FlyBase Allele Report: Dmel\grh[IM]

General Information

Symbol

Dmel\grh^IM

Species

D. melanogaster

Name

FlyBase ID

FBal0005208

Feature type

allele

Associated gene

Dmel\grh

Associated Insertion(s)

Carried in Construct

Key Links

Genomic Maps

JBrowse

Allele class

amorphic allele - genetic evidence

Mutagen

ethyl methanesulfonate

Nature of the Allele

Allele class

amorphic allele - genetic evidence

(Ostrowski et al., 2002)

Mutagen

ethyl methanesulfonate

(Tearle and Nusslein-Volhard, 1987, Nusslein-Volhard et al., 1984)

Progenitor genotype

Cytology

Description

Nonsense mutation: TAT to TAA stop-codon introduction in exon seven, within the DNA-binding domain.

(Paré et al., 2012)

Mutations Mapped to the Genome

Curation Data

Type

Location

Additional Notes

References

point_mutation

2R:17,828,845..17,828,845 [+]

Nucleotide change:

T17828845A

Reported nucleotide change:

T?A

Amino acid change:

Reported amino acid change:

Y?term

Comment:

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

(Paré et al., 2012)

Variant Molecular Consequences

Associated Sequence Data

DDBJ / EMBL / GenBank

DNA sequence

Protein sequence

UniProtKB/Swiss-Prot

UniProtKB/TrEMBL

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

cephalopharyngeal skeleton

(Tearle and Nusslein-Volhard, 1987)

cephalopharyngeal skeleton | embryonic stage

(Kim and McGinnis, 2011)

chaeta | somatic clone

(Lee and Adler, 2004)

chaeta | somatic clone | increased number

(Lee and Adler, 2004)

embryonic/first instar larval cuticle

(Ostrowski et al., 2002)

embryonic/larval cuticle

(Kim and McGinnis, 2011)

embryonic/larval epidermis | embryonic stage 17

(Kim and McGinnis, 2011)

epicuticle

(Gangishetti et al., 2012)

eye | somatic clone

(Lee and Adler, 2004)

eye photoreceptor cell | somatic clone

(Lee and Adler, 2004)

larval thoracic perisympathetic organ (with Df(2R)Pcl7B)

(Baumgardt et al., 2009)

ommatidium | somatic clone

(Lee and Adler, 2004)

procuticle

(Gangishetti et al., 2012)

thoracic neuroblast NB5-6 (with Df(2R)Pcl7B)

(Baumgardt et al., 2009)

ventral denticle belt

(Tearle and Nusslein-Volhard, 1987)

wing | somatic clone

(Lee and Adler, 2004)

wing hair | cell non-autonomous | somatic clone

(Lee and Adler, 2004)

wing hair | cell non-autonomous | somatic clone | increased number

(Lee and Adler, 2004)

wing hair | somatic clone

(Lee and Adler, 2004)

wing hair | somatic clone | increased number

(Lee and Adler, 2004)

wing margin bristle | somatic clone

(Lee and Adler, 2004)

wing vein | ectopic | somatic clone

(Lee and Adler, 2004)

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.

(Gangishetti et al., 2012)

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

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

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

(Kim and McGinnis, 2011)

grh^IM/+ mutant flies exhibit temperature-induced mobility defects.

(Kucherenko et al., 2011)

The number of SELK neurons is normal in grh^IM mutant animals.

(Losada-Pérez et al., 2010)

grh^IM/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.

(Baumgardt et al., 2009)

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

(Mace et al., 2005)

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.

(Lee and Adler, 2004)

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).

(Ostrowski et al., 2002)

grh^IM mutant embryos have a defective head skeleton and weak denticles.

(Tearle and Nusslein-Volhard, 1987)

Head skeleton glassy.

(Nusslein-Volhard et al., 1984)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

NOT Enhanced by

Statement

Reference

grh^IM has abnormal planar polarity | somatic clone phenotype, non-enhanceable by in¹

(Lee and Adler, 2004)

grh^IM has abnormal planar polarity | somatic clone phenotype, non-enhanceable by mwh¹

(Lee and Adler, 2004)

NOT suppressed by

Statement

Reference

grh^IM has abnormal planar polarity | somatic clone phenotype, non-suppressible by mwh¹

(Lee and Adler, 2004)

grh^IM has abnormal planar polarity | somatic clone phenotype, non-suppressible by in¹

(Lee and Adler, 2004)

NOT Enhancer of

Statement

Reference

grh^IM is a non-enhancer of abnormal planar polarity | somatic clone phenotype of in¹

(Lee and Adler, 2004)

grh^IM is a non-enhancer of abnormal planar polarity | somatic clone phenotype of mwh¹

(Lee and Adler, 2004)

NOT Suppressor of

Statement

Reference

grh^IM is a non-suppressor of abnormal planar polarity | somatic clone phenotype of in¹

(Lee and Adler, 2004)

grh^IM is a non-suppressor of abnormal planar polarity | somatic clone phenotype of mwh¹

(Lee and Adler, 2004)

Other

Statement

Reference

Df(3R)Exel6184/+, grh^IM has abnormal neuroanatomy | third instar larval stage phenotype

(Marrone et al., 2011)

Phenotype Manifest In

NOT Enhanced by

Statement

Reference

grh^IM has wing hair | somatic clone phenotype, non-enhanceable by in¹

(Lee and Adler, 2004)

grh^IM has wing hair | increased number | somatic clone phenotype, non-enhanceable by in¹

(Lee and Adler, 2004)

grh^IM has wing hair | somatic clone phenotype, non-enhanceable by mwh¹

(Lee and Adler, 2004)

grh^IM has wing hair | increased number | somatic clone phenotype, non-enhanceable by mwh¹

(Lee and Adler, 2004)

NOT suppressed by

Statement

Reference

grh^IM has wing hair | somatic clone phenotype, non-suppressible by in¹

(Lee and Adler, 2004)

grh^IM has wing hair | somatic clone phenotype, non-suppressible by mwh¹

(Lee and Adler, 2004)

grh^IM has wing hair | increased number | somatic clone phenotype, non-suppressible by in¹

(Lee and Adler, 2004)

grh^IM has wing hair | increased number | somatic clone phenotype, non-suppressible by mwh¹

(Lee and Adler, 2004)

NOT Enhancer of

Statement

Reference

grh^IM/grh[+] is a non-enhancer of indirect flight muscle cell phenotype of Dys^RNAi.NH2.UAS, Scer\GAL4^Act.PU

(Kucherenko et al., 2011)

grh^IM/grh[+] is a non-enhancer of indirect flight muscle cell phenotype of Dg^RNAi.UAS, Scer\GAL4^Act.PU

(Kucherenko et al., 2011)

grh^IM is a non-enhancer of wing hair | somatic clone phenotype of mwh¹

(Lee and Adler, 2004)

grh^IM is a non-enhancer of wing hair | increased number | somatic clone phenotype of mwh¹

(Lee and Adler, 2004)

grh^IM is a non-enhancer of wing hair | somatic clone phenotype of in¹

(Lee and Adler, 2004)

grh^IM is a non-enhancer of wing hair | increased number | somatic clone phenotype of in¹

(Lee and Adler, 2004)

NOT Suppressor of

Statement

Reference

grh^IM is a non-suppressor of wing hair | somatic clone phenotype of mwh¹

(Lee and Adler, 2004)

grh^IM is a non-suppressor of wing hair | increased number | somatic clone phenotype of mwh¹

(Lee and Adler, 2004)

grh^IM is a non-suppressor of wing hair | somatic clone phenotype of in¹

(Lee and Adler, 2004)

grh^IM is a non-suppressor of wing hair | increased number | somatic clone phenotype of in¹

(Lee and Adler, 2004)

Other

Statement

Reference

Df(3R)Exel6184/+, grh^IM has lamina plexus | third instar larval stage phenotype

(Marrone et al., 2011)

Additional Comments

Genetic Interactions

Statement

Reference

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

grh^IM Dg^O86 double heterozygous flies do not exhibit indirect flight muscle degeneration.

One copy of grh^IM does not enhance the indirect flight muscle degeneration seen when Dys^{dsRNA.NH2.Scer\UAS} is expressed under the control of Scer\GAL4^Act.PU.

One copy of grh^IM does not enhance the indirect flight muscle degeneration seen when Dg^{dsRNA.Scer\UAS} is expressed under the control of Scer\GAL4^tub.PU.

grh^IM Dg³²³ double heterozygous flies do not exhibit indirect flight muscle degeneration.

(Kucherenko et al., 2011)

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

Combination of Dg^O86 in heterozygous state with a single copy of grh^IM does not significantly affect the frequency of lamina plexus defects in the third instar larvae.

(Marrone et al., 2011)

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

(Lee and Adler, 2004)

Xenogenetic Interactions

Statement

Reference

Complementation and Rescue Data

Partially rescued by

grh^IM is partially rescued by Scer\GAL4^e22c/grh^UAS.cKa

(Kim and McGinnis, 2011)

grh^IM is partially rescued by grh^2A.UAS/Scer\GAL4^e22c

(Kim and McGinnis, 2011)

grh^IM is partially rescued by grh^PanA.UAS/Scer\GAL4^e22c

(Kim and McGinnis, 2011)

grh^IM is partially rescued by Scer\GAL4^e22c/grh^2E.UAS

(Kim and McGinnis, 2011)

Comments

Expression of grh^Scer\UAS.cKa in the epidermis under the control of Scer\GAL4^e22c partially rescues the cuticle and head skeleton defects seen in grh^IM embryos.

Expression of grh^2A.Scer\UAS in the epidermis under the control of Scer\GAL4^e22c partially rescues the cuticle and head skeleton defects seen in grh^IM embryos.

Expression of grh^{PanA.Scer\UAS} in the epidermis under the control of Scer\GAL4^e22c partially rescues the cuticle and head skeleton defects seen in grh^IM embryos.

Expression of grh^2E.Scer\UAS in the epidermis under the control of Scer\GAL4^e22c partially rescues the cuticle and head skeleton defects seen in grh^IM embryos.

Expression of grh^Scer\UAS.cKa in the epidermis under the control of Scer\GAL4^e22c rescues the defects in epidermal barrier integrity seen in stage 17 grh^IM homozygous embryos. Epidermal barrier regeneration following wounding is also rescued.

Expression of grh^2A.Scer\UAS in the epidermis under the control of Scer\GAL4^e22c rescues the defects in epidermal barrier integrity seen in stage 17 grh^IM homozygous embryos. Epidermal barrier regeneration following wounding is only partially rescued.

Expression of grh^{PanA.Scer\UAS} in the epidermis under the control of Scer\GAL4^e22c rescues the defects in epidermal barrier integrity seen in stage 17 grh^IM homozygous embryos. However epidermal barrier regeneration following wounding is only partially rescued.

Expression of grh^2E.Scer\UAS in the epidermis under the control of Scer\GAL4^e22c rescues the defects in epidermal barrier integrity seen in stage 17 grh^IM homozygous embryos. Epidermal barrier regeneration following wounding is also rescued.

(Kim and McGinnis, 2011)

Images (0)

Mutant

Wild-type

Stocks (2)

Bloomington

3270

cn¹ grh^IM bw¹/SM6a

Kyoto

106949

cn¹ grh^IM bw¹ speck¹/CyO

Notes on Origin