Open Close
General Information
Symbol
Dmel\shgg119
Species
D. melanogaster
Name
FlyBase ID
FBal0050503
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Mutagen
Nature of the Allele
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
deletion
Comment:

An in-frame deletion of four conserved amino acids.

Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Cytology
Nature of the lesion
Statement
Reference

shgg119 has an in-frame deletion of four conserved amino acids in the membrane-proximal lamininG domain in the extracellular domain.

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

shgg119/+ mutants embryos show no defects in development or survival.

Homozygous embryos have sporadic tracheal branch breaks.

shgg119 mutants exhibit disrupted embryonic head cuticle.

Embryos maternally and zygotically mutant for shgg119 show widespread cell dissociation during gastrulation, but some cells form epithelial folds.

Cells in epithelial folds and rosettes of embryos maternally and zygotically mutant for shgg119 are pear-shaped with a constricted and extended apical domain, whereas wild type cells adopt a columnar shape.

Homozygous mutant embryos show defects in head involution - the embryo secretes cuticle without head structures.

Homozygous female germ line clones give rise to egg chambers with misplaced oocytes in 7% of cases.

Class I allele: lacks portions of the head cuticle and has defects in head involution. Trunk cuticle is intact. 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
Phenotype Manifest In
Enhanced by
Enhancer of
Statement
Reference

shg[+]/shgg119 is an enhancer of phenotype of p120ctn308

NOT Enhancer of
Other
Additional Comments
Genetic Interactions
Statement
Reference

One copy of shgg119 causes a significant enhancement of the cuticle defects seen in α-Cat1 mutant embryos. >99% of embryos display a strong head defect and 21% show defects in the ventral cuticle.

The tracheal tube length defects caused by varif00033 are not enhanced if the embryos are also mutant for shgg119.

The tracheal tube length defects caused by convR278 are not enhanced if the embryos are also mutant for shgg119.

Loss of Rho1rev220 enhances the shgg119 phenotype. Most double mutants have holes in their ventral epidermis that are not present in most shgg119 single mutants. As both Rho1rev220 and shgg119 affect head involution, the enhancement of this phenotype may simply reflect additive effects. However, because loss of Rho1rev220 does not affect integrity of the ventral epidermis, enhancement of this aspect of the phenotype is likely to reflect a genetic interaction.

Rho1rev220 enhances the weak shgg119 phenotype, leading to more severe embryonic defects. The percentage of phenotypically-wild-type embryos is reduced from approximately 7.6% in shgg119 embryos to approximately 0.5% in shgg119 Rho1rev220 mutants. The majority of shgg119 Rho1rev220 mutants (approximately 54%) exhibit ventral holes in the embryonic cuticle, compared to 21.7% in shgg119 mutants and 0.4% in Rho1rev220 mutants.

In shg-/shg+ the viability of p120ctn308 homozygotes is reduced to 20-60% of their shg+/shg+ siblings.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Comments
Images (0)
Mutant
Wild-type
Stocks (0)
Notes on Origin
Discoverer
Comments
Comments
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (2)
References (9)