FlyBase Allele Report: Dmel\rdgB[9]

FB2026_01 , released March 12, 2026

FB2026_01 , released March 12, 2026

Allele: Dmel\rdgB⁹

General Information

Symbol

Dmel\rdgB⁹

Species

D. melanogaster

Name

FlyBase ID

FBal0014486

Feature type

allele

Associated gene

Associated Insertion(s)

Carried in Construct

Also Known As

rdgB^KS222

Key Links

Genomic Maps

Allele class

Mutagen

ethyl methanesulfonate

Nature of the Allele

Allele class

Mutagen

ethyl methanesulfonate

(Inoue et al., 1989)

Progenitor genotype

Cytology

Description

The premature stop codon is within the PITP domain.

(Paetkau et al., 1999)

Amino acid replacement: Q147term.

(Paetkau et al., 1999)

Mutations Mapped to the Genome

Curation Data

Type

Location

Additional Notes

References

X:13,769,167..13,769,167 [+]

Nucleotide change:

C13769167T

Amino acid change:

Q147term | rdgB-PA; Q147term | rdgB-PB; Q147term | rdgB-PC; Q147term | rdgB-PD; Q147term | rdgB-PE; Q147term | rdgB-PF; Q147term | rdgB-PG; Q147term | rdgB-PH; Q147term | rdgB-PI; Q147term | rdgB-PJ; Q147term | rdgB-PK

Reported amino acid change:

Q147term

Comment:

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

(Paetkau et al., 1999)

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

endoplasmic reticulum-plasma membrane contact site

(Nath et al., 2020)

eye photoreceptor cell

(Chakrabarti et al., 2015, Garcia-Murillas et al., 2006)

(Stark and Carlson, 1982)

(Stark et al., 1983)

(LaLonde et al., 2005, Paetkau et al., 1999, Sahly et al., 1994)

outer photoreceptor cell

(Nath et al., 2020)

photoreceptor cell R1

(Paetkau et al., 1999, Stark et al., 1983, Stark and Carlson, 1982, Miller et al., 1981)

photoreceptor cell R2

(Paetkau et al., 1999, Stark et al., 1983, Stark and Carlson, 1982, Miller et al., 1981)

photoreceptor cell R3

(Paetkau et al., 1999, Stark et al., 1983, Stark and Carlson, 1982, Miller et al., 1981)

photoreceptor cell R4

(Paetkau et al., 1999, Stark et al., 1983, Stark and Carlson, 1982, Miller et al., 1981)

photoreceptor cell R5

(Paetkau et al., 1999, Stark et al., 1983, Stark and Carlson, 1982, Miller et al., 1981)

photoreceptor cell R6

(Paetkau et al., 1999, Stark et al., 1983, Stark and Carlson, 1982, Miller et al., 1981)

photoreceptor neuron

(Hardie et al., 2001, Sahly et al., 1992, Inoue et al., 1989)

photoreceptor neuron | adult stage

(Bulthoff, 1982)

plasma membrane

(Nath et al., 2020)

(Kumari et al., 2022, Nath et al., 2020, LaLonde et al., 2005, Paetkau et al., 1999, Lee et al., 1994, Stark et al., 1983, Harris and Stark, 1977)

retina | adult stage

(Basak et al., 2021, Yadav et al., 2018)

retina | cell autonomous | somatic clone

(Harris and Stark, 1977)

retina | conditional

(Chakrabarti et al., 2015)

(Wang and Montell, 2006, LaLonde et al., 2005, Lee et al., 1994)

rhabdomere | adult stage

(Basak et al., 2021)

rhabdomere of eye photoreceptor cell | adult stage | progressive

(Yadav et al., 2015)

rhabdomere of eye photoreceptor cell | decreased number

(Nath et al., 2020)

(Paetkau et al., 1999, Minke et al., 1990)

(Paetkau et al., 1999, Minke et al., 1990)

(Paetkau et al., 1999, Minke et al., 1990)

(Paetkau et al., 1999, Minke et al., 1990)

(Paetkau et al., 1999, Minke et al., 1990)

(Paetkau et al., 1999, Minke et al., 1990)

Detailed Description

Statement

Reference

rdgB⁹ adults show decreased retinal electrical response to green light (decreased amplitude), compared to controls.

(Kumari et al., 2022)

rdgB⁹ adults exhibit progressive retinal degeneration (with substantial loss of rhabdomere integrity) under constant dark condition, a reduced electroretinogram amplitude and a reduced rate of PIP2 and PI4P recovery.

Dark-reared rdgB⁹ adults exhibit a reduction in the endoplasmic reticulum-plasma membrane contact site density in outer photoreceptors at eclosion.

(Nath et al., 2020)

rdgB⁹ homozygotes exhibit a severe decrease in electroretinogram peak amplitude, a decrease in light sensitivity and severe retinal degeneration in individuals exposed to 12 h:12 h light-dark regime, as compared to controls.

(Yadav et al., 2018)

Compared to wild type, rdgB⁹ photoreceptors produce a very small receptor potential in response to light. rdgB⁹ mutants show light-dependent retinal degeneration.

(Chakrabarti et al., 2015)

rdgB⁹ mutant adults display progressive degeneration phenotype of rhabdomeres in peripheral photoreceptors, which are completely lost by day 5 post-eclosion, whereas the central UV-sensitive photoreceptor is spared. 1-day-old (i.e. prior to the onset of detectable retinal degeneration) rdgB⁹ adults show significantly decreased electroretinogram amplitude (the reduction is more pronounced in flies that had been exposed to light than those kept in darkness until testing) as well as reduced sensitivity to light of increasing intensity compared to wild-type.

(Yadav et al., 2015)

rdgB⁹ flies undergo age-dependent loss of the rhabdomeres; 6 day-old-flies that have been raised under a light/dark cycle have few rhabdomeres left.

(Wang and Montell, 2006)

Electroretinograms show that, 1 day after eclosion, rdgB⁹ mutants do not respond appropriately to light stimulus even though retinal degeneration is not obvious. Retinal degeneration is apparent in 3-day old rdgB⁹ mutant eyes: rhabdomeres are decreased in size and vacuolation has increased. 7 days after eclosion, ommatidial architecture is completely destroyed in rdgB⁹ mutant eyes.

(LaLonde et al., 2005)

Response of rdgB⁹ photoreceptors to moderate flashes of light are indistinguishable from wild type under control conditions, providing the flies are strictly dark reared. Quantum bumps are indistinguishable from wild type. Mutant photoreceptors exposed to La³⁺ show no recovery after a light stimulus of sufficient intensity and duration to induce complete decay, in contrast to wild type (which recover within about 90 seconds). In the absence of La³⁺ the same light stimulus usually results in responses which fail to terminate, leaving channels constitutively activated. Relatively dim flashes repeated at 30 second intervals in a Ca²⁺ free solution result in an exponential and irreversible reduction in sensitivity in mutant photoreceptors (in wild type the response recovers fully between flashes).

(Hardie et al., 2001)

10 day old rdgB⁹ flies raised in a 12 hour light:dark cycle show massive retinal degeneration, and completely lack photoreceptors and rhabdomeres R1-R6. The electroretinogram light response amplitude is reduced compared to wild-type and the off transient is absent.

(Paetkau et al., 1999)

Third instar foraging larvae show negative photobehaviour indistinguishable from the wild-type response to light. Third instar larvae show a decrease in negative phototaxis from the onset of wandering culminating in random photobehaviour indistinguishable from the response of wild-type larvae.

(Sawin-McCormack et al., 1995)

Flies retain large, regular rhabdomeres and exhibit a few holes in their retina if maintained in the dark for over one week. After a week at 12h light dark cycles rhabdomeres become very small and irregular in shape and many holes appear in the retina. rdgB⁹; P{DG_q2-203} lines show no gross histological changes in their retinas after one week in the dark. rdgB⁹; P{DG_q1-203} lines show signs of degeneration, small irregular rhabdomeres and holes in the retina.

(Lee et al., 1994)

Application of calcium channel blockers to eyes over a 7 day period largely inhibit light-dependent degeneration of photoreceptor cells.

(Sahly et al., 1992)

Abnormal olfactory behaviour. EAG defect.

(Woodard et al., 1992)

Microvilli of degenerating rhabdomeres separate and collapse and the detritus they generate is immunopositive to anti-actin.

(Blest et al., 1991)

Rhabdomeres R1-R6 degenerate in flies exposed to light or phorbol esters. Early stages of degeneration are characterised by the appearance of vesicles between the microvilli, phagocytotic vacuoles in the cytoplasm, and partial internalisation of the whole rhabdomere into the cytoplasm. Later, shedding of the rhabdomeres is observed. Rhabdomeres R7 and R8 remain intact.

(Minke et al., 1990)

Photoreceptor degeneration is induced by light stimulation.

(Inoue et al., 1989)

The ocelli are normal in 3 week old flies.

(Stark et al., 1989)

The retina appears fairly normal in newly emerged flies but degenerates with age, particularly the R1-R6 receptors. The lamina is striated into neat cartridges in the newly emerged fly, but appears degenerate and disorganised in older flies. The medulla appears relatively normal at all ages from newly emerged to 3 week old flies. R1-R6 photopigment levels are one-third to one-half of normal in newly emerged flies, and decline within a week to undetectable levels.

(Stark et al., 1983)

Receptor mutant. Orientation effect is almost absent in the fixation Y-maze.

(Bulthoff, 1982)

Photoreceptor cells R7 and R8 are normal. Newly emerged mutant flies have a normal peripheral retina and normal optic neuropiles. By 3 days after eclosion the soma of only one peripheral photoreceptor cell per ommatidium usually shows degenerative ultrastructural changes; the cytoplasm is filled with electron dense bodies, residual bodies, secondary lysosomes, liposomes and an electron dense network immediately beneath the rhabdomere, which appears to be composed of aggregated ribosomes. Strands of microvillar membrane appear to detach from the rhabdomere and partly autophaged mitochondria are seen. The axon terminals of these cells are very degenerate. At one week after eclosion an electron dense meshwork pervades the entire cell, and few if any cytoplasmic organelles can be recognised. At this time, most R1-R6 photoreceptor cells and their axons are degenerate. Lamina interneurons do not show any transsynaptic degeneration, but have a larger diameter than normal, and are misaligned. By three weeks after eclosion only amorphous, dense, vacuolated vestiges of the peripheral photoreceptor cells remain. Epithelial glia have multiplied and filled in any gaps in the lamina ganglionaris produced by the degenerating R1-R6 axons.

(Stark and Carlson, 1982)

Flies show light-induced inactivation and degeneration of photoreceptor cells R1-R6. Flies do not show phototaxis in response to extremely dim light stimuli.

(Miller et al., 1981)

Retinal degeneration is occurring by 24 hours after eclosion in mutant flies kept in the light and at 72 hours degeneration is well underway in almost all mutant flies. No retinal degeneration is seen in 5 day old flies kept in darkness at 18^oC. Dark-to-light shifts indicate that it is the adult photoreceptor cell that is sensitive to light induced degeneration. Mosaic analysis indicates that the degeneration defects are autonomous to the retina. Retinal degeneration in constant light or in darkness is temperature sensitive. Photoreceptors R7 and R8 are preserved in almost every ommatidium in 7 day old mutant flies. The electroretinogram (ERG) of 7 day old flies shows reduced receptor potentials and the absence of on-transients. The prolonged depolarising afterpotential produced by exposing dark raised mutant flies to intense 470nm light is abnormal and results in the photoreceptors becoming completely unresponsive to light.

(Harris and Stark, 1977)

External Data

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Enhanced by

Statement

Reference

rdgB⁹ has abnormal neurophysiology | adult stage phenotype, enhanceable by Esyt2^KO/Esyt2^KO

(Nath et al., 2020)

rdgB⁹ has abnormal neurophysiology phenotype, enhanceable by PIP5K59B¹⁸

(Chakrabarti et al., 2015)

NOT Enhanced by

Statement

Reference

rdgB⁹ has abnormal neurophysiology phenotype, non-enhanceable by sktl^Δ20

(Chakrabarti et al., 2015)

rdgB⁹ has abnormal neurophysiology phenotype, non-enhanceable by PIP4K²⁹

(Chakrabarti et al., 2015)

Suppressed by

Statement

Reference

rdgB⁹ has abnormal neurophysiology | adult stage phenotype, suppressible by pnut[+]/pnut^XP

(Kumari et al., 2022)

rdgB⁹ has abnormal neurophysiology | adult stage phenotype, suppressible by PIP5K59B^{RNAi.UAS.L.cKa}/Scer\GAL4^ninaE.PT

(Kumari et al., 2022)

rdgB⁹ has abnormal neurophysiology phenotype, suppressible by Scer\GAL4^ninaE.PD/Pld^UAS.cLa

(LaLonde et al., 2005)

NOT suppressed by

Statement

Reference

rdgB⁹ has abnormal sensory perception | adult stage phenotype, non-suppressible by vib^Ubi.PG

(Yadav et al., 2015)

Suppressor of

Statement

Reference

rdgB⁹ is a suppressor of abnormal neurophysiology | dominant | adult stage phenotype of pnut^XP

(Kumari et al., 2022)

Phenotype Manifest In

Enhanced by

Statement

Reference

rdgB⁹ has rhabdomere of eye photoreceptor cell | decreased number phenotype, enhanceable by Esyt2^KO/Esyt2^KO

(Nath et al., 2020)

rdgB⁹ has retina phenotype, enhanceable by Esyt2^KO/Esyt2^KO

(Nath et al., 2020)

rdgB⁹ has plasma membrane phenotype, enhanceable by Esyt2^KO/Esyt2^KO

(Nath et al., 2020)

rdgB⁹ has outer photoreceptor cell phenotype, enhanceable by Esyt2^KO/Esyt2^KO

(Nath et al., 2020)

rdgB⁹ has endoplasmic reticulum-plasma membrane contact site phenotype, enhanceable by Esyt2^KO/Esyt2^KO

(Nath et al., 2020)

rdgB⁹ has eye photoreceptor cell phenotype, enhanceable by PIP5K59B¹⁸

(Chakrabarti et al., 2015)

rdgB⁹ has retina | conditional phenotype, enhanceable by PIP5K59B¹⁸

(Chakrabarti et al., 2015)

rdgB⁹ has eye photoreceptor cell phenotype, enhanceable by CG11426^UAS.GFP/Scer\GAL4^ninaE.PT

(Garcia-Murillas et al., 2006)

NOT Enhanced by

Statement

Reference

rdgB⁹ has eye photoreceptor cell phenotype, non-enhanceable by sktl^Δ20

(Chakrabarti et al., 2015)

rdgB⁹ has retina | conditional phenotype, non-enhanceable by sktl^Δ20

(Chakrabarti et al., 2015)

rdgB⁹ has eye photoreceptor cell phenotype, non-enhanceable by PIP4K²⁹

(Chakrabarti et al., 2015)

rdgB⁹ has retina | conditional phenotype, non-enhanceable by PIP4K²⁹

(Chakrabarti et al., 2015)

Suppressed by

Statement

Reference

rdgB⁹ has retina phenotype, suppressible by pnut[+]/pnut^XP

(Kumari et al., 2022)

rdgB⁹ has retina phenotype, suppressible by PIP5K59B^{RNAi.UAS.L.cKa}/Scer\GAL4^ninaE.PT

(Kumari et al., 2022)

rdgB⁹ has eye photoreceptor cell phenotype, suppressible by laza²²

(Garcia-Murillas et al., 2006)

rdgB⁹ has rhabdomere phenotype, suppressible by Pis^ninaE.PW

(Wang and Montell, 2006)

rdgB⁹ has retina phenotype, suppressible by Scer\GAL4^ninaE.PD/Pld^UAS.cLa

(LaLonde et al., 2005)

rdgB⁹ has retina phenotype, suppressible by norpA^su76

(Paetkau et al., 1999)

rdgB⁹ has retina phenotype, suppressible by norpA^su68

(Paetkau et al., 1999)

rdgB⁹ has retina phenotype, suppressible by norpA^su99

(Paetkau et al., 1999)

rdgB⁹ has retina phenotype, suppressible by ninaE^su71

(Paetkau et al., 1999)

rdgB⁹ has retina phenotype, suppressible by stops⁶⁹

(Paetkau et al., 1999)

rdgB⁹ has retina phenotype, suppressible by su(rdgB)82⁸²

(Paetkau et al., 1999)

rdgB⁹ has retina phenotype, suppressible by Su(rdgB)83⁸³

(Paetkau et al., 1999)

rdgB⁹ has retina phenotype, suppressible by stops¹⁰²

(Paetkau et al., 1999)

rdgB⁹ has retina phenotype, suppressible by stops¹⁰³

(Paetkau et al., 1999)

rdgB⁹ has retina phenotype, suppressible by stops¹⁰⁴

(Paetkau et al., 1999)

rdgB⁹ has retina phenotype, suppressible by Su(rdgB)116¹¹⁶

(Paetkau et al., 1999)

rdgB⁹ has eye photoreceptor cell phenotype, suppressible by trp¹

(Paetkau et al., 1999)

rdgB⁹ has ommatidium phenotype, suppressible by trp¹

(Paetkau et al., 1999)

rdgB⁹ has phenotype, suppressible by norpA^suII

(Stark et al., 1983, Harris and Stark, 1977)

rdgB⁹ has phenotype, suppressible by norpA^suIII

(Harris and Stark, 1977)

rdgB⁹ has photoreceptor cell R1 phenotype, suppressible by norpA^EE5

(Harris and Stark, 1977)

rdgB⁹ has photoreceptor cell R2 phenotype, suppressible by norpA^EE5

(Harris and Stark, 1977)

rdgB⁹ has photoreceptor cell R3 phenotype, suppressible by norpA^EE5

(Harris and Stark, 1977)

rdgB⁹ has photoreceptor cell R4 phenotype, suppressible by norpA^EE5

(Harris and Stark, 1977)

rdgB⁹ has photoreceptor cell R5 phenotype, suppressible by norpA^EE5

(Harris and Stark, 1977)

rdgB⁹ has photoreceptor cell R6 phenotype, suppressible by norpA^EE5

(Harris and Stark, 1977)

rdgB⁹ has phenotype, suppressible by norpA^suI

(Harris and Stark, 1977)

NOT suppressed by

Statement

Reference

rdgB⁹ has rhabdomere of eye photoreceptor cell | adult stage | progressive phenotype, non-suppressible by vib^Ubi.PG

(Yadav et al., 2015)

rdgB⁹ has retina phenotype, non-suppressible by Scer\GAL4^ninaE.PD/Pld^UAS.cLa

(LaLonde et al., 2005)

rdgB⁹ has eye photoreceptor cell phenotype, non-suppressible by inaC²

(Paetkau et al., 1999)

rdgB⁹ has ommatidium phenotype, non-suppressible by inaC²

(Paetkau et al., 1999)

rdgB⁹ has phenotype, non-suppressible by Hdc^JK910

(Harris and Stark, 1977)

Suppressor of

Statement

Reference

rdgB⁹ is a suppressor of retina phenotype of pnut^XP

(Kumari et al., 2022)

rdgB⁹ is a suppressor of retina phenotype of Pld^UAS.cLa, Scer\GAL4^ninaE.PD

(LaLonde et al., 2005)

Other

Statement

Reference

Hsap\KCNJ2^UAS.EGFP, Scer\GAL4^ninaE.PT, rdgB⁹ has photoreceptor neuron phenotype

(Hardie et al., 2001)

Additional Comments

Genetic Interactions

Statement

Reference

rdgB⁹ Esyt2^KO exhibit substantially greater rhabdomeral degeneration than rdgB⁹ when flies are reared for 2 days under conditions of 12-h L/D cycle.

(Nath et al., 2020)

PIP5K59B¹⁸, but not sktl^Δ20 or PIP4K²⁹, exacerbates the reduced electrical response to light and retinal degeneration phenotypes of rdgB⁹.

(Chakrabarti et al., 2015)

The progressive retinal degeneration as well as reduced electroretinogram amplitude characteristic for rdgB⁹ mutant adults cannot be suppressed by expression of vib^Ubi.PG.

(Yadav et al., 2015)

Expression of CG11426^{Scer\UAS.T:Avic\GFP} under the control of Scer\GAL4^ninaE.PT enhances the photoreceptor degeneration seen in rdgB⁹ flies.

laza²² slows the rate of photoreceptor degeneration seen in rdgB⁹ flies.

(Garcia-Murillas et al., 2006)

The degeneration of rhabdomeres in rdgB⁹ flies is greatly suppressed by expression of Pis^ninaE.PW.

(Wang and Montell, 2006)

Expression of Pld^Scer\UAS.cLa under the control of Scer\GAL4^ninaE.PD suppresses the defective light response phenotype of 1 day-old rdgB⁹ mutants.

The retinal degeneration phenotype observed upon expression of Pld^Scer\UAS.cLa under the control of Scer\GAL4^ninaE.PD when flies are raised under continuous light for 1 or 3 days is suppressed in a rdgB⁹ mutant background. Conversely, expression of Pld^Scer\UAS.cLa under the control of Scer\GAL4^ninaE.PD does not prevent or slow the rate of retinal degeneration seen in rdgB⁹ flies.

(LaLonde et al., 2005)

The retinal degeneration phenotype of rdgB⁹ flies is suppressed by norpA^su76, norpA^su68, norpA^su99, ninaE^su71, su(rdgB)69⁶⁹, su(rdgB)82⁸², Su(rdgB)83⁸³, su(rdgB)69¹⁰², su(rdgB)69¹⁰³, su(rdgB)69¹⁰⁴, or Su(rdgB)116¹¹⁶. inaC² does not significantly alter the deep pseudopupil loss of rdgB⁹ flies and fails to suppress the photoreceptor degeneration and ommatidial disorganisation seen in these flies at 6 days after eclosion. trp¹ does not slow the initiation of deep pseudopupil loss of rdgB⁹ flies, but dramatically suppresses photoreceptor degeneration and ommatidial disorganisation in these flies.

(Paetkau et al., 1999)

The initial photopigment level is increased and then decreases more slowly in rdgB⁹ flies also carrying norpA⁵⁶ or norpA⁷. The retinal degeneration phenotype is inhibited by norpA⁵⁶.

(Stark et al., 1983)

Acph-1ⁿ¹¹ does not prevent, but delays, the retinal degeneration seen in rdgB⁹ flies. rdgB⁹ ort¹ double mutants do not show degeneration of photoreceptor cells at 18^oC even after 20 days in constant light. However, at 25^oC they do show degeneration after about 10 days, independent of light condition. norpA⁷ rdgB⁹ double mutants have normal looking R1-6 photoreceptors even after 20 days in constant light at 18^oC. Retinal degeneration in rdgB⁹ flies is not suppressed by Hdc^JK910. norpA⁵⁵ rdgB⁹ double mutants have almost no electroretinogram receptor potential and do not show retinal degeneration. norpA⁵⁶ rdgB⁹ double mutants have a normal electroretinogram but do not show retinal degeneration.

(Harris and Stark, 1977)

Xenogenetic Interactions

Statement

Reference

After a light stimulus just sufficient to induce decay, the photoreceptor cell IRK current is suppressed in rdgB⁹ flies expressing Hsap\KCNJ2^{Scer\UAS.T:Avic\GFP-EGFP} under the control of Scer\GAL4^ninaE.PT (as occurs in a rdgB⁺ background), but the current recovers at most about 50% over a period of several minutes (in flies expressing Hsap\KCNJ2^{Scer\UAS.T:Avic\GFP-EGFP} under the control of Scer\GAL4^ninaE.PT in a rdgB⁺ background full recovery with a half-time of about 30 seconds is seen).

(Hardie et al., 2001)

Complementation and Rescue Data

Rescued by

rdgB⁹ is rescued by rdgB^UAS.cYa/Scer\GAL4^GMR.PU

(Basak et al., 2021)

rdgB⁹ is rescued by Scer\GAL4^ninaE.PU/rdgB^UAS.cYa

(Yadav et al., 2018)

rdgB⁹ is rescued by rdgB^UAS.cYa/Scer\GAL4^GMR.PF

(Yadav et al., 2018)

rdgB⁹ is rescued by rdgB^PITPd.UAS/Scer\GAL4^GMR.PF

(Yadav et al., 2018)

rdgB⁹ is rescued by rdgB^UAS.cYa

(Yadav et al., 2015)

rdgB⁹ is rescued by rdgB^PITP.UAS

(Yadav et al., 2015)

Partially rescued by

rdgB⁹ is partially rescued by rdgB^DDHD-4A.UAS/Scer\GAL4^GMR.PU

(Basak et al., 2021)

rdgB⁹ is partially rescued by Scer\GAL4^ninaE.PU/rdgB^FF-AA.UAS

(Yadav et al., 2018)

rdgB⁹ is partially rescued by Scer\GAL4^ninaE.PU/rdgB^PITPd.UAS

(Yadav et al., 2018)

Not rescued by

rdgB⁹ is not rescued by rdgB^{ΔDDHD-LNS2.UAS}/Scer\GAL4^GMR.PU

(Basak et al., 2021)

rdgB⁹ is not rescued by rdgB^LNS2Δ.UAS/Scer\GAL4^GMR.PU

(Basak et al., 2021)

rdgB⁹ is not rescued by Scer\GAL4^ninaE.PU/rdgB^FFD-AAA.UAS

(Yadav et al., 2018)

rdgB⁹ is not rescued by rdgB^{T59E.PITP.UAS}

(Yadav et al., 2015)

rdgB⁹ is not rescued by rdgB^{T59A.PITP.UAS}

(Yadav et al., 2015)

rdgB⁹ is not rescued by rdgB^{PITP.K61A.UAS}

(Yadav et al., 2015)

rdgB⁹ is not rescued by rdgB^{PITP.N90F.UAS}

(Yadav et al., 2015)

rdgB⁹ is not rescued by rdgB^K61A.UAS

(Yadav et al., 2015)

rdgB⁹ is not rescued by rdgB^YW-AA.UAS

(Yadav et al., 2015)

Comments

The severe decrease in electroretinogram peak amplitude observed in rdgB⁹ homozygotes is fully rescued by the expression of rdgB^Scer\UAS.cYa or rdgB^{PITPd.Scer\UAS}, is partially rescued by the expression of rdgB^{FF-AA.Scer\UAS}, and is not rescued by the expression of rdgB^{FFD-AAA.Scer\UAS} (expression under the control of Scer\GAL4^ninaE.PU).

The severe retinal degeneration observed in rdgB⁹ homozygotes exposed to 12 h:12 h light-dark regime is fully and partially rescued by the expression of rdgB^Scer\UAS.cYa and rdgB^{FF-AA.Scer\UAS}, respectively, under the control of under the control of Scer\GAL4^ninaE.PU.

The decreased light sensitivity observed in rdgB⁹ homozygotes is fully rescued by the expression of rdgB^Scer\UAS.cYa and partially rescued by the expression of rdgB^{FF-AA.Scer\UAS} or rdgB^{PITPd.Scer\UAS}. This decreased light sensitivity is also fully rescued by the expression of either rdgB^Scer\UAS.cYa or rdgB^{PITPd.Scer\UAS} under the control of Scer\GAL4^GMR.PF.

(Yadav et al., 2018)

The progressive retinal degeneration, reduced electroretinogram amplitude and sensitivity to light of increasing intensity characteristic for rdgB⁹ mutant adults can be fully rescued by expression of either rdgB^Scer\UAS.cYa or rdgB^{PITP.Scer\UAS} under the control of Scer\GAL4^ninaE.PU.

The progressive retinal degeneration as well as reduced electroretinogram amplitude characteristic for rdgB⁹ mutant adults cannot be rescued by expression of any of the following: rdgB^{T59A.PITP.Scer\UAS}, rdgB^{T59E.PITP.Scer\UAS}, rdgB^{PITP.K61A.Scer\UAS}, rdgB^{PITP.N90F.Scer\UAS}, rdgB^{K61A.Scer\UAS} or rdgB^{YW-AA.Scer\UAS} under the control of Scer\GAL4^ninaE.PU.

(Yadav et al., 2015)

Images (0)

Mutant

Wild-type

Stocks (1)

27337

Notes on Origin

Discoverer

Comments

Comments

Alleles can be ranked with respect to how much R7 and R8 are affected in each mutant; rdgB⁵ > rdgB⁷ > rdgB⁶ = rdgB⁸ > rdgB¹ = rdgB⁹.

(Harris and Stark, 1977)

No genetic or interallelic interaction with rdgC³⁰⁶.

(Steele and O'Tousa, 1990)

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (4)

Reported As

Symbol Synonym

rdg^K222

(Woodard et al., 1992)

rdgB⁹

(Mishra et al., 2024, Kumari et al., 2022, Basak et al., 2021, Nath et al., 2020, Trivedi et al., 2020, Balakrishnan et al., 2018, Yadav et al., 2018, Chakrabarti et al., 2015, Hardie et al., 2015, Yadav et al., 2015, LaLonde et al., 2005)

rdgB^ks222

(Garcia-Murillas et al., 2006, LaLonde et al., 2005)

Name Synonyms

Secondary FlyBase IDs

References (39)

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