Amino acid replacement: Q22term.
Mutation is predicted to truncate the protein before the Ran-binding domain.
C15682868T
Q22term | Impbeta11-PA
Q22term
Site of nucleotide substitution in mutant inferred by FlyBase based on reported amino acid change.
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.
Impβ1170 has abnormal neuroanatomy phenotype, enhanceable by witA12/wit[+]
Impβ1170 has abnormal neuroanatomy phenotype, enhanceable by wit[+]/witHA1
Impβ1170 has abnormal neuroanatomy phenotype, non-enhanceable by n-syb[+]/nSybF33
Impβ1170, wit[+]/witHA1 has abnormal neuroanatomy phenotype, suppressible by witUAS.cMa/Scer\GAL4elav.PLu
Impβ1170 has abnormal neurophysiology phenotype, suppressible by saxQ263D.UAS.Tag:HA/Scer\GAL4RapGAP1-OK6
Impβ1170 has abnormal neuroanatomy phenotype, non-suppressible by n-syb[+]/nSybF33
Impβ1170 has abnormal neurophysiology phenotype, non-suppressible by Scer\GAL4RapGAP1-OK6/tkvQ253D.UAS.cNb
Impβ1170 has abnormal neurophysiology phenotype, non-suppressible by Scer\GAL4G14/tkvQ253D.UAS.cNb
Impβ1170 has abnormal neurophysiology phenotype, non-suppressible by Scer\GAL4G14/saxQ263D.UAS.Tag:HA
Impβ1170 is an enhancer of abnormal neuroanatomy phenotype of witA12
Impβ1170 is an enhancer of abnormal neuroanatomy phenotype of witHA1
Ranbp11[+]/Impβ1170 is a non-enhancer of abnormal neuroanatomy phenotype of nSybF33
Ranbp11[+]/Impβ1170 is a non-suppressor of abnormal neuroanatomy phenotype of nSybF33
Impβ1170, Mad10 has abnormal neuroanatomy phenotype
Impβ1170 has bouton phenotype, suppressible by Scer\GAL4RapGAP1-OK6/tkvQ253D.UAS.cNb
Impβ1170 has bouton phenotype, suppressible by saxQ263D.UAS.Tag:HA/Scer\GAL4RapGAP1-OK6
Impβ1170, wit[+]/witHA1 has bouton phenotype, suppressible by witUAS.cMa/Scer\GAL4elav.PLu
Impβ1170 has bouton phenotype, non-suppressible by Scer\GAL4G14/tkvQ253D.UAS.cNb
Impβ1170 has bouton phenotype, non-suppressible by Scer\GAL4G14/saxQ263D.UAS.Tag:HA
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.
Impβ1170 is rescued by Scer\GAL4ey.PH/Impβ11UAS.EGFP
Impβ1170 is rescued by Scer\GAL4elav.PLu/Impβ11UAS.EGFP
Impβ1170 is rescued by Scer\GAL4da.G32/Impβ11UAS.EGFP
Impβ1170 is not rescued by Scer\GAL4G14/Impβ11UAS.EGFP
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.