Based on Experimental Evidence ( 0 )
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
Disease-implicated variant(s)
Phenotypic Data
Phenotypic Class
Phenotype Manifest In

border follicle cell & filopodium | somatic clone

border follicle cell & filopodium | somatic clone | cell non-autonomous

Detailed Description

shg1 somatic clones in an otherwise wild-type background are excluded from the neuroepithelium, form rosettes beneath the outer optic anlage and undergo apoptosis in late third instar larvae. shg1 mutant cells do not show signs of differentiation or neurogenesis.

In contrast to wild-type, shg1 mutant germline stem cell and somatic stem cell clones are not maintained in the testis. However, progeny of shg1 mutant somatic stem cells do contribute to the apical hub at a frequency similar to progeny from wild-type somatic stem cells.

The ommatidial under-rotation of Scer\GAL4hs.2sev>shgdCR3h.Scer\UAS.T:Avic\GFP-rs eyes is enhanced in flies with a shg1/+ background.

Clones mutant for shg1 in the imaginal wing disc have a roundish smooth shape and their cells are apically constricted.

Homozygous mutant embryos lack a head and ventral epidermis, which results in a lack of head and ventral cuticle. When homozygous somatic clones are made in nurse cells or border cells, the border cells are prevented from penetrating between nurse cells. The oocyte is also often mislocalized in clones, both germ-line clones and somatic clones in the follicle cells. When somatic clones are made in the follicle cells, mutant cells sort away from wild-type generating a smooth boundary at the interface.

Border cells in ovaries where the nurse cells are somatic clones of shg1, fail to migrate and do not form long (20-40 μm) or intermediate length (10-20 μm) cellular extensions. This is also the case for border cells that are part of a shg1 somatic clone, whether or not the adjacent nurse cells are also shg1 mutant.

When homozygous somatic clones are made in the thoracic epithelium, mutant cells have a smaller apical surface than their wild-type neighbours. Apical-basal polarity is defective in these cells.

Homozygous female germ line clones give rise to egg chambers with misplaced oocytes in 73% of cases. Region 2 cysts never stretch across the whole width of the germarium, thereby preventing the positioning of the oocyte in the centre of the flattened disk. The oocyte occupies random positions in these cysts. The misplaced oocytes are properly determined and have a normal karyosome. The oocyte is misplaced in 23% of mosaic cysts which contain a homozygous clone that includes the follicle cells at the posterior of the cyst. The misplaced oocyte lies adjacent to the wild-type follicle cells in these mosaic cysts. The oocyte is correctly localised in mosaic cysts where the homozygous clone includes only lateral or anterior follicle cells.

Eggs chambers of homozygous female germline clones show a number of defects, including mispositioning of the oocyte and disruptions of the actin cytoskeleton (such as floating ring canals). Nurse cells are an irregular size and shape and can be multinucleate. Nurse cell dumping is inhibited.

shg1/shg2 transheterozygotes exhibit lack of head skeleton, loss of ventral cuticle and the appearance of holes in the lateral cuticle. Heterozygous embryos are completely normal.

embryonic lethal. Embryonic cuticle has many small holes with necrotic rims. Head grossly distorted. Weak alleles show head defects and irregular flaws in segmentation pattern.

External Data
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhancer of
NOT Enhancer of
Suppressor of
Phenotype Manifest In
Enhancer of

shg[+]/shg1 is an enhancer of ommatidium phenotype of Scer\GAL4hs.2sev, nmoUAS.cUa

shg1 is an enhancer of ommatidium phenotype of S05671

shg1 is an enhancer of wing phenotype of Scer\GAL4en-e16E, armUAS.cWa

NOT Enhancer of

shg1 is a non-enhancer of ommatidium phenotype of FrlDN.UAS, Scer\GAL4sev.EP

Suppressor of
Additional Comments
Genetic Interactions

Presence of shg1 does not significantly alter eye phenotypes seen in flies with FrlDN.Scer\UAS driven by Scer\GAL4sev.EP.

shg1/+ enhances the ommatidial over-rotation phenotype which is caused by expression of nmoScer\UAS.cUa under the control of Scer\GAL4hs.2sev.

The ommatidial rotation defects observed in ecspok hemizygous adult eyes are partially suppressed by shg1/+.

Heterozygous shg1, significantly enhances the ommatidial misrotation phenotype seen S05671/+ animals.

37% of shg1/+ ; knk1/+ double heterozygous embryos have a fragmented cuticle phenotype. 31% of shg1/+ ; zepLP13/+ double heterozygous embryos have a fragmented cuticle phenotype.

Scer\GAL4arm.PS mediated expression of one or two doses of argos::shgi.Scer\UAS.T:Hsap\MYC fails to rescue the shg1/shg2 mutant phenotype. Scer\GAL4arm.PS mediated expression of argos::shgi.Scer\UAS.T:Hsap\MYC in shg1 heterozygotes causes adhesion defects; 10-20% embryos exhibit strong head defects and holes in the ventral cuticle.

Xenogenetic Interactions
Complementation and Rescue Data
Partially rescued by

Scer\GAL4arm.PS mediated expression of shgScer\UAS.cSa rescues the cuticle to wild type and rescues most embryos to hatching.

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Stocks (1)
Notes on Origin
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (6)
References (25)