FB2024_03 , released June 25, 2024
Allele: Dmel\grn7L
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General Information
Symbol
Dmel\grn7L
Species
D. melanogaster
Name
FlyBase ID
FBal0005216
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
grn7L12
Key Links
Nature of the Allele
Progenitor genotype
Cytology
Description

11bp deletion of bases 379 to 389. This deletion results in a frameshift and produces a truncated protein that diverges from wild-type grn after 52 amino acids and lacks both zinc fingers.

Mutations Mapped to the Genome
Curation Data
Type
Location
Additional Notes
References
Variant Molecular Consequences
Associated Sequence Data
DNA sequence
Protein sequence
 
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 )
 
Disease-implicated variant(s)
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
Statement
Reference

grn7L mutant embryos do not show morphological abnormalities in the midgut.

85% of intersegmental nerves show defective muscle 1/9 innervations in grnSPJ9/grn7L embryos.

In grn7L/Df(3R)dsx3 mutants the intersegmental nerve (ISN) motor axons are stalled at muscles 2/10, leading to a near complete loss of innervation (~12-18%) of the dorsal-most muscles 1/9. In addition, grn7L/Df(3R)dsx3 mutants display aberrant innervation of muscle 8. In affected hemisegments, a grossly normal pattern of axonal projections to the dorsal muscles 2/10 is observed, indicating that aCC and/or RP2, and at least one of the U motoneurons project aberrantly to muscle 8.

grn7L/Df(3R)dsx3 mutants display a partially penetrant muscle patterning phenotype, evident as an imprecise insertion of muscles 21-24 into the body wall.

In grn7L/Df(3R)dsx3 mutants, the intersegmental nerve fails to innervate muscles 1/9, but axonal projections are still observed contacting muscles 2/10.

In grn7L/Df(3R)dsx3 mutants, approximately 36% of hemisegments show ectopic innervation of muscle 8, together with defasciculation of aCC and RP2 motor axons. Muscle 9 is not innervated (by U1), while U axon terminals contact muscles field 2/10.

grn7L/Df(3R)dsx10M embryos have an abnormal head skeleton with aberrant lateralgraten and dorsal bridge. The stigmatophore does not protrude (in contrast to wild type) and the filzkorper is short. Other cuticular structures are normal. The number of stigmatophore cells abutting the posterior spiracular chamber and the number of cell tiers does not change during development in mutant embryos, in contrast to wild type. Germline clonal analysis indicates that grn is not required maternally. No abnormalities are seen when homozygous clones occupy the wing or distal leg segments. Clones on the proximal leg segments often severely affect the shape of the femur and tibia, which become shorter and broader than in wild type. In these cases the segments are approximately 1/3 shorter and 1/3 broader than normal, but leg segmentation is normal. The number of leg trichomes is normal. The shape of homozygous clones in the leg disc is similar to that of wild-type twin clones.

No changes in phenotype of tor13D embryos.

External Data
Interactions
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Phenotypic Class
Phenotype Manifest In
Additional Comments
Genetic Interactions
Statement
Reference

grn7L GATAe2 double mutant embryos do not show morphological abnormalities in the midgut.

unc-58/+ ; grn7L/+ double heterozygous embryos show guidance defects in the intersegmental nerve.

The defects in intersegmental nerve innervation of muscles 1/9 are partially rescued by expression of unc-5Scer\UAS.T:Ivir\HA1,T:SS-wg under the control of Scer\GAL4eve.RN2.

Expression of zfh1Scer\UAS.cPa in the aCC/RP2 neurons, under the control of Scer\GAL4eve.RN2 can only partially rescue the grn7L/Df(3R)dsx3 motoneuron phenotype, with muscle 1/9 innervation increasing to 34% compared with the more severe (approximately 12%) grn7L/Df(3R)dsx3 mutant phenotype.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Partially rescued by
Comments

Expression of grnScer\UAS.cBa in the aCC/RP2 neurons, under the control of Scer\GAL4eve.RN2 efficiently rescues grn7L/Df(3R)dsx3 mutant axon pathfinding (with 100% muscle 1/9 innervation). By contrast, expression of grnScer\UAS.cBa in the U motoneurons, under the control of Scer\GAL4eve.CQ2 only partially rescues the grn7L/Df(3R)dsx3 mutant phenotypes, with approximately 54% of muscles 1/9 being innervated.

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Mutant
Wild-type
Stocks (2)
Notes on Origin
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External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (6)
References (16)