FlyBase Allele Report: Dmel\trp[9]

General Information

Symbol

Dmel\trp⁹

Species

D. melanogaster

Name

FlyBase ID

FBal0017163

Feature type

allele

Associated gene

Dmel\trp

Associated Insertion(s)

Carried in Construct

Also Known As

trp³⁴³, trp^P343

Key Links

Genomic Maps

JBrowse

Allele class

loss of function allele

Mutagen

ethyl methanesulfonate

Nature of the Allele

Allele class

loss of function allele

(Leung et al., 2000)

Mutagen

ethyl methanesulfonate

Progenitor genotype

Cytology

Description

Mutation in the first base of the 5' splice site of intron 7.

(Wang et al., 2005)

Nucleotide substitution: G?A.

(Wang et al., 2005)

Mutations Mapped to the Genome

Curation Data

Type

Location

Additional Notes

References

point_mutation

3R:29,917,798..29,917,798 [-]

Nucleotide change:

G29917798A

Reported nucleotide change:

G?A

Comment:

G to A mutation in the splice donor site of intron 7.

(Wang et al., 2005)

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

abnormal neuroanatomy

(Wang et al., 2005)

abnormal neurophysiology

(Rosenbaum et al., 2011, Leung et al., 2008, Meyer et al., 2006, Wang et al., 2005)

abnormal neurophysiology, with trp^3.cHa

(Hong et al., 2002)

abnormal neurophysiology, with trp^1234.cHa

(Hong et al., 2002)

abnormal neurophysiology (with trp^idl-B-1)

(Sanxaridis and Tsunoda, 2010)

abnormal neurophysiology (with trp^idl-B-2)

(Sanxaridis and Tsunoda, 2010)

abnormal neurophysiology | adult stage, with trp^S936A.ninaE

(Voolstra et al., 2017)

abnormal neurophysiology | adult stage, with trp^S936D.ninaE

(Voolstra et al., 2017)

abnormal neurophysiology | adult stage | somatic clone

(Huang et al., 2015)

abnormal neurophysiology | recessive

(Badsha et al., 2012)

abnormal smell perception | dominant

(Badsha et al., 2012)

abnormal visual behavior

(Leung et al., 2000, Li et al., 1999)

increased cell death | adult stage | progressive | somatic clone

(Huang et al., 2015)

Phenotype Manifest In

eye | somatic clone

(Huang et al., 2015)

eye photoreceptor cell

(Meyer et al., 2006)

eye photoreceptor cell | somatic clone

(Huang et al., 2015)

photoreceptor neuron

(Agam et al., 2000, Haab et al., 2000, Leung et al., 2000, Li et al., 1999)

retina | adult stage, with trp^S936A.ninaE

(Voolstra et al., 2017)

retina | adult stage, with trp^S936D.ninaE

(Voolstra et al., 2017)

retina | conditional

(Rosenbaum et al., 2011)

retina | somatic clone

(Huang et al., 2015)

rhabdomere

(Wang et al., 2005, Kosloff et al., 2003)

rhabdomere, with trp^3.cHa

(Hong et al., 2002)

rhabdomere, with trp^1234.cHa

(Hong et al., 2002)

rhabdomere of eye photoreceptor cell | somatic clone

(Huang et al., 2015)

Detailed Description

Statement

Reference

Like wild-type, trp⁹ heterozygous flies carrying any of the following transgenic alleles: trp^ninaE.PV, trp^S936D.ninaE or trp^S936D.ninaE do not display oscillating voltage electroretinogram (ERG) response upon constant light stimulation.

Dark-adapted trp⁹/+;trp^ninaE.PV flies show no significant changes in the onset of the frequency-locked response to oscillating light of either low (10Hz) or high (70Hz) frequency compared to wild-type flies, no defects are observed in light-adapted flies at high frequency either.

The frequency response of light-adapted trp⁹/+;trp^S936A.ninaE flies to oscillating light of gradually increasing frequencies is comparable to controls at both low and high stimulus frequencies. Dark-adapted flies show no significant changes in the onset of the frequency-locked response to oscillating light of low (10Hz) frequency, but unlike wild-type flies they display a quick (<0.3s) frequency-locked response also at high (70Hz) frequency (wild-type flies take about 8s). Light-adapted flies at high frequency show normal quick onset, same as wild-type.

The electroretinogram response of light-adapted trp⁹/+;trp^S936D.ninaE flies to oscillating light of gradually increasing frequencies is comparable to controls at lower stimulus frequencies, but mean oscillation amplitude of the response drops significantly at higher frequencies relative to controls. Dark-adapted flies show no significant changes in the onset of the frequency-locked response to oscillating light of either low (10Hz) or high (70Hz) frequency compared to wild-type flies. However, there is no difference in the timing of the onset of frequency-locked response between dark-adapted and light-adapted flies as both take about 8s to show response (similar to the onset time of dark-adapted controls), whereas in light-adapted wild-type flies it takes less than 0.3s until they display frequency-locked response.

(Voolstra et al., 2017)

trp⁹ mutant adults show normal preference for less solid sucrose-agarose food than a harder one (higher agarose conc., same sucrose content) one in a two-way food choice assay.

(Zhang et al., 2016)

The integrity of photoreceptor cells show light-dependent degeneration (including loss of rhabdomere structures in the retina) in trp⁹/trp⁹ homozygous mutant clones in the eye (in 10 day old flies compared to 1 day old); ERG recordings show a transient response to light.

(Huang et al., 2015)

The gustatory aversion of mutant flies to 6mM camphor in a two way-choice test is not significantly different from that seen in wild-type flies.

(Zhang et al., 2013)

trp⁹ homozygotes show decreased avoidance to CO2, as compared to heterozygous and wild-type controls; in agreement, mutants show decreased electrophysiological responses of the basiconica rich region of the 3rd antennal segment to CO2 exposure, as compared to controls.

(Badsha et al., 2012)

trp⁹ mutants show a decline in the light response towards baseline during prolonged intense light.

(Richter et al., 2011)

Mutants show an abnormal, transient response during prolonged light stimulation compared to wild type.

trp⁹ mutants exhibit retinal degeneration. There is no sign of secretory pathway membrane accumulations. At 2 weeks, mutants display a severe retinal phenotype - this is significantly attenuated when flies are reared in constant darkness.

(Rosenbaum et al., 2011)

Mutant flies exhibit the wild type avoidance of aristolochic acid in food choice assays.

(Kim et al., 2010)

Mutant adults show normal avoidance of 1% citronellal in a direct airborne repellent test (DART) assay.

(Kwon et al., 2010)

Mutant third instar larvae show the same preference for 17.5[o]C over 14[o]C in a two-way choice test as do wild-type controls.

(Kwon et al., 2010)

trp^idl-B-1/trp⁹ and trp^idl-B-2/trp⁹ animals show a transient electroretinogram response.

(Sanxaridis and Tsunoda, 2010)

trp⁹ mutants retain a preference for 18[o]C (i.e. are thermotactic).

(Kwon et al., 2008)

Mutants have no prolonged depolarising afterpotential in their electroretinogram in response to blue light stimulus. The mutant flies have a prolonged refractory period after stimulation.

(Leung et al., 2008)

The light-triggered translocation of trpl^{ninaE.T:Avic\GFP-EGFP} is abolished in trp⁹ flies.

(Meyer et al., 2008)

The light response of trp⁹ mutants is very different to wild-type flies, which have a sustained response during illumination and the response to the first and second light pulses are virtually identical. Intensity-response relationships (V-log I curves) of trp⁹ mutants are shifted to higher levels of light intensity by about 1 log unit as compared to wild-type flies.

trpl^{ninaE.T:Avic\GFP-EGFP} is not internalised in trp⁹ mutant photoreceptors.

(Meyer et al., 2006)

The maximum rate of capa stimulated fluid transport in Malpighian tubules from trp⁹ animals is not significantly different from that of wild-type tubules, and the basal rate of secretion is also unaffected.

(Macpherson et al., 2005)

Mutant flies have electroretinogram defects, showing only a transient response to light (60% deactivation time is 1.5 +/- 0.2 seconds).

Mutant flies show light-dependent degeneration of rhabdomeres; when maintained under a 12 hour light-12 hour dark cycle rhabdomeres begin to disappear between 7-10 days after eclosion, and almost no rhabdomeres remain after 14 days. In contrast, when maintained in the dark, the number of rhabdomeres per ommatidium does not decrease, even 30 days after eclosion, although the size of the rhabdomeres is reduced in 30 day old mutant flies compared to wild-type controls.

(Wang et al., 2005)

trp⁹ mutants do not exhibit the light dependent architectural changes seen in wild-type rhabdomeres.

(Kosloff et al., 2003)

trp⁹ flies carrying trp^3.cHa have severely mutant electroretinograms. trp⁹ flies carrying trp^1234.cHa have severely mutant electroretinograms. The rhabdomeres appear normal in trp⁹ flies at 0, 3 and 7 days after eclosion. trp⁹ flies carrying trp^3.cHa have nearly normal rhabdomeres at day 0 post-eclosion, although some rhabdomeres appear to be splitting up. By day 3 post-eclosion, most rhabdomeres are no longer detectable. trp⁹ flies carrying trp^1234.cHa show degeneration of the rhabdomeres. trp⁹ flies carrying trp^124.cHa have normal rhabdomeres at 0, 3 and 7 days after eclosion.

(Hong et al., 2002)

In normal Ca²⁺, the light induced current (LIC) in trp⁹ mutant photoreceptors decays towards baseline with two distinct kinetic components; a rapid (subsecond) decay which is similar to, although slightly slower than, the Ca²⁺-dependent inactivation seen in wild-type photoreceptors, and a much slower decay which returns the current to baseline over a period of 1-5 seconds. Stimuli that induce decay under normal conditions still induce decay in Ca²⁺-free conditions. However, the fast component is absent and responses now decay with a single exponential time course which is about 3 times faster than the slower component seen in the presence of Ca²⁺.

(Hardie et al., 2001)

The trp⁹ ERG shows the typical decline towards baseline during illumination, whereas the Ca²⁺ signal is transient and relatively small. Anoxia initially activates the slow and small phase of the voltage response, though the second faster phase of the voltage and Ca²⁺ signal are of significantly smaller amplitude than wild type. This effect persists for as long as the anoxia is applied. No significant change in ^Ca<up>2+</up> out is observed during the initial 2 mins of anoxia.

(Agam et al., 2000)

ERG shows no sustained response during prolonged light stimulation, reduced peak amplitude and longer than normal response latency.

(Leung et al., 2000)

The small electroretinogram responses seen in trp^P365/trp⁹ flies are not "transient" but have a maintained component that persists throughout the duration of the stimulus.

(Yoon et al., 2000)

The phenotypes of inaF^P106x, trp⁹ and trp² are similar with respect to rapid time course of decay of potential during stimulus, V-logI curves, latency and recovery of response from a previous stimulation.

(Li et al., 1999)

trp⁹ photoreceptors in zero extracellular calcium sustain robust light-induced currents.

(Scott et al., 1997)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

NOT Enhanced by

Statement

Reference

trp⁹ has abnormal smell perception | dominant phenotype, non-enhanceable by trpl³⁰²/trpl³⁰²

(Badsha et al., 2012)

trp⁹ has abnormal neurophysiology | recessive phenotype, non-enhanceable by trpl³⁰²/trpl³⁰²

(Badsha et al., 2012)

Suppressed by

Statement

Reference

trp⁹ has abnormal neuroanatomy phenotype, suppressible by Calx^B

(Wang et al., 2005)

trp⁹ has abnormal neuroanatomy phenotype, suppressible by Arr2⁵

(Wang et al., 2005)

Enhancer of

Statement

Reference

trp⁹ is an enhancer of abnormal visual behavior phenotype of trpl³⁰²

(Li et al., 1999)

NOT Enhancer of

Statement

Reference

trp⁹ is a non-enhancer of decreased cell number | somatic clone | progressive phenotype of Pect²⁹, Scer\FLP1^ey.PU

(Zhao and Wang, 2020)

trp⁹/trp⁹ is a non-enhancer of abnormal smell perception | dominant phenotype of trpl³⁰²

(Badsha et al., 2012)

trp⁹/trp⁹ is a non-enhancer of abnormal neurophysiology | recessive phenotype of trpl³⁰²

(Badsha et al., 2012)

Suppressor of

Statement

Reference

trp⁹ is a suppressor of visible phenotype of rdgA¹

(Georgiev et al., 2005)

trp⁹ is a suppressor of abnormal neuroanatomy phenotype of Calx^B

(Wang et al., 2005)

NOT Suppressor of

Statement

Reference

trp⁹ is a non-suppressor of decreased cell number | somatic clone | progressive phenotype of Pect²⁹, Scer\FLP1^ey.PU

(Zhao and Wang, 2020)

Other

Statement

Reference

trp⁹, trpl³⁰² has abnormal neurophysiology | recessive phenotype

(Badsha et al., 2012)

trp⁹, trpl³⁰² has abnormal neurophysiology phenotype

(Krause et al., 2008, Huang et al., 2004)

trp⁹, trp^D621G, trpl³⁰² has abnormal neurophysiology | adult stage phenotype

(Liu et al., 2007)

trp⁹, trp^D621E, trpl³⁰² has abnormal neurophysiology | adult stage phenotype

(Liu et al., 2007)

trp⁹, trp^D621N, trpl³⁰² has abnormal neurophysiology | adult stage phenotype

(Liu et al., 2007)

trp⁹, trp^D621N, trpl³⁰² has abnormal neuroanatomy | adult stage | progressive phenotype

(Liu et al., 2007)

trp⁹, trpl³⁰² has abnormal circadian rhythm | recessive phenotype

(Yang et al., 1998)

trp⁹, trpl^unspecified has abnormal visual behavior phenotype

(Scott et al., 1997)

Phenotype Manifest In

Suppressed by

Statement

Reference

trp⁹ has rhabdomere phenotype, suppressible by Calx^B

(Wang et al., 2005)

trp⁹ has rhabdomere phenotype, suppressible by Arr2⁵

(Wang et al., 2005)

Enhancer of

Statement

Reference

trp⁹ is an enhancer of photoreceptor neuron phenotype of trpl³⁰²

(Li et al., 1999)

NOT Enhancer of

Statement

Reference

trp⁹ is a non-enhancer of rhabdomere | somatic clone | decreased number phenotype of Pect²⁹, Scer\FLP1^ey.PU

(Zhao and Wang, 2020)

trp⁹ is a non-enhancer of eye photoreceptor cell | somatic clone | decreased number phenotype of Pect²⁹, Scer\FLP1^ey.PU

(Zhao and Wang, 2020)

Suppressor of

Statement

Reference

trp⁹ is a suppressor of eye phenotype of rdgA¹

(Georgiev et al., 2005)

trp⁹ is a suppressor of rhabdomere phenotype of Calx^B

(Wang et al., 2005)

trp⁹ is a suppressor of phenotype of rdgA¹

(Raghu et al., 2000)

trp⁹ is a suppressor of ommatidium & microvillus phenotype of rdgA¹

(Raghu et al., 2000)

trpl³⁰²/trp⁹ is a suppressor of ommatidium & microvillus phenotype of rdgA¹

(Raghu et al., 2000)

trp⁹ is a suppressor of ommatidium phenotype of rdgA¹

(Raghu et al., 2000)

trpl³⁰²/trp⁹ is a suppressor of ommatidium phenotype of rdgA¹

(Raghu et al., 2000)

NOT Suppressor of

Statement

Reference

trp⁹ is a non-suppressor of eye photoreceptor cell | somatic clone | decreased number phenotype of Pect²⁹, Scer\FLP1^ey.PU

(Zhao and Wang, 2020)

trp⁹ is a non-suppressor of rhabdomere | somatic clone | decreased number phenotype of Pect²⁹, Scer\FLP1^ey.PU

(Zhao and Wang, 2020)

Other

Statement

Reference

trp⁹, trpl³⁰² has ommatidium phenotype

(Krause et al., 2008)

trp⁹, trp^D621G, trpl³⁰² has photoreceptor | adult stage phenotype

(Liu et al., 2007)

trp⁹, trp^D621E, trpl³⁰² has photoreceptor | adult stage phenotype

(Liu et al., 2007)

trp⁹, trp^D621N, trpl³⁰² has photoreceptor | adult stage phenotype

(Liu et al., 2007)

trp⁹, trp^D621N, trpl³⁰² has rhabdomere | adult stage | progressive phenotype

(Liu et al., 2007)

Hsap\KCNJ2^{R228Q.UAS.EGFP}, trp⁹ has photoreceptor phenotype

(Gu et al., 2005)

trp⁹, trpl³⁰² has retina phenotype

(Huang et al., 2004)

trp⁹, trpl³⁰² has photoreceptor neuron phenotype

(Agam et al., 2000, Haab et al., 2000)

Trpγ^hs.N.Tag:MYC, trp⁹ has retina phenotype

(Xu et al., 2000)

trp⁹, trpl^unspecified has photoreceptor neuron phenotype

(Scott et al., 1997)

Additional Comments

Genetic Interactions

Statement

Reference

Electroretinograms of trp⁹, trpl³⁰² double homozygotes show a complete lack of response to light stimuli, as compared to either single mutant.

(Badsha et al., 2012)

The trpl³⁰²; trp⁹ double mutant has no functional trp and trpl channels and shows no response to light.

(Richter et al., 2011)

Illumination of dissociated, patch-clamped ommatidia from trp⁹;trpl³⁰² double mutants show activation of the whole phototransduction cascade, do not show any light-induced current or Ca[2+] influx, but do show a normal light-dependent modulation of the delayed rectifier current mediated by Shab channels. Increasing the light level by a factor of ten results in an upregulation of approximately 30% and recovery to baseline within 30 minutes, similar to wildtype controls.

(Krause et al., 2008)

trp⁹;trpl³⁰² double mutant flies expressing any of the following: trp^D621N, trp^D621E or trp^D621G show significant changes in their photoreceptor ionic selectivity profile (decreased permeability for Ca[2+] and Mg[2+] in particular) and alleviated channel block by Mg[2+] and ruthenium red as well as other neurophysiological defects: The flies expressing trp^D621N also display decreased single channel conductance and much slower kinetics of the light response and strongly increased rate of light-induced retinal degeneration (with most rhabdomeres entirely absent or exhibiting extensive signs of disruption of the microvillar structure, the cell bodies also contained multivesicular bodies) compared to controls. The flies expressing trp^D621E exhibit decreased effective pore diameter and decreased single channel conductance compared to controls. They however do not display increased rate of light-induced retinal degeneration. The flies expressing trp^D621G also show much slower kinetics of the light response and decreased single channel conductance as well as altered rectification characteristics.

Flies expressing trp^D626G in the trp⁹;trpl³⁰² double mutant background show photoreceptor ionic selectivity profile, rectification characteristics, Mg[+] and ruthenium red channel block that are comparable to controls.

(Liu et al., 2007)

trp⁹; trpl³⁰² individual photoreceptors form the correct number of synapses per

presynaptic terminal independently of cartridge composition. The photoreceptor terminals of these mutants show an increase in glial invaginations.

(Hiesinger et al., 2006)

The retinal degeneration phenotype of rdgA¹ flies is suppressed by trp⁹ (as assayed by the presence of a crisp pseudopupil in the double mutant flies).

(Georgiev et al., 2005)

capa stimulated fluid transport rates are significantly reduced in Malpighian tubules from trpl³⁰² trp⁹ animals compared to control tubules, while the basal rate of secretion is unaffected.

(Macpherson et al., 2005)

The retinal degeneration seen in both Calx^B and trp⁹ single mutant flies when they are maintained under a 12 hour light-12 hour dark cycle is suppressed in Calx^B trp⁹ double mutants; most ommatidia in the double mutants contain the normal number of rhabdomeres at 14 days after eclosion.

Arr2⁵ partially suppresses the retinal degeneration seen in trp⁹ single mutant flies when they are maintained under a 12 hour light-12 hour dark cycle; the double mutants contain the normal number of rhabdomeres at 14 days after eclosion, although the size of the rhabdomeres is reduced compared to controls.

trpl³⁰² ; trp^L612F.ninaE trp⁹ flies have a wild-type electroretinogram response.

trpl³⁰² ; trp^ninaE.PW trp⁹ flies have a wild-type electroretinogram response.

trpl³⁰² ; trp^R671Q.ninaE trp⁹ flies have a transient electroretinogram response to a 10 second pulse of light.

(Wang et al., 2005)

trp⁹ ; trpl³⁰² double mutants show a reduced depolarisation response to anoxia in the photoreceptors compared to wild-type flies; the amplitude of anoxia-induced depolarisation in the double mutants is half that of wild type and the response kinetics are much slower than normal.

(Huang et al., 2004)

In trp⁹,trpl³⁰² double mutants the second, large phase depolarization response to anoxia (caused by N₂ and measured in the eye by extracellular voltage change recordings), fails, indicating that the small but not the large phase of the response resulted from accumulation of K⁺ in the extracellular space. In trp⁹, trpl³⁰² double mutants the Ca²⁺ response to anoxia is virtually abolished.

(Agam et al., 2000)

Excised patches from rhabdomeral membranes show no sustained spontaneous activity nor high frequency burst-like behavior in trp⁹,trpl³⁰² double mutants.

(Haab et al., 2000)

Ommatidial appearance of rdgA¹ is largely restored to wild type by mutants at the trp locus, though defects detectable at the EM level remain. These residual defects are suppressed in the triple mutant with trpl³⁰². These anatomical rescue effects are paralleled by rescue of electrophysiological defects of rdgA¹ mutants. Double rdgA¹, trp mutants show age dependent retinal degeneration.

(Raghu et al., 2000)

The addition of trpγ^{hs.N.T:Hsap\MYC} to trp⁹ flies greatly suppresses the electroretinogram (ERG) responses to light stimulus.

(Xu et al., 2000)

Double mutant analysis comparing the receptor potentials of trpl³⁰² with inaF^P106x; trpl³⁰² or trp²; trpl³⁰² or trp⁹; trpl³⁰² showed that the effects of inaF^P106x are as severe as those of trp² and are specific to the trp channel.

(Li et al., 1999)

Behavioural rhythms of trp⁹ trpl³⁰² double mutants show reduced resetting in response to a pulse of light.

(Yang et al., 1998)

trpl^unspecified; trp⁹ double mutant photoreceptors have no light-induced currents. The photoreceptors of trpl^unspecified; trp⁹ double mutant flies carrying trpl^trp.PS show transient responses to long pulses of light. The photoreceptors of trpl^unspecified; trp⁹ double mutant flies carrying trpl^CBS1.trp or trpl^CBS2.trp show robust inward currents for the duration of the stimulus in response to long pulses of light. trp⁹; Cam³⁵²/Camⁿ³³⁹ double mutant photoreceptors do not have transient light responses.

(Scott et al., 1997)

Xenogenetic Interactions

Statement

Reference

The presence of trp::trpl^{ninaE.trp1-675.trpl681-1124.T:Avic\GFP-EGFP} in trpl³⁰²; trp⁹ double mutants results in a response to light that declines towards baseline during prolonged intense light.

The presence of trp::trpl^{ninaE.trpl1-336.T:Avic\GFP-EGFP} in trpl³⁰²; trp⁹ double mutants results in a response to light that declines towards baseline during prolonged intense light.

The presence of trp::trpl^{ninaE.trpl1-336.trp328-675.trpl681-1124.T:Avic\GFP-EGFP} in trpl³⁰²; trp⁹ double mutants results in a response to light that declines towards baseline during prolonged intense light.

The presence of trp::trpl^{ninaE.trp1-328.trpl336-681.trp675-1275.T:Avic\GFP-EGFP} in trpl³⁰²; trp⁹ double mutants results in a response to light that declines towards baseline during prolonged intense light.

(Richter et al., 2011)

In trp⁹ photoreceptors expressing Hsap\KCNJ2^{R228Q.Scer\UAS.T:Avic\GFP-EGFP} channels, the PIP₂ sensitive current is suppressed by a significantly greater extent than in wild-type photoreceptors.

(Gu et al., 2005)

Complementation and Rescue Data

Fails to complement

Rescued by

trp⁹ is rescued by trp^{ninaE.Tag:SBP}

(Chen et al., 2015)

trp⁹ is rescued by trp^hs.PM

(Wang et al., 2005)

trp⁹ is rescued by trp^ninaE.PW

(Wang et al., 2005)

trp⁹ is rescued by trp^L612F.ninaE

(Wang et al., 2005)

trp⁹ is rescued by trp^+mHa

(Hong et al., 2002)

trp⁹ is rescued by trp^124.cHa

(Hong et al., 2002)

Comments

Expression of trp^{ninaE.T:Zzzz\SBP} rescues the electroretinogram defects of trp⁹ flies.

(Chen et al., 2015)

trp^ttd4 in trans with trp⁹ displays complete inhibition of trpl^{ninaE.T:Avic\GFP-EGFP} internalisation in the light.

Light-raised trp^ttd2 in trans with trp⁹ shows partial translocation of trpl^{ninaE.T:Avic\GFP-EGFP} from the rhabdomere to the cell body.

(Meyer et al., 2008)

Images (0)

Mutant

Wild-type

Stocks (2)

Bloomington

9046

w^*; trp⁹

25082

w^*; P{hs-trp.M}3, trp⁹

Notes on Origin

Discoverer

Pak.

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (5)

Reported As

Symbol Synonym

Trp⁹

(Bajar et al., 2022)

trp³⁴³

(Nath et al., 2025, Nhuchhen Pradhan et al., 2025, Pradhan et al., 2024, Dhakal et al., 2022, Chen et al., 2021, Chen and Montell, 2020, Liu et al., 2020, Zhao and Wang, 2020, Rimal and Lee, 2019, Asteriti et al., 2017, Zhang et al., 2016, Cerny et al., 2015, Chen et al., 2015, Hardie et al., 2015, Huang et al., 2015, Sengupta et al., 2013, Zhang et al., 2013, Badsha et al., 2012, Rosenbaum et al., 2011, Elsaesser et al., 2010, Sanxaridis and Tsunoda, 2010, Satoh et al., 2010, Krause et al., 2008, Meyer et al., 2008, Rosenzweig et al., 2008, Sanxaridis et al., 2007, Hiesinger et al., 2006, Rosenbaum et al., 2006, Georgiev et al., 2005, Gu et al., 2005, Macpherson et al., 2005, Hardie et al., 2004, Huang et al., 2004, Tsunoda et al., 2001, Li and Montell, 2000, Raghu et al., 2000, Xu et al., 2000)

trp⁹

(Bajar et al., 2022, Mu et al., 2019, Chen et al., 2017, Meyer et al., 2008)

trp^p343

(Haab et al., 2000)

Name Synonyms

Secondary FlyBase IDs

References (72)

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