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General Information
Symbol
Dmel\grhIM
Species
D. melanogaster
Name
FlyBase ID
FBal0005208
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Key Links
Nature of the Allele
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
Nucleotide change:

T17828845A

Reported nucleotide change:

T?A

Amino acid change:

Y661term | grh-PH; Y661term | grh-PI; Y931term | grh-PJ; Y382term | grh-PK; Y931term | grh-PL; Y327term | grh-PN; Y327term | grh-PO; Y661term | grh-PP

Reported amino acid change:

Y?term

Comment:

Reported as Y29@ relative to the sequence in Figure 1.

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

Nonsense mutation: TAT to TAA stop-codon introduction in exon seven, within the DNA-binding 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 )
 
Disease-implicated variant(s)
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
Statement
Reference

The inner two layers of the cuticle (epicuticle and procuticle) appear to have mixed in mutant larvae, resulting in bloated animals that die before hatching.

The larval cuticle in grhIM homozygotes is weak and easily ruptured and the head skeleton is grainy and discontinuous.

Stage 17 homozygous grhIM embryos display defects in epidermal barrier integrity (an inability to exclude dye from the body cavity). This defect is not observed in grhIM heterozygous embryos.

grhIM homozygous stage 17 embryos do not regain epidermal barrier integrity following wounding. Efficient regeneration of the barrier occurs in grhIM heterozygotes.

grhIM/+ mutant flies exhibit temperature-induced mobility defects.

The number of SELK neurons is normal in grhIM mutant animals.

grhIM/Df(2R)Pcl7B mutants show an increase in the number of ap NB5-6T neuroblasts from 4 to 6. Frequent loss of dorsal neurohemal organ innervation is observed in 75% of animals.

Mutant embryos show an abnormal wound healing response after wounding with a sterile micropipette.

When homozygous mutant somatic clones are made in the wing, polarity defects are seen. Multiple wing hairs are sometimes seen, and the hairs are more erect than wild-type. The majority of clones show signs of weak domineering non-autonomy consisting of a small number of multiple wing hairs and/or hairs of abnormal polarity. When pupal wing clones are examined, it is seen that the multiple hair cell phenotype tends to be stronger in larger clones. In some clones not all cells produce multiple hairs. In addition an apparent delay in hair development is seen in many clones. Other phenotypes are also seen in mutant somatic clones. Most wings show ectopic wing veins. There is often disruption to the pattern of marginal bristles and occasionally polyploid cells. Large clones result in bulges of the wing and the region of the clone. Clones in the abdomen have reduced pigmentation and/or multiple hair phenotypes. The reduced pigmentation is most obvious in regions that are darkly pigmented but it could be seen elsewhere. In addition to the reduced pigmentation the clone cells often show a strong multiple hair cell phenotype. In abdominal areas that normally produce few hairs, a strong multiple a strong multiple hair cell phenotype is not seen and in some cases there appears to be a loss of hairs. Clones in the notum have reduced pigmentation. The hair phenotypes of these clones varies from an increased number of hairs to a loss of hairs. Lateral clones usually display a multiple hair cell phenotype, while medial clones often, but not invariably have a reduced number of hairs. Flies carrying mutant clones have rough spots on the eye. This phenotype is associated with ommatidia that show incorrect chirality, incorrect rotation and an abnormal number of photoreceptor cells.

When homozygous embryos are mechanically devitellinised the resulting cuticle preparations stretch to a greater extent than wild-type cuticles, resulting in inflated cuticles ("blimp" phenotype).

grhIM mutant embryos have a defective head skeleton and weak denticles.

Head skeleton glassy.

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

grhIM is a non-suppressor of abnormal planar polarity | somatic clone phenotype of in1

Other
Phenotype Manifest In
NOT Enhanced by
Statement
Reference

grhIM has wing hair | somatic clone phenotype, non-enhanceable by in1

grhIM has wing hair | increased number | somatic clone phenotype, non-enhanceable by in1

grhIM has wing hair | somatic clone phenotype, non-enhanceable by mwh1

grhIM has wing hair | increased number | somatic clone phenotype, non-enhanceable by mwh1

NOT suppressed by
Statement
Reference

grhIM has wing hair | somatic clone phenotype, non-suppressible by in1

grhIM has wing hair | increased number | somatic clone phenotype, non-suppressible by in1

grhIM has wing hair | somatic clone phenotype, non-suppressible by mwh1

grhIM has wing hair | increased number | somatic clone phenotype, non-suppressible by mwh1

NOT Enhancer of
Statement
Reference

grhIM is a non-enhancer of wing hair | somatic clone phenotype of mwh1

grhIM is a non-enhancer of wing hair | increased number | somatic clone phenotype of mwh1

grhIM is a non-enhancer of wing hair | somatic clone phenotype of in1

grhIM is a non-enhancer of wing hair | increased number | somatic clone phenotype of in1

NOT Suppressor of
Statement
Reference

grhIM is a non-suppressor of wing hair | somatic clone phenotype of mwh1

grhIM is a non-suppressor of wing hair | increased number | somatic clone phenotype of mwh1

grhIM is a non-suppressor of wing hair | somatic clone phenotype of in1

grhIM is a non-suppressor of wing hair | increased number | somatic clone phenotype of in1

Other
Additional Comments
Genetic Interactions
Statement
Reference

grh Dys double heterozygous flies (grhIM/Df(3R)Exel6184) do not exhibit indirect flight muscle degeneration.

grhIM DgO86 double heterozygous flies do not exhibit indirect flight muscle degeneration.

One copy of grhIM does not enhance the indirect flight muscle degeneration seen when DysdsRNA.NH2.Scer\UAS is expressed under the control of Scer\GAL4Act.PU.

One copy of grhIM does not enhance the indirect flight muscle degeneration seen when DgdsRNA.Scer\UAS is expressed under the control of Scer\GAL4tub.PU.

grhIM Dg323 double heterozygous flies do not exhibit indirect flight muscle degeneration.

Combination of Df(3R)Exel6184 in heterozygous state with a single copy of grhIM results in a significantly increased frequency of lamina plexus defects in the third instar larval brain in the double heterozygotes.

Combination of DgO86 in heterozygous state with a single copy of grhIM does not significantly affect the frequency of lamina plexus defects in the third instar larvae.

When grhIM mutant clones are made in an in1 mutant wing the grhIM phenotype is still seen. When grhIM mutant clones are made in an mwh1 mutant wing the grhIM phenotype is still seen. A slight additive effect is seen on the phenotype.

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

Expression of grhScer\UAS.cKa in the epidermis under the control of Scer\GAL4e22c partially rescues the cuticle and head skeleton defects seen in grhIM embryos.

Expression of grh2A.Scer\UAS in the epidermis under the control of Scer\GAL4e22c partially rescues the cuticle and head skeleton defects seen in grhIM embryos.

Expression of grhPanA.Scer\UAS in the epidermis under the control of Scer\GAL4e22c partially rescues the cuticle and head skeleton defects seen in grhIM embryos.

Expression of grh2E.Scer\UAS in the epidermis under the control of Scer\GAL4e22c partially rescues the cuticle and head skeleton defects seen in grhIM embryos.

Expression of grhScer\UAS.cKa in the epidermis under the control of Scer\GAL4e22c rescues the defects in epidermal barrier integrity seen in stage 17 grhIM homozygous embryos. Epidermal barrier regeneration following wounding is also rescued.

Expression of grh2A.Scer\UAS in the epidermis under the control of Scer\GAL4e22c rescues the defects in epidermal barrier integrity seen in stage 17 grhIM homozygous embryos. Epidermal barrier regeneration following wounding is only partially rescued.

Expression of grhPanA.Scer\UAS in the epidermis under the control of Scer\GAL4e22c rescues the defects in epidermal barrier integrity seen in stage 17 grhIM homozygous embryos. However epidermal barrier regeneration following wounding is only partially rescued.

Expression of grh2E.Scer\UAS in the epidermis under the control of Scer\GAL4e22c rescues the defects in epidermal barrier integrity seen in stage 17 grhIM homozygous embryos. Epidermal barrier regeneration following wounding is also rescued.

Images (0)
Mutant
Wild-type
Stocks (2)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (5)
References (29)