FB2025_01 , released February 20, 2025
Allele: Dmel\Impβ1170
Open Close
General Information
Symbol
Dmel\Impβ1170
Species
D. melanogaster
Name
FlyBase ID
FBal0246520
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Key Links
Genomic Maps

Allele class
Nature of the Allele
Allele class
Progenitor genotype
Cytology
Description

Amino acid replacement: Q22term.

Mutation is predicted to truncate the protein before the Ran-binding domain.

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

C15682868T

Amino acid change:

Q22term | Impbeta11-PA

Reported amino acid change:

Q22term

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 ( 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

Ranbp1170 flies exhibit defects in phototaxis and abnormalities in the ERG.

Ranbp1170 mutant eye clones lack 'on' and 'off' transients in their ERGs in response to brief exposures to light.

Ranbp1170 mutant eyes do not exhibit any gross abnormalities in photoreceptor axon projections: R1-R6 endings appear to terminate appropriately in the lamina, and normal terminals appear in the layers of the medulla that receive the endings of photoreceptors R7 and R8.

Lamina from Ranbp1170 mutant animals exhibit a wild-type structure, the R1-R6 photoreceptors appear normal, synapses can be seen with T-bar ribbons, presynaptic densities and clusters of vesicles. Small clear vesicles are normal in size but more numerous at mutant terminals. The cross-sectional area of the terminal profile is also significantly increased, resulting in normal vesicle density. In addition, capitate projections are almost absent from mutant terminals.

Maternal germline clones homozygous for Ranbp1170 do not lay eggs.

Although the size of their muscle fibers is normal, Ranbp1170/Df(2R)ΔM22-103 mutant larvae exhibit a 30% reduction in bouton number when compared to either control larvae or heterozygote mutant larvae. Ranbp1170/Df(2R)ΔM22-103 mutants show a similar 30% decrease in bouton density. Synaptic footprints, a sign that boutons have retracted, were scant in both mutant and control. There is no preferential loss of Ib or Is boutons in Ranbp1170/Df(2R)ΔM22-103 neuromuscular junctions, but arbor length and bouton diameter are both slightly decreased when compared to control. The geometry of the synapse is altered in Ranbp1170/Df(2R)ΔM22-103 mutants with axonal branches remaining close to the inter-muscular cleft rather than spreading across the width of the muscle.

The amplitude of excitatory junctional potentials (EJPs) in larval muscle 6 is reduced by 40% in Ranbp1170/Df(2R)ΔM22-103 mutants. Vesicles also fuse spontaneously at the NMJ, giving rise to quantal events or miniature EJPs. Ranbp1170/Df(2R)ΔM22-103 mutants release vesicles at a lower frequency, about 65% less than control. There is also a small, but statistically significant decrease in the amplitude of the mEJPs. Quantal content, or the number of vesicles released per action potential, is reduced by 30% in Ranbp1170/Df(2R)ΔM22-103 mutants when corrected for nonlinear summation.

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

Impβ1170 has abnormal neuroanatomy phenotype, non-enhanceable by n-syb[+]/nSybF33

Suppressed by
NOT suppressed by
Enhancer of
Statement
Reference
NOT Enhancer of
Statement
Reference

Ranbp11[+]/Impβ1170 is a non-enhancer of abnormal neuroanatomy phenotype of nSybF33

NOT Suppressor of
Statement
Reference

Ranbp11[+]/Impβ1170 is a non-suppressor of abnormal neuroanatomy phenotype of nSybF33

Other
Phenotype Manifest In
Enhanced by
Statement
Reference

Impβ1170 has bouton phenotype, enhanceable by witA12/wit[+]

Impβ1170 has bouton phenotype, enhanceable by wit[+]/witHA1

NOT Enhanced by
Statement
Reference

Impβ1170 has bouton phenotype, non-enhanceable by n-syb[+]/nSybF33

Suppressed by
NOT suppressed by
Statement
Reference

Impβ1170 has bouton phenotype, non-suppressible by n-syb[+]/nSybF33

Enhancer of
Statement
Reference

Ranbp11[+]/Impβ1170 is an enhancer of bouton phenotype of witA12

Ranbp11[+]/Impβ1170 is an enhancer of bouton phenotype of witHA1

NOT Enhancer of
Statement
Reference

Ranbp11[+]/Impβ1170 is a non-enhancer of bouton phenotype of nSybF33

NOT Suppressor of
Statement
Reference

Ranbp11[+]/Impβ1170 is a non-suppressor of bouton phenotype of nSybF33

Other
Statement
Reference
Additional Comments
Genetic Interactions
Statement
Reference

Ranbp1170/Mad10 double mutants exhibit a 15% reduction in synaptic bouton number.

Ranbp1170/+; witA12/+ double heterozygous larvae exhibit significantly fewer boutons than either wild-type or each heterozygous allele alone.

Ranbp1170/+; witHA1/+ double heterozygous larvae exhibit significantly fewer boutons than either wild-type or each heterozygous allele alone.

Larvae heterozygous for Ranbp1170 and n-sybF33 exhibit normal synaptic arbors.

Neuronal expression of witScer\UAS.cMa (under the control of Scer\GAL4elav.PLu reverses the reduction in bouton number in Ranbp1170/+ ; witHA1/+ larvae.

Expression of tkvQ253D.Scer\UAS.cNb in motor neurons (under the control of Scer\GAL4OK6) rescues bouton number and EJP phenotypes in Ranbp1170 mutants, although mEJP frequency is not rescued.

Expression of tkvQ253D.Scer\UAS.cNb in muscle (under the control of Scer\GAL4G14) does not rescue bouton number or mEJP and EJP phenotypes in Ranbp1170 mutants.

Expression of saxQ263D.Scer\UAS.T:Ivir\HA1 in motor neurons (under the control of Scer\GAL4OK6) rescues bouton number and EJP phenotypes in Ranbp1170 mutants, although mEJP frequency is not rescued.

Expression of saxQ263D.Scer\UAS.T:Ivir\HA1 in muscle (under the control of Scer\GAL4G14) does not rescue bouton number or mEJP and EJP phenotypes in Ranbp1170 mutants.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Comments

Expression of Ranbp11Scer\UAS.T:Avic\GFP-EGFP in photoreceptors under the control of Scer\GAL4ey.PH fully restores the on and off transients in Ranbp1170 mutant eye clones.

Expression of Ranbp11Scer\UAS.T:Avic\GFP-EGFP in all tissues (with a Scer\GAL4da.G32 driver) or in neurons (with a Scer\GAL4elav.PLu driver) rescues the reduction in bouton number/muscle surface area in Ranbp1170 mutants. Expression of Ranbp11Scer\UAS.T:Avic\GFP-EGFP in muscle (with a Scer\GAL4G14 driver) does not rescue this phenotype in Ranbp1170 mutants.

The observed defects in quantal content and EJP amplitude in Ranbp1170 are fully rescued upon expression of Ranbp11Scer\UAS.T:Avic\GFP-EGFP in the nervous system under the control of Scer\GAL4elav.PLu. Although quantal content is somewhat increased by transgene expression in muscle (under the control of Scer\GAL4G14), it does not correspond to a statistically significant restoration of EJP amplitude. Separately, neither neuronal nor muscle expression of Ranbp11Scer\UAS.T:Avic\GFP-EGFP is adequate to restore mEJP frequency or amplitude to control levels; however, concurrent expression in both neurons and muscle significantly increases mini frequency. mEJP amplitude is not rescued.

Images (0)
Mutant
Wild-type
Stocks (0)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (4)
Reported As
Symbol Synonym
Name Synonyms
Secondary FlyBase IDs
    References (3)