Open Close
General Information
Symbol
Dmel\shg2
Species
D. melanogaster
Name
FlyBase ID
FBal0015609
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
shgIH, shg1H, shgIH81
Nature of the Allele
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
point mutation
Nucleotide change:
G21050864A
Amino acid change:
G1489D | shg-PA
Reported amino acid change:
G?D
Comment:
Site of nucleotide substitution in mutant inferred by FlyBase based on reported amino acid change.
point mutation
Nucleotide change:
G21051743A
Amino acid change:
G1196E | shg-PA
Reported amino acid change:
G?E
Comment:
Site of nucleotide substitution in mutant inferred by FlyBase based on reported amino acid change.
Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Cytology
Nature of the lesion
Statement
Reference
shg2 has two mutations: mis-sense changes in a conserved aminao acid in the lamininG domain and in a conserved residue in the cytoplasmic tail at the C-terminal end of the arm-binding site.
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 )
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
embryonic epidermis & embryonic head
embryonic trachea & cortical actin cytoskeleton
Detailed Description
Statement
Reference
shg2 heterozygous embryos do not show obvious dorsal closure defects, as compared to controls.
An average of 0.6 PGCs remain outside the midgut in embryos from mothers carrying one copy of shg2, with 29% of embryos exhibiting a phenotype.
shgR64a/shg2 embryos have abnormal gonads that exhibit both somatic gonadal precursor cluster fusion defects and compaction defects.
shg2 homozygous embryos do not progress to 1st instar larval stage due to moderate (49%) to severe (42% and 9%) defects in the embryonic head and ventral cuticle. shg2 heterozygotes do not exhibit a visible phenotype nor a reduction in viability.
Cell attachments in the tracheal branches of shg2/shgE17B mutant embryos are loosened and broken in several places, and adherens junctions appear diffuse and discontinuous. These phenotypes are more severe in the unicellular dorsal branch than the multicellular dorsal trunk.
shg2 mutant embryos display disorganised nervous systems, but the nervous system is not hyper-neuralised.
shg2 embryos show defective branch fusion and interruptions in the tubes. The tracheal cells have a rounded shape and tracheal branches tend to break. The accumulation of cortical actin is decreased in the tubules relative to controls.
Posterior spiracles in shg2 zygotic mutant embryos fail to invaginate. This invagination failure is not due to problems of cell elongation.
The ommatidial under-rotation of Scer\GAL4hs.2sev>shgdCR3h.Scer\UAS.T:Avic\GFP-rs eyes is enhanced in flies with a shg2/+ background.
shg2 mutants exhibit disrupted head and, to varying degrees, ventral epidermis. Approximately 4.5% of shg2 mutants are apparently wild-type. The majority (approximately 55%) of these mutants exhibit a fragmentary ventral cuticle phenotype. Approximately 11.4% of mutants exhibt holes in their embryonic ventral cuticle. Approximately 13.7% of shg2 mutants exhibit a dorsal cuticle phenotype.
52% of shg2 embryos show defective cardiac cell alignment. This phenotype is recessive.
Zygotic shg2 mutant embryos show disorganization of epithelial tissues in the head and the ventral epidermis.
In shg2 homozygous embryos gonad compaction is sometimes initiated, but often does not proceed to completion. The three clusters of somatic gonadal precursors (SGPs) from parasegments (PS) 10-12 are able to associate correctly with one another, and with germ cells, to form a cohesive group. However, these cells often remain loosely associated and spread over more than one parasegment, rather than compacting tightly in PS10. In the most severe cases, compaction from PS10-12 to PS10 appears completely blocked. In weaker examples, compaction is initiated but not completed, resulting in partially compacted and misshapen gonads. Phenotypes are weaker these embryos (3% severe, 50% weak, n=36) than in shgg317 homozygotes.
Mutant embryos are unable to form trachea and in some cases to complete tracheal fusion at the adherens junction. At segment boundaries where fusion does not occur. F-Actin containing fusion tracks are absent.
Homozygous mutant embryos show holes in the ventral cuticle.
The gonadal mesoderm fails to fully coalesce into an embryonic gonad in mutant embryos.
The optic placode does not invaginate in mutant embryos and remains at the surface. The placode cells lose contact and dissociate. Loss of epithelial integrity and an increase in cell death is seen in the head epidermis, resulting in partial or full exposure of the brain in late mutant embryos. Cells of the optic lobe and Bolwig's organ do not differentiate structurally.
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.
shg2/Df(2R)E2 embryos have tracheal defects; dorsal trunk cell fusion is blocked.
Homozygous female germ line clones give rise to egg chambers with misplaced oocytes in 46% of cases. This phenotype is apparent in the germarium; although region 2b cysts usually have a wild-type arrangement of germ cells in homozygous germ line clones, the oocyte never protrudes into the follicle cell layer when the cyst enters region 3, and frequently occupies a lateral position. 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.
Germline clones generate mutant germ cells that are not adherent to each other, nor to the follicle epithelium. Mutation has no effect on the number of germ cells or on their positioning in the egg chamber. Border follicle cells never enter the nurse cell cluster and instead remain stuck in the follicle cell layer. Border cells retain their motility but do not reach their target position. Also the onset of centripetal follicle cell migration is slightly delayed. These follicle cells often take the wrong pathway, causing defects in cytoplasm transport into the oocyte, nurse cell regression and gross distortion of the egg shape and structure. No fertilised eggs are obtained.
shg1/shg2 transheterozygotes exhibit lack of head skeleton, loss of ventral cuticle and the appearance of holes in the lateral cuticle.
Intermediate embryonic tracheal phenotype.
Class III allele: lacks most of the head and ventral epidermis. In germ-line clones, no eggs are recovered.
Mutants show gross disorganization of epithelial tissues in the head, ventral epidermis, Malpighian tubules and tracheal ducts. Malpighian tubule tip cells are present and differentiate into neurons, as in wild type. Tracheal tip cells are also present. Phenotype is alleviated by shghs.PU.
The principal midgut epithelial cells spread over the visceral mesoderm but do not become columnar, they maintain a rounded to cuboidal shape, and do not form a monolayer. At later stages (stage 14-17) the principle midgut epithelial cells become attached to the visceral mesoderm and gradually adopt a more wild type appearence. By the time the embryos are fully differentiated, no difference from wild type can be seen.
External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhanced by
Statement
Reference
Suppressed by
Statement
Reference
shgE17D/shg2 has lethal phenotype, suppressible by P{FlyFos-045685}
Enhancer of
Statement
Reference
Suppressor of
Statement
Reference
shg[+]/shg2 is a suppressor | partially of visible phenotype of CycEJP
Other
Phenotype Manifest In
Enhanced by
Suppressed by
Statement
Reference
Enhancer of
Statement
Reference
shg[+]/shg2 is an enhancer of amnioserosa | dorsal closure stage phenotype of jub54
shg[+]/shg2 is an enhancer of wing disc phenotype of CskGD9345, Scer\GAL4ptc-559.1
shg[+]/shg2 is an enhancer of egg chamber phenotype of RanBPMCB-6232-3/RanBPMΔ
shg[+]/shg2 is an enhancer of ovary phenotype of RanBPMCB-6232-3/RanBPMΔ
shg2 is an enhancer of ommatidium phenotype of S05671
shg2 is an enhancer of ommatidium phenotype of S48-5
shg[+]/shg2 is an enhancer of phenotype of p120ctn308
Suppressor of
Statement
Reference
shg[+]/shg2 is a suppressor of eye phenotype of Scer\GAL4GMR.PU, miple1UAS.Tag:HA
shg[+]/shg2 is a suppressor of eye phenotype of Scer\GAL4hs.2sev, miple1UAS.Tag:HA
shg[+]/shg2 is a suppressor | partially of eye phenotype of CycEJP
shg2 is a suppressor of denticle belt phenotype of arm3
Other
Additional Comments
Genetic Interactions
Statement
Reference
The dorsal closure defects observed in both jub54 and Df(1)jubII maternal-zygotic mutant embryos are enhanced by shg2 heterozygosity.
A shg2 heterozygous mutant background enhances the actin remodelling and subsequent basolateral invasion of epithelial cells seen in flies expressing CskGD9345 in a stripe of cells at the anterior/posterior boundary of the larval wing disc under the control of Scer\GAL4ptc-559.1.
A shg2 heterozygous mutant background suppresses the eye roughness seen in flies expressing miple1Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4GMR.PU. A shg2 heterozygous mutant background enhances the ommatidial rotation phenotype seen in flies expressing miple1Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4hs.2sev.
More than 50% of gonads do not form correctly in enaC14-06/+, shg2/+ transheterozygous embryos.
Embryos from Jafrac1KG05372, shg2 trans-heterozygous mothers display a statistically insigificant enhancement of the primordial germline cell adherence defect compared to single shg2 mutants. These mothers produce embryos with an average of 0.9 primordial germline cells left outside of the midgut with 26% of embryos affected.
shg2 p130CAS1 double heterozygotes do not exhibit a visible phenotype nor a reduction in viability. shg2; p130CAS1 double homozygotes arrest in late embryogenesis (and thereby do not hatch). Athough most of the embryos form at least partial cuticles, absence of p130CAS1 significantly enhances shg2 single mutant cuticle defects, with shg2; p130CAS1 mutant embryos showing severe defects that essentially eliminate head and ventral cuticle, while incomplete dorsal closure is reflected by the presence of holes in the dorsal cuticle.
The reduction in viability of RanBPMΔ/RanBPMCB-6232-3 mutants is dominantly enhanced in a shg2 heterozygous background. Ovaries of RanBPMCB-6232-3 shg2/RanBPMΔ survivors exhibit defects not seen in either RanBPMCB-6232-3/RanBPMΔ or shg2 heterozygotes alone, such as frequent follicle cell multilayering at the poles of egg chambers, severe egg chamber fusion, and loss of epithelial integrity so that many germline cells are no longer surrounded by a somatic cell layer.
One copy of shg2 enhances the tracheal epithelium defects seen when Src42ACA.Scer\UAS is expressed under the control of Scer\GAL4btl.PS. The dorsal trunk is broken in many places and cells are more rounded. Expressing Src42ACA.Scer\UAS in a homozygous shg2 background results in complete cell dissociation.
Coinjection of Cad88CcLa and Cad88Ca.cLa increases the frequency of spiracle defects in shg2 mutant embryos. Likewise, coinjection of Cad96CbcLa and Cad96Cba.cLa increases the spiracle defect phenotype of shg2 embryos. Cell elongation is not affected.
The salivary gland defects seen in embryos expressing Rac1L89.Scer\UAS under the control of Scer\GAL4fkh.PH are strongly suppressed by shg2/+.
The shg2 embryonic cuticle phenotype is partially suppressed by Rho1rev220. Approximately 4.5% of shg2 mutants are phenotypically wild-type, while 5.9% of Rho1rev220 shg2 double mutants are wild-type. Approximately 39.9% of double mutants exhibit ventral holes in the cuticle compared to 11.4% in the single shg21 mutant, with 55% of shg2 mutants exhibiting fragmentary ventral cuticle, while only 46.3% of the double mutants exhibit this phenotype. In summary, over 80% of Rho1rev220 shg2 double mutants have ventral holes or fragmentary ventral cuticle. This illustrates the general suppression of the shg2 phenotype in a Rho1rev220 background.
sli2/+, shg2/+ double mutant embryos show defective cardiac cell alignment; a phenotype not observed in either single heterozygote.
Heterozygous shg2, significantly enhances the ommatidial misrotation phenotype seen S05671/+ animals.
S48-5/shg2 mutants show 40.56%+-5.21 misrotated ommatidia compared to 9.55%+-1.43 seen in S48-5 mutants alone.
In shg-/shg+ the viability of p120ctn308 homozygotes is reduced to 20-60% of their shg+/shg+ siblings.
Heterozygosity for shg2 results in lethality in Abl4/+ embryos derived from homozygous Abl4 female germline clones. Heterozygosity for shg2 results in lethality in Abl1/+ embryos derived from homozygous Abl1 female germline clones. 70% of the lethal progeny of females with homozygous Abl4 germline clones mated to shg2/+ ; Abl4/+ males have cuticles that are reduced in size with a large dorsal-anterior hole.
shg2, Df(2R)E2, embryos with α-CatScer\UAS.T:Avic\GFP-sg driven by Scer\GAL4btl.PS, show largely disordered tracheal branching. No successful dorsal trunk fusions are seen in these embryos.
Dominantly suppresses the segment polarity phenotype of hemizygous arm3 embryos.
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.
Xenogenetic Interactions
Statement
Reference
The lethality of shgE17D/shg2 animals is rescued if they are carrying the P{FlyFos-045685} construct (which contains D. pseudoobscura pseudoobscura fosmid sequence that includes the region orthologous to shg).
Complementation and Rescue Data
Comments
The addition of shgScer\UAS.cOa to shg2, Df(2R)E2, α-CatScer\UAS.T:Avic\GFP-sg, Scer\GAL4btl.PS flies rescues their tracheal phenotypes to nearly wild-type. Tracheal patterning is normal, although tracheal branches and connectives in the embryos are less extend than in wild-type. The addition of shgScer\UAS.cOa, shgScer\UAS.T:Avic\GFP-rs, or shgmNcGSP.Scer\UAS.T:Avic\GFP-rs driven by Scer\GAL4btl.PS to shg2/Df(2R)E2 flies rescues the tracheal fusion phenotype. The addition of shgdCR3h.Scer\UAS.T:Avic\GFP-rs, shgdCR4h.Scer\UAS.T:Avic\GFP-rs, or shgdEx.Scer\UAS.T:Avic\GFP-rs, driven by Scer\GAL4btl.PS to shg2/Df(2R)E2 flies partially rescues the tracheal fusion phenotype. The addition of shgdCPc3.Scer\UAS.T:Avic\GFP-rs, shgdCR4.Scer\UAS.T:Avic\GFP-rs,shgdNc.Scer\UAS.T:Avic\GFP-rs, shgdCL3.Scer\UAS.T:Avic\GFP-rs, shginNcHA.Scer\UAS.T:Avic\GFP-rs, driven by Scer\GAL4btl.PS to shg2/Df(2R)E2 flies fails to rescue the tracheal fusion phenotype.
Scer\GAL4arm.PS mediated expression of shgScer\UAS.cSa rescues the cuticle to wild type and rescues most embryos to hatching.
Images (0)
Mutant
Wild-type
Stocks (2)
Notes on Origin
Discoverer
Comments
Comments
Stronger allele than shgg119.
Intermediate strength allele.
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (6)
References (58)