FB2024_03 , released June 25, 2024
Allele: Dmel\RopG27
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General Information
Symbol
Dmel\RopG27
Species
D. melanogaster
Name
FlyBase ID
FBal0048940
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Key Links
Genomic Maps

Nature of the Allele
Progenitor genotype
Cytology
Description

Amino acid replacement: Q311term.

Mutations Mapped to the Genome
Curation Data
Type
Location
Additional Notes
References
Nucleotide change:

C4137884T

Amino acid change:

Q311term | Rop-PA; Q311term | Rop-PB

Reported amino acid change:

Q311term

Comment:

Site of nucleotide substitution in mutant inferred by FlyBase based on reported amino acid change.

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 ( 1 )
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

RopG27/RopG27 embryos display defects in the growth of the dendritic arbor in the dorsal class I and IV dendritic arborizing (da) neurons, including reduction in outgrowth of both primary dendrites and secondary lateral branches.

RopG27/RopG27 class IV da neurons in larval somatic clones first manifest defects (dendrites thinning) in dendritic growth at 72hrs after egg laying (AEL) and the phenotype (severely reduced dendritic complexity due to loss of branching, reduction in number of dendritic intersections, varicosities or terminal dendrites fragmentation) gets progressively worse at later stages of larval life, especially in terminal dendrites that show heightened sensitivity to loss of Rop. Axon growth of RopG27 mutant da neurons however appears normal until late in larval life (144hrs AEL) when axons show thinning and varicosities along the terminals.

Germ-line clones of this mutant often produce miniature eggs with greatly reduced surface volumes. Membranes in mature oocytes are also not intact.

Heterozygous larvae show a 35% decrease in the amplitude of the excitatory junctional potential in the muscle at the neuromuscular junction compared to control larvae, and a 79% reduction in miniature EJP frequency.

Embryos have little or no cuticle (epidermally derived structures are also abnormal), embryos fail to hatch into larvae. Trachea do not appear to be disrupted but they fail to fill with air in later embryos, possibly because they collapse due to insufficient cuticle deposition. Defects in the extracellular accumulation of secreted products was observed in other tissues: Malpighian tubules do not contain uric acid, the lumen of salivary glands contains severely reduced glue protein levels and the gut contents are incompletely digested due to lack of digestive enzymes. Morphology of the CNS is altered, fails to dissociate from the ventral epidermis and fails to shorten in mature embryos.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Suppressed by
Enhancer of
Statement
Reference

RopG27/Rop[+] is an enhancer of visible phenotype of Scer\GAL4GMR.PF, bchsEP2299

Suppressor of
Statement
Reference
Other
Phenotype Manifest In
Additional Comments
Genetic Interactions
Statement
Reference

Sec5E13/RopG27 transheterozygous third instar larvae show decreased number of terminal dendritic branches in the class IV dendritic arborizing neurons compared to either Sec5E13/+ or RopG27/+ single heterozygotes.

Sec6Ex15/RopG27 transheterozygous third instar larvae show decreased number of terminal dendritic branches in the class IV dendritic arborizing neurons compared to either Sec6Ex15/+ or RopG27/+ single heterozygotes.

Expression of temperature-sensitive shi1.Scer\UAS under the control of Scer\GAL4109(2)80 in RopG27/RopG27 somatic clones ameliorates the loss of dendritic terminal branches displayed by RopG27/RopG27 class IV dendritic arborizing (da) neurons in third instar larvae (shifted to non-permissive temperature at 48hrs after egg laying and examined at 96hrs). Compared to controls kept under the same temperature regimen the shi1.Scer\UAS expressing RopG27/RopG27 class IV da neurons show increased number of dendrite crossings.

Heterozygosity for RopG27 does not enhance the wing phenotype caused by expression of two copies of Sep4Scer\UAS.cMa under the control of Scer\GAL4da.G32.

Xenogenetic Interactions
Statement
Reference

RopG27/+ fully suppresses the increased excitatory junction potential (EJP) amplitude and decreased failure rate seen in Hsap\HD128Q.FL.Scer\UAS, Scer\GAL4elav-C155 animals at 0.25 mM Ca[2+].

RopG27/+ suppresses the reduced number of rhabdomeres per ommatidium phenotype seen in Hsap\HD128Q.FL.Scer\UAS, Scer\GAL4GMR.PF animals at 20 days.

Complementation and Rescue Data
Comments

Ectopic expression of RopScer\UAS.T:Hsap\MYC,T:Avic\GFP-NYFP under Scer\GAL4109(2)80 in the RopG27/RopG27 class IV da neurons in third instar larvae somatic clones fully rescues the dendritic growth defects of RopG27 mutant neurons.

Images (0)
Mutant
Wild-type
Stocks (2)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (3)
References (13)