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General Information
Symbol
Dmel\shgk03401
Species
D. melanogaster
Name
FlyBase ID
FBal0050505
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
shgP34-1, shg-lacZ
Nature of the Allele
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Cytology
Nature of the lesion
Statement
Reference

P{lacW} is inserted behind nucleotide 368 of the 5' untranslated region of the shg cDNA.

Insertion components
P{lacW}shgk03401
Product class / Tool use(s)
Encoded product / tool
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
Detailed Description
Statement
Reference

Mutant embryos show defects in epithelial wound repair during the contraction phase; actin cable assembly is impaired, leading to initially jagged wound boundaries and irregularly shaped wounds. Wound closure is eventually achieved by non-uniform contraction of leading edge areas a few cells wide which accumulate actin.

Embryos that are maternally mutant for shgk03401 display impaired wound repair. In comparison with wild-type controls, these embryos show excessive expansion upon ablation, as well as defects in actin ring assembly. Nevertheless, these embryos heal eventually.

In late 3rd instar larval discs, at the stage of ommatidial rotation, clones of shgk03401 show robust rotation defects. Within mutant tissue, about 50% of ommatidia do not initiate rotation and several others rotate less in comparison with wild-type clusters of the same stage. Rotation defects are apparent in both in small and large shgk03401 clones. There is no significant evidence for apicobasal polarity defects in the clones. Mosaic ommatidia containing shgk03401 clones do not have a higher probability of rotating correctly when both R3 and R4 are wild type. Wild-type preclusters that are directly adjacent to shgk03401 interommatidial cells can also fail to rotate correctly.

The ommatidial under-rotation of Scer\GAL4hs.2sev>shgdCR3h.Scer\UAS.T:Avic\GFP-rs eyes is enhanced in Scer\GAL4hs.2sev>shgdCR3h.Scer\UAS.T:Avic\GFP-rs; shgk03401/+ flies.

Expression of shgScer\UAS.cSa under the control of Scer\GAL4hs.2sev increases the number of ommatidial clusters that initiate rotation correctly in shgk03401 clones.

shgk03401 mutant follicle cell clones exhibit a loss of epithelial integrity resulting in defects in cell sorting and oocyte mis-positioning. Approximately 5% of stage 10 egg chambers show slight migration delays when border cells are mutant.

Heterozygous shgk03401, significantly enhances the ommatidial misrotation phenotype seen S05671/+ animals.

The head cuticle is missing in homozygous embryos, although most embryos only show minor defects in the ventral trunk cuticle. 12% of embryos have a more severe phenotype in which the entire ventral cuticle is missing.

When homozygous somatic clones are made in the thoracic epithelium the orientation of division of pIIa relative to the pI division axis is significantly more variable than wild-type. 39% of pIIa cells divide at an α angle of more than 20o (compared to 2% for wild-type).

Cardioblasts remain rounded in homozygous embryos, in contrast to wild type where they adopt a crescent shape. There is no lumen between the cardioblasts and no adherens junctions between them. Amnioserosa cells are still attached to the ventral surface of the cardioblasts, in contrast to wild type.

shgk03401/shgR6 flies are semi-viable. Border follicle cell migration is substantially delayed in many cases in shgk03401/shgR6 follicles. Approximately 65% of the border cell clusters that have not reached the oocyte at stage 10 are located between nurse cells and only 35% of border cell clusters do not penetrate between nurse cells.

The oocyte is mislocalised in 29.5% of stage 7-9 shgk03401/shgR6 follicles.

Homozygous female germ line clones give rise to egg chambers with misplaced oocytes in 18% of cases.

Class II allele: lacks most of the head cuticle and has small holes in the ventral cuticle. Germ line clones give rise to only a few eggs, giving rise to embryos with Class III and class IV phenotypes.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhanced by
Suppressed by
NOT suppressed by
Enhancer of
NOT Enhancer of
Suppressor of
Statement
Reference

shg[+]/shgk03401 is a suppressor of increased cell death | heat sensitive phenotype of Scer\GAL4sd-SG29.1, Src64BUY1332

shg[+]/shgk03401 is a suppressor of decreased cell growth | heat sensitive phenotype of Scer\GAL4sd-SG29.1, Src64BUY1332

shg[+]/shgk03401 is a suppressor | partially of visible phenotype of CycEJP

NOT Suppressor of
Statement
Reference

shgk03401 is a non-suppressor of lethal | pupal stage phenotype of Cskj1D8/CskS030003

Other
Phenotype Manifest In
Enhanced by
Suppressed by
Enhancer of
NOT Enhancer of
Statement
Reference
Suppressor of
Statement
Reference
NOT Suppressor of
Statement
Reference

shg[+]/shgk03401 is a non-suppressor of ommatidium phenotype of Scer\GAL4hs.2sev, nmoUAS.cUa

Other
Additional Comments
Genetic Interactions
Statement
Reference

shgk03401 partially suppresses the decreased number of macrophages within the germ band of mrvaEP3102 stage 12 embryos.

Presence of shgk03401 does not significantly alter eye phenotypes seen in flies with FrlDN.Scer\UAS driven by Scer\GAL4sev.EP.

The disorganised ommatidial lattice and supernumerary primary pigment cells phenotype observed in either Vav2 or Vav3 homozygotes is strongly enhanced by combination with shgk03401 in heterozygous state but the proportion of ommatidia with extra cone cells is not further increased.

RhoL10-161;shgk03401 double homozygous mutant embryos display the normal number of haemocytes migrating into the tail region of the embryo.

p130CAS1 homozygotes in combination with heterozygous shgk03401 severely reduce viability.

shgk03401; p130CAS1 double homozygotes arrest in late embryogenesis (and thereby do not hatch) and are considered semi-lethal. Athough most of the embryos form at least partial cuticles, absence of p130CAS1 significantly enhances shgk03401 single mutant cuticle defects, with shgk03401; 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.

shgk03401 mutant larval brain cells expressing Ras85DV12.Scer\UAS under the control of Scer\GAL4Act5C.PI exhibit a weak invasive phenotype and can invade the ventral nerve cord (this phenotype occurs with 20% penetrance).

shgk03401 mutant larval brain cells expressing both Ras85DV12.Scer\UAS and egrScer\UAS.cIa under the control of Scer\GAL4Act5C.PI generate into invasive tumours that can invade the ventral nerve cord (this phenotype occurs with 88% penetrance).

Expression of Ras85DV12.Scer\UAS, egrScer\UAS.cIa and bskDN.Scer\UAS, under the control of Scer\GAL4Act5C.PI in shgk03401 mutant larval cephalic complexes (brain, eye and antennal discs) induces tumor invasion of the ventral nerve cord.

Overexpression of hepCA.Scer\UAS in shgk03401 mutant cephalic cells (i.e. cells in the larval brain and eye-antennal discs) expressing Ras85DV12.Scer\UAS results in neither enhanced tumour growth nor metastatic behaviour.

The proportion of shgk03401 embryos showing the severe ventral cuticle phenotype is completely suppressed by rho9 and is enhanced by expression of btl::EgfrScer\UAS.T:λ\cI-DD under the control of Scer\GAL4da.G32.

Xenogenetic Interactions
Statement
Reference

shgk03401/+ does not suppress the decreased lifespan seen in flies with expression of Hsap\HTTQ93.ex1p.Scer\UAS driven by Scer\GAL4elav.PU or Scer\GAL4Eaat1.PR.

Expression of shg::α-Catshg.ΔCyt.Scer\UAS can suppress the shgk03401 mutant follicle cell clone phenotype (follicle cell sorting, loss of epithelial integrity, and oocyte positioning).

Expression of shg::α-Catshg.ΔCyt.Scer\UAS is not able to suppress the migration defects of shgk03401 mutant border cell clones.

shg::α-CatScer\UAS.fl can suppress shgk03401 clone phenotypes such as follicle cell sorting, loss of epithelial integrity, and oocyte mis-positioning, as well as the migration defects of shgk03401 mutant border cell clones.

Complementation and Rescue Data
Comments

Expression of shgScer\UAS.cSa can suppress the shgk03401 mutant follicle cell clone phenotype (follicle cell sorting, loss of epithelial integrity, and oocyte positioning).

Expression of shgScer\UAS.cSa can suppress the migration defects of shgk03401 mutant border cell clones.

Images (0)
Mutant
Wild-type
Stocks (2)
Notes on Origin
Discoverer

wcd1 was isolated a second site mutation on a chromosome also mutant for shgk03401.

Separable from: wcd1.

Comments
Comments

Complements: l(2)0305003050. Complements: l(2)0720607206. Complements: Xbp1k13803.

Weak allele. Transposase induced excision of the P{lacW} can be accompanied by reversion of the mutant phenotype.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (9)
References (40)