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General Information
Symbol
Dmel\shgg317
Species
D. melanogaster
Name
FlyBase ID
FBal0028554
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
Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Cytology
Nature of the lesion
Statement
Reference
Caused by aberration
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
shgg317 mutant embryos display defects in the actin dynamics in the amnioserosa cells compared to controls.
In embryos from females heterozygous for shgg317, an average of 3.7 PGCs are left outside the midgut with 64% of embryos exhibiting a phenotype.
In shgg317 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. During ensheathment of germ cells by gonadal mesoderm in these embryos the gonadal mesoderm cells fail to make cellular extensions between and around the germ cells. Phenotypes are stronger in these embryos than in shg2 homozygotes. This is true, both for the compaction phenotype (22% severe, 41% weak, n=49 in shgg317 homozygotes; 3% severe, 50% weak, n=36 in shg2 homozygotes) and the ensheathment phenotype, but the severity of these two phenotypes do not correlate with each other. In male shgg317 homozygous embryos male specific gonadal precursors often fail to join the posterior of the male gonad (42% male embryos n=49). Offspring from heterozygous shgg317/+ females are viable, but the embryos have a significant germ cell migration defect. Offspring from the reciprocal cross using shgg317/+ males show no germ cell migration defect.
Class IV allele: mutants lack all head and ventral cuticle, and show segmental defects in lateral epidermis or dorsal and lateral epidermis. Defects are evident in the neurectoderm, Malpighian tubules, optic lobe precursor, PNS and SNS. In germ-line clones, no eggs are recovered.
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 appearance. 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
Phenotype Manifest In
Enhanced by
Statement
Reference
shgg317 has germline cell | maternal effect phenotype, enhanceable by Jafrac1[+]/Jafrac1KG05372
Suppressed by
Statement
Reference
shgg317 has neurogenic region phenotype, suppressible by Nint.hs
shgg317 has Malpighian tubule phenotype, suppressible by ctC145
Enhancer of
Statement
Reference
Other
Statement
Reference
Additional Comments
Genetic Interactions
Statement
Reference
shgg317/+ enhances the frequency of ensheathment defects in raw134.47/raw155.27 mutants. Homozygous shgg317 does so even at a greater frequency.
67.8% of gonads do not form correctly in enaC14-06/+, shgg317/+ transheterozygous embryos, compared to 28.8% in enaC14-06/+ and 37.3% in shgg317/+ single heterozygotes.
Embryos from Jafrac1KG05372, shgg317 trans-heterozygous mothers display a significantly enhanced primordial germline cell adherence defect compared to single shgg317 mutants. These mothers produce embryos with an average of 6.2 primordial germline cells left outside of the midgut with 91% of embryos affected.
Src42A6-1 notum phenotypes are enhanced in a shgg317/+ background; in some Src42A6-1; shgg317/+ flies the right and left halves of the notum appear completely separated.
Neurectoderm defect is rescued by Nint.hs. Malpighian tubule defect of shgg317 is rescued by ctC145. The zonula adherens of many epithelial cells is unaffected by zygotic loss of shg function.
Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Comments
Images (0)
Mutant
Wild-type
Stocks (0)
Notes on Origin
Discoverer
Comments
Comments
Strong allele. Visceral mesoderm develops normally.
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (4)
Reported As
Name Synonyms
Secondary FlyBase IDs
    References (10)