FlyBase Allele Report: Dmel\norpA[P24]

28bp deletion (nucleotides 2710 to 2737, nucleotide numbering as in FBrf0047660). This deletes 9 amino acid residues, and causes a frameshift which results in the substitution of 24 amino acids residues followed by a premature termination codon.

(Pearn et al., 1996)

Mutations Mapped to the Genome

Curation Data

Type

Location

Additional Notes

References

deletion

X:4,359,416..4,359,443 [+]

Comment:

28bp deletion which causes a frameshift, resulting in the substitution of 24 amino acids residues followed by a premature termination codon.

(Pearn et al., 1996)

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 ( 1 )

Disease

Evidence

References

model of retinal disease

CEA

(Kristaponyte et al., 2012)

Modifiers Based on Experimental Evidence ( 1 )

Disease

Interaction

References

ameliorates photosensitive epilepsy

modeled by Cpes^KO

(Kunduri et al., 2018)

model of retinal disease

is exacerbated by ninaE^StoA

(Kristaponyte et al., 2012)

Comments on Models/Modifiers Based on Experimental Evidence ( 0 )

Disease-implicated variant(s)

Phenotypic Data

Phenotypic Class

abnormal behavior | larval stage | recessive

(Busto et al., 1999)

abnormal chemosensory behavior | adult stage

(Kwon et al., 2010)

abnormal circadian rhythm

(Hamblen-Coyle et al., 1992)

abnormal locomotor rhythm

(Klarsfeld et al., 2004)

abnormal memory | adult stage, with norpA^ninaE.PW

(Melnattur et al., 2014)

abnormal neuroanatomy

(Kristaponyte et al., 2012)

abnormal neuroanatomy | third instar larval stage

(Yuan et al., 2011)

abnormal neurophysiology

(Wang et al., 2008, Hardie et al., 2003, Knox et al., 2003, McKay et al., 1995)

abnormal neurophysiology, with norpA^C1094S.hs

(Hardie et al., 2002, Cook et al., 2000)

abnormal neurophysiology | adult stage

(Ni et al., 2017, Kwon et al., 2010)

abnormal neurophysiology | recessive

(Kim et al., 2003)

abnormal phototaxis

(Gao et al., 2008)

abnormal phototaxis | larval stage

(Hassan et al., 2000)

abnormal smell perception

(Riesgo-Escovar et al., 1995)

abnormal taste perception | recessive

(Kim et al., 2010)

abnormal thermotaxis

(Kwon et al., 2008)

abnormal thermotaxis | larval stage

(Shen et al., 2011)

abnormal thermotaxis | third instar larval stage

(Sokabe et al., 2016)

abnormal visual behavior

(Zerr et al., 1990, Kulkarni et al., 1988)

decreased cell number | adult stage | progressive

(Panda et al., 2018)

increased cell death

(Wang et al., 2009, Hsu et al., 2004)

increased cell death | conditional

(Lee et al., 2013)

Phenotype Manifest In

adult olfactory receptor neuron ab11a

(Kwon et al., 2010)

dendrite | third instar larval stage

(Yuan et al., 2011)

endoplasmic reticulum-plasma membrane contact site

(Nath et al., 2020)

eye

(Zerr et al., 1990)

eye photoreceptor cell

(Meyer et al., 2006)

eye photoreceptor cell | adult stage

(Shieh et al., 2023)

eye photoreceptor cell | progressive

(Panda et al., 2018)

LNv neuron | third instar larval stage

(Yuan et al., 2011)

maxillary palp

(Riesgo-Escovar et al., 1995)

ommatidium

(Wang et al., 2014, Sahly et al., 1994)

ommatidium | adult stage | conditional

(Thakur et al., 2016)

outer photoreceptor cell

(Nath et al., 2020)

photoreceptor

(Kim et al., 2003)

photoreceptor cell R1

(Pearn et al., 1996)

photoreceptor cell R2

(Pearn et al., 1996)

photoreceptor cell R3

(Pearn et al., 1996)

photoreceptor cell R4

(Pearn et al., 1996)

photoreceptor cell R5

(Pearn et al., 1996)

photoreceptor cell R6

(Pearn et al., 1996)

photoreceptor neuron

(Wang et al., 2014, Kristaponyte et al., 2012, Wang et al., 2009)

photoreceptor neuron, with norpA^C1094S.hs

(Hardie et al., 2002)

retina

(Lee, 2012, Wang et al., 2009, Hsu et al., 2004, Kim et al., 2003)

retina | adult stage

(Cao et al., 2018)

retina | adult stage | conditional

(Thakur et al., 2016)

retina | conditional

(Chakrabarti et al., 2015, Lee et al., 2013)

rhabdomere

(Wang et al., 2014, Kristaponyte et al., 2012, Lee, 2012, Kosloff et al., 2003)

rhabdomere | adult stage

(Shieh et al., 2023, Cao et al., 2018)

Detailed Description

Statement

Reference

norpA³⁶ flies reared in dark exhibit a reduction in the endoplasmic reticulum-plasma membrane contact site density in outer photoreceptors at eclosion.

(Nath et al., 2020)

norpA³⁶ mutant adults show severe retinal degeneration (lost and damaged rhabdomeres) already after six days in light/dark cycles.

(Cao et al., 2018)

norpA³⁶ homozygous adults do not exhibit structural abnormalities in the cortical glia.

(Kunduri et al., 2018)

norpA³⁶ adults exhibit retinal degeneration (normal numbered eye photoreceptor cells on the day of eclosion followed by a progressively decreased number of eye photoreceptor cells) when compared to controls.

(Panda et al., 2018)

norpA³⁶ homozygous adults display a complete loss of retinal response to light in electro-retinograms, but maintain a rhythmic behavior under constant darkness conditions after previous training in 12h:12h light:dark cycles, and do not present obvious defects in arousal in response to a light pulse during the night period, as compared to controls.

(Ni et al., 2017)

norpA³⁶ homozygous mutant late third instar larvae show impaired temperature selection and unlike controls display no strong preference for cooler temperatures (18[o]C) in a temperature gradient.

(Sokabe et al., 2016)

The number of rhodopsin1-containing vesicles (RLVs) per ommatidium in norpA³⁶ homozygous adults both pre- and post-illumination is elevated compared to controls and the flies display light-dependent retinal degeneration.

(Thakur et al., 2016)

norpA³⁶ mutants undergo light-dependent retinal degeneration.

(Chakrabarti et al., 2015)

Adults expressing norpA^ninaE.PW in a norpA³⁶ background have a significant reduction in short-term aversive visual (blue/green) memory, compared to controls, with no effect on blue/green preference or heat (laser) avoidance.

(Melnattur et al., 2014)

Upon continuous exposure to white light for 6 days, norpA³⁶ mutants exhibit reduced numbers of rhabdomeres compared to control flies. In addition, ommatidial organisation is often aberrant in these mutants, indicating that the photoreceptor cells are undergoing a progressive demise.

(Wang et al., 2014)

norpA³⁶/norpA³⁶ flies show progressive retinal degeneration within 3-4 days of exposure to constant light (wild type flies show no signs of retinal degeneration even after 7 days of constant light).

(Lee et al., 2013)

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)

The degeneration of norpA³⁶ photoreceptors is marked by the age-dependent progressive deterioration of rhabdomeres. As norpA³⁶ flies age in a 12 hour light/dark cycle, rhabdomeres become smaller and eventually disappear at ~9 days post-eclosion. In contrast, the size of rhabdomeres in wild-type R1-R6 cells remains constant for up to 28 days.

(Kristaponyte et al., 2012)

Mutant flies show retinal degeneration (lack of deep pseudopupil) after 5 days in constant light. The rhabdomeres show severe deterioration.

(Lee, 2012)

Mutant larvae show defects in discrimination between 18[o]C and 24[o]C in a binary choice thermotaxis assay compared to controls.

Mutant larvae show reduced turning behaviour compared to control larvae when they move into a 24[o]C zone from an 18[o]C zone (turning behaviour when they move from an 18[o]C zone into a 24[o]C zone is similar in both mutant and wild-type larvae).

(Shen et al., 2011)

Wild-type larvae display differences in their LN(v) dendrite length when exposed to constant darkness versus constant light. In contrast, such light induced changes are absent in norpA³⁶ mutants.

(Yuan et al., 2011)

Mutants display a reduced aversion to aristolochic acid and fewer aristolochic acid-induced action potentials in tip recordings compared to wild type.

(Kim et al., 2010)

The citronellal-evoked action potential frequency in ab12 basiconic sensilla in the antenna of mutant flies is not significantly different from wild type.

(Kwon et al., 2010)

Mutant flies show significantly reduced avoidance of citronellal in a direct airborne repellent test (DART) assay.

ab11a olfactory receptor neurons (ORNs) in the antenna show a higher citronellal-evoked action potential frequency in mutant flies compared to in wild type.

(Kwon et al., 2010)

norpA³⁶ mutant class IV dendritic arborization neurons do not exhibit any defects in light response.

(Xiang et al., 2010)

norpA³⁶ mutants undergo rapid retinal degeneration such that the animals have detectable loss of photoreceptor cells by 4 days and are almost devoid of photoreceptor cells by day 10.

(Wang et al., 2009)

norpA³⁶ mutants fail to discriminate between wavelengths in the UV and green spectrum.

(Gao et al., 2008)

Whole cell patch-clamped dissociated ommatidia from norpA³⁶ mutants (also carrying trp⁹ to prevent the low level of spontaneous trp channel activity seen in norpA³⁶ mutants), upon light stimulation, do not show a light response nor any indication of Shab-mediated light-dependent modulation of the delayed rectifier current.

(Krause et al., 2008)

norpA³⁶ mutants are thermotaxis defective, losing the 18[o]C versus 24[o]C preference found in wild-type.

norpA³⁶ larvae are unable to distinguish between 18 and 19-24[o]C. In the 26-30[o]C range, norpA³⁶ show reduced thermotactic behaviour and they show a wild-type preference for 18[o]C over either 14-16[o]C or 32[o]C.

(Kwon et al., 2008)

norpA³⁶ flies entrained to 12 hour light: 12 hour dark cycles and then exposed to 8 hour delayed light-dark (LD) cycles are able to resynchronise to the new light regime.

norpA³⁶ flies that are entrained to 12 hour light: 12 hour dark cycles ( 12:12 LD) and are then shifted to 9:9 , 13:13 or 14:14 LD cycles routinely re-entrain to behave in synchrony with the novel non-24 hour cycles.

(Dolezelova et al., 2007)

norpA³⁶ mutant photoreceptors form the correct number of synapses per presynaptic terminal independently of cartridge composition.

(Hiesinger et al., 2006)

No light-dependent translocation of trpl^{ninaE.T:Avic\GFP-EGFP} to the cell body is observed in norpA³⁶ mutant photoreceptors.

(Meyer et al., 2006)

Uptake of 0.5-100mM trehalose solution by norpA³⁶ mutant flies is normal, as is the electrical response of associated sensory neurons to stimulations of long labellar taste bristles with 0.8-400mM trehalose

(Ueno et al., 2006)

norpA³⁶ pupal photoreceptors show normal endocytosis of ninaE.

(Satoh and Ready, 2005)

norpA³⁶ rhabdomeres show signs of early stages of degeneration at 1 day of age. The rhabdomeres appear smaller and less organized; photoreceptor cell bodies are reduced in size, and pigment cells swell to occupy this space. At later stages of degeneration rhabdomeres are further deteriorated, and cell bodies are shrunken with many aberrant vesicles and electron-dense material.

(Hsu et al., 2004)

norpA³⁶ mutants exhibit no signs of retinal degeneration when raised for 6 days in constant darkness.

(Iakhine et al., 2004)

At high-light intensity, norpA³⁶ flies are able to resynchronize to a shift in the light-dark schedule of 8 hours. However, at 1000-fold lower light intensity, norpA³⁶ mutants take longer to synchronize to new schedules than wild-type flies.

Exposing norpA³⁶ flies to constant light results in arrhythmicity, as with wild-type flies.

(Klarsfeld et al., 2004)

A small approximately 15pA noisy inward current is detected in norpA³⁶ in whole-cell recordings of photoreceptors on establishment of the whole-cell configuration. This noisy current gradually subsides and eventually reveals isolated 1-2pA events and finally, after about 20 minutes, a quiet base line. At this point, brief flashes of light induce tiny (less than 2pA) light responses consisting of little more than a train of miniature "quantum bumps", which last for several minutes. In the absence of ATP in the electrode, the spontaneous activity seen on establishment of the whole-cell configuration initially increases in magnitude during a period of several minutes, and then decays again during 15-20 minutes, revealing single quantum bump-like events with amplitudes that are restored to near wild-type levels, but terminate more slowly than normal.

(Hardie et al., 2003)

norpA³⁶ mutants exhibit a complete loss of photoreceptor response to light.

(Kim et al., 2003)

Mutant flies show no response to light (measured using an electroretinogram (ERG) recording).

(Knox et al., 2003)

norpA³⁶ mutants do not exhibit the light dependent architectural changes seen in wild-type rhabdomeres.

(Kosloff et al., 2003)

The amplitude of quantum bumps in photoreceptors is smaller in animals expressing norpA^C1094S.hs in a norpA³⁶ background than in wild type (when ATP is present in the intracellular solution during recordings).

(Hardie et al., 2002)

The dendritic arborisation of the lateral neurons appears normal in mutant third instar larvae.

(Malpel et al., 2002)

The effect of anoxia as measured in the eye by extracellular voltage change recordings is similar to that of wild type. The Ca²⁺ signal has a faster onset than wild type and overshoots after anoxia is removed.

(Agam et al., 2000)

Patch-clamp whole cell recordings show termination of light-induced currents that is four orders of magnitude slower than wild type in flies carrying norpA^C1094S.hs in a norpA³⁶ background.

(Cook et al., 2000)

The larval response to light is abolished in mutants (as measured by a "checker assay").

(Hassan et al., 2000)

Wild-type larvae reduce their path lengths and show increased head swinging when exposed to light. This response is abolished in norpA³⁶ larvae. Wild-type larvae show a greater change in direction when lights are turned on or off (light (L) to dark (D), or D to L transition) than in the absence of a light transition (D to D). The amplitude of change of direction is greater for the D to L than for the L to D transition. This light-induced difference in the amplitude of change of direction for L to D and D to L transitions is abolished in norpA³⁶ larvae. The difference between the change of direction at the L to D transition and in the absence of a light transition (D to D) is not affected in norpA³⁶ larvae.

(Busto et al., 1999)

Linolenic acid can activate light sensitive channels in mutant photoreceptors.

(Chyb et al., 1999)

Newly fertilised homozygous females elicit as much courtship from wild-type males as do newly fertilised wild-type females. Newly fertilised homozygous females extrude their ovipositors at a much lower frequency than control females.

(Bubis et al., 1998)

The lamina of norpA³⁶ flies shows no difference in volume between flies kept in constant darkness and flies kept under 16 hour light/8 hour dark conditions.

(Barth et al., 1997)

The DHP-sensitive current is reduced. Application of TPA (phorbol 12-myrisatae 13-acetate) and PDD (phorbol 12,13-didecanoate), activators of PKC, rescues the current in mutant fibres without significantly affecting the normal current. 4αPDD (4α-phorbol 12,13-didecanoate), an inactive analog of PDD, does not affect the normal or mutant current. BIM (bisindolylmaleimide), an inhibitor of PKC, reduces the current in normal fibres without affecting the mutant current. DOG (sn-1,2-dioctanoyl-glycarol), analog of diacylglycerol increases the current in the mutant fibres.

(Gu and Singh, 1997)

ERG recordings show no response to a 2-sec orange light pulse.

(Shieh et al., 1997)

The electroretinogram (ERG) of norpA³⁶ flies shows almost no response at any stimulus intensity. Newly eclosed homozygous flies have R1 to R6 rhabdomeres similar in size and pattern to wild-type flies, but six week old homozygous flies completely lack photoreceptors R1 to R6.

(Pearn et al., 1996)

norpA³⁶ flies show no electroretinogram (ERG) or prolonged depolarising afterpotential (PDA) response. norpA³⁶ flies carrying norpA^ninaE.PM have a more normal ERG and PDA response.

(McKay et al., 1995)

The amplitude of visual response is 0. The amplitude response to vapours of all odorants tested in the maxillary palp is significantly reduced. The antennal response is unaffected. Maxillary palps have no gross anatomical defects and the electrical conduction properties are normal.

(Riesgo-Escovar et al., 1995)

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)

Retinas of norpA³⁶; rdgB² mutants fail to degenerate in the dark or light, rdgB²; P{DG_q1-203} retinas degenerate in the dark and norpA³⁶; rdgB²; P{DG_q1-203} triple mutant retinas fail to degenerate in the light or dark.

(Lee et al., 1994)

At normal extracellular calcium concentration an intense excitation light does not induce any light evoked inward current (LIC) in the photoreceptor, light induced elevation of calcium is absent.

(Peretz et al., 1994)

Males have white eyes. Flies are blind.

(Stark et al., 1993)

Short cycle duration, the evening peak of activity is shifted to an earlier time than wild type.

(Hamblen-Coyle et al., 1992)

norpA³⁶ partially suppresses the arrhythmicity of some homozygous e¹ flies.

(Newby and Jackson, 1991)

Sex-dependent enhancement in pertussis toxin catalysed ADP-ribosylation with respect to wild type: attributed in part to an increase in the α subunit of the G₀-like protein.

(Guillen et al., 1990)

Flies are blind.

(Zerr et al., 1990)

Visually blind males show multiple orientations similar to nonA⁹ males during courtship, the pulse song is wild-type.

(Kulkarni et al., 1988)

no ERG

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

NOT Enhanced by

Statement

Reference

Cnoc\ChR1::Csub\ChR^{CsChrimson.IVS.20xUAS.Venus}, Scer\GAL4^0273-G4, norpA^P24 has abnormal locomotor behavior | adult stage | conditional phenotype, non-enhanceable by Gthe\ACR1^{lexAop.d.EYFP}/Ecol\lexA^GMR38G08

(Stern et al., 2019)

Suppressed by

Statement

Reference

Cnoc\ChR1::Csub\ChR^{CsChrimson.IVS.20xUAS.Venus}, Scer\GAL4^0273-G4, norpA^P24 has abnormal locomotor behavior | adult stage | conditional phenotype, suppressible | conditional | partially by Gthe\ACR1^{lexAop.d.EYFP}/Ecol\lexA^GMR13F02

(Stern et al., 2019)

norpA^P24 has decreased cell number | adult stage | progressive phenotype, suppressible by Scer\GAL4^ninaE.PU/Hsap\PLD2^UAS.cPa

(Panda et al., 2018)

norpA^P24 has decreased cell number | adult stage | progressive phenotype, suppressible by Scer\GAL4^ninaE.PU/Hsap\PLD1^UAS.cPa

(Panda et al., 2018)

cry⁰¹, norpA^P24 has abnormal circadian rhythm | adult stage phenotype, suppressible by trp^MB03672/trp^MB03672

(Ni et al., 2017)

cry⁰¹, norpA^P24 has abnormal circadian rhythm | adult stage phenotype, suppressible by trpl^MB10553/trpl^MB10553

(Ni et al., 2017)

ninaE¹⁷, norpA^P24, norpA^ninaE.PW has abnormal neurophysiology | adult stage phenotype, suppressible by Rh7^UAS.cNa/Scer\GAL4^ninaE.PT

(Ni et al., 2017)

ninaE¹⁷, norpA^P24, norpA^ninaE.PM has abnormal neurophysiology | adult stage phenotype, suppressible | partially by ninaE^E194Q

(Zheng et al., 2015)

ninaE¹⁷, norpA^P24, norpA^ninaE.PM has abnormal neurophysiology | adult stage phenotype, suppressible by ninaE^D124N

(Zheng et al., 2015)

ninaE¹⁷, norpA^P24, norpA^ninaE.PM has abnormal neurophysiology | adult stage phenotype, suppressible | partially by ninaE^D96N

(Zheng et al., 2015)

ninaE¹⁷, norpA^P24, norpA^ninaE.PM has abnormal neurophysiology | adult stage phenotype, suppressible by ninaE^D203N

(Zheng et al., 2015)

ninaE¹⁷, norpA^P24, norpA^ninaE.PM has abnormal neurophysiology | adult stage phenotype, suppressible by ninaE^D147N

(Zheng et al., 2015)

norpA^P24 has increased cell death | conditional phenotype, suppressible by Osi21^MB01450/Osi21^die4

(Lee et al., 2013)

norpA^P24 has increased cell death | conditional phenotype, suppressible by Osi21^VDRC.cUa/Scer\GAL4^ninaE.PTa

(Lee et al., 2013)

norpA^P24 has abnormal neuroanatomy phenotype, suppressible by ninaE^StoA/ninaE^Δ356

(Kristaponyte et al., 2012)

norpA^P24 has abnormal neuroanatomy phenotype, suppressible by ninaE^Δ356

(Kristaponyte et al., 2012)

norpA^P24 has abnormal neuroanatomy phenotype, suppressible by ninaE^StoA

(Kristaponyte et al., 2012)

norpA^P24 has increased cell death phenotype, suppressible by Tsc1^UAS.cGa/Scer\GAL4^GMR.PU

(Wang et al., 2009)

norpA^P24 has increased cell death phenotype, suppressible by gig^UAS.cTa/Scer\GAL4^GMR.PU

(Wang et al., 2009)

norpA^P24 has increased cell death phenotype, suppressible by Atg1^{ninaE.Tag:MYC}

(Wang et al., 2009)

norpA^P24 has abnormal thermotaxis phenotype, suppressible by rdgC³⁰⁶

(Kwon et al., 2008)

norpA^P24 has increased cell death phenotype, suppressible by Dronc^GMR.PH

(Hsu et al., 2004)

norpA^P24 has increased cell death phenotype, suppressible by BacA\p35^GMR.PH

(Hsu et al., 2004)

NOT suppressed by

Statement

Reference

Cnoc\ChR1::Csub\ChR^{CsChrimson.IVS.20xUAS.Venus}, Scer\GAL4^0273-G4, norpA^P24 has abnormal locomotor behavior | adult stage | conditional phenotype, non-suppressible by Gthe\ACR1^{lexAop.d.EYFP}/Ecol\lexA^GMR38G08

(Stern et al., 2019)

norpA^P24 has increased cell death phenotype, non-suppressible by Diap1^GMR.PH

(Hsu et al., 2004)

norpA^P24 has increased cell death phenotype, non-suppressible by Df(3L)H99

(Hsu et al., 2004)

Enhancer of

Statement

Reference

norpA^P24/norpA^P24 is an enhancer of abnormal circadian rhythm | adult stage phenotype of cry⁰¹

(Ni et al., 2017)

NOT Enhancer of

Statement

Reference

norpA^P24 is a non-enhancer of decreased cell number | somatic clone | progressive phenotype of Pect²⁹, Scer\FLP1^ey.PU

(Zhao and Wang, 2020)

Suppressor of

Statement

Reference

norpA^P24 is a suppressor | conditional | partially of abnormal locomotor behavior | adult stage | conditional phenotype of Cnoc\ChR1::Csub\ChR^{CsChrimson.IVS.20xUAS.Venus}, Scer\GAL4^0273-G4

(Stern et al., 2019)

norpA^P24 is a suppressor of paralytic | adult stage | progressive | conditional phenotype of Cpes^KO

(Kunduri et al., 2018)

norpA^P24 is a suppressor of abnormal locomotor behavior | adult stage | progressive | conditional phenotype of Cpes^KO

(Kunduri et al., 2018)

norpA^P24 is a suppressor of abnormal phototaxis phenotype of Crei\ChR2^UAS.cSa, Scer\GAL4^{Orco.2.642.Hsim\VP22}

(Bellmann et al., 2010)

norpA^P24 is a suppressor of abnormal phototaxis phenotype of Egra\PACα^UAS.cSLa, Scer\GAL4^{Orco.2.642.Hsim\VP22}

(Bellmann et al., 2010)

norpA^P24 is a suppressor | partially of increased cell death phenotype of ninaE^pp100

(Iakhine et al., 2004)

norpA^P24 is a suppressor of photoperiod response variant phenotype of cry^b

(Klarsfeld et al., 2004)

NOT Suppressor of

Statement

Reference

norpA^P24 is a non-suppressor of decreased cell number | somatic clone | progressive phenotype of Pect²⁹, Scer\FLP1^ey.PU

(Zhao and Wang, 2020)

norpA^P24 is a non-suppressor of abnormal neuroanatomy | adult stage phenotype of Cpes^KO

(Kunduri et al., 2018)

norpA^P24 is a non-suppressor of abnormal neurophysiology phenotype of Ih^f03355

(Hu et al., 2015)

Other

Statement

Reference

ninaE¹⁷, norpA^P24, norpA^ninaE.PW has abnormal neurophysiology | adult stage phenotype

(Ni et al., 2017)

ninaE¹⁷, norpA^P24, norpA^ninaE.PM has abnormal neurophysiology | adult stage phenotype

(Zheng et al., 2015)

Osi21^+tLa, Osi21^MB01450/Osi21^die4, norpA^P24 has increased cell death | conditional phenotype

(Lee et al., 2013)

Crei\ChR2^UAS.cUa.YFP, Scer\GAL4^Foma1, norpA^P24 has abnormal behavior | heat sensitive phenotype

(de Vries and Clandinin, 2012)

cry⁰¹, norpA^P24 has abnormal locomotor rhythm phenotype

(Dolezelova et al., 2007)

cry⁰², norpA^P24 has abnormal locomotor rhythm phenotype

(Dolezelova et al., 2007)

cry⁰³, norpA^P24 has abnormal locomotor rhythm phenotype

(Dolezelova et al., 2007)

Phenotype Manifest In

Enhanced by

Statement

Reference

norpA^P24 has rhabdomere | adult stage phenotype, enhanceable by Plc21C^JF01210/Scer\GAL4^GMR.PF

(Shieh et al., 2023)

norpA^P24 has rhabdomere | adult stage phenotype, enhanceable by Pkc53E^HMC04134/Scer\GAL4^GMR.PF

(Shieh et al., 2023)

norpA^P24 has eye photoreceptor cell | adult stage phenotype, enhanceable by Pkc53E^HMC04134/Scer\GAL4^GMR.PF

(Shieh et al., 2023)

norpA^P24 has rhabdomere | adult stage phenotype, enhanceable by inaC^JF02391/Scer\GAL4^GMR.PF

(Shieh et al., 2023)

Suppressed by

Statement

Reference

norpA^P24 has rhabdomere | adult stage phenotype, suppressible | partially by Scer\GAL4^GMR.PF/Pld^HMS00529

(Shieh et al., 2023)

norpA^P24 has eye photoreceptor cell | progressive phenotype, suppressible by Scer\GAL4^ninaE.PU/Hsap\PLD1^UAS.cPa

(Panda et al., 2018)

norpA^P24 has eye photoreceptor cell | progressive phenotype, suppressible by Scer\GAL4^ninaE.PU/Hsap\PLD2^UAS.cPa

(Panda et al., 2018)

norpA^P24 has rhabdomere phenotype, suppressible by Scer\GAL4^Act5C.PU/w^JF01901/Vps35^UAS.Tag:HA

(Wang et al., 2014)

norpA^P24 has ommatidium phenotype, suppressible by Scer\GAL4^Act5C.PU/w^JF01901/Vps35^UAS.Tag:HA

(Wang et al., 2014)

norpA^P24 has photoreceptor neuron phenotype, suppressible by Scer\GAL4^Act5C.PU/w^JF01901/Vps35^UAS.Tag:HA

(Wang et al., 2014)

norpA^P24 has rhabdomere phenotype, suppressible by Scer\GAL4^Act5C.PU/w^JF01901/Vps26^UAS.Tag:V5

(Wang et al., 2014)

norpA^P24 has ommatidium phenotype, suppressible by Scer\GAL4^Act5C.PU/w^JF01901/Vps26^UAS.Tag:V5

(Wang et al., 2014)

norpA^P24 has photoreceptor neuron phenotype, suppressible by Scer\GAL4^Act5C.PU/w^JF01901/Vps26^UAS.Tag:V5

(Wang et al., 2014)

norpA^P24 has retina | conditional phenotype, suppressible by Osi21^MB01450/Osi21^die4

(Lee et al., 2013)

norpA^P24 has retina | conditional phenotype, suppressible by Osi21^VDRC.cUa/Scer\GAL4^ninaE.PTa

(Lee et al., 2013)

norpA^P24 has photoreceptor neuron phenotype, suppressible by ninaE¹⁷/ninaE^Δ356

(Kristaponyte et al., 2012)

norpA^P24 has photoreceptor neuron phenotype, suppressible by ninaE¹⁷/ninaE^StoA

(Kristaponyte et al., 2012)

norpA^P24 has rhabdomere phenotype, suppressible by ninaE¹⁷/ninaE^Δ356

(Kristaponyte et al., 2012)

norpA^P24 has rhabdomere phenotype, suppressible by ninaE¹⁷/ninaE^StoA

(Kristaponyte et al., 2012)

norpA^P24 has retina phenotype, suppressible by diehard1^diehard1/diehard1^diehard1

(Lee, 2012)

norpA^P24 has retina phenotype, suppressible by diehard3^diehard3/diehard3^diehard3

(Lee, 2012)

norpA^P24 has photoreceptor neuron phenotype, suppressible by gig^UAS.cTa/Tsc1^UAS.cGa/Scer\GAL4^GMR.PU

(Wang et al., 2009)

norpA^P24 has retina phenotype, suppressible by gig^UAS.cTa/Tsc1^UAS.cGa/Scer\GAL4^GMR.PU

(Wang et al., 2009)

norpA^P24 has retina phenotype, suppressible by Atg1^{ninaE.Tag:MYC}

(Wang et al., 2009)

norpA^P24 has photoreceptor neuron phenotype, suppressible by Atg1^{ninaE.Tag:MYC}

(Wang et al., 2009)

norpA^P24 has retina phenotype, suppressible by Dronc^GMR.PH

(Hsu et al., 2004)

norpA^P24 has retina phenotype, suppressible by BacA\p35^GMR.PH

(Hsu et al., 2004)

norpA^P24 has phenotype, suppressible by ninaE^ΔAsn20

(Kurada and O'Tousa, 1995)

norpA^P24 has phenotype, suppressible by ninaE¹²

(Kurada and O'Tousa, 1995)

norpA^P24 has phenotype, suppressible by ninaE¹⁷

(Kurada and O'Tousa, 1995)

norpA^P24 has phenotype, suppressible by ninaE^205UAA

(Kurada and O'Tousa, 1995)

norpA^P24 has phenotype, suppressible by ninaE^309UAA

(Kurada and O'Tousa, 1995)

norpA^P24 has phenotype, suppressible by ninaE⁵

(Kurada and O'Tousa, 1995)

norpA^P24 has phenotype, suppressible by ninaE⁶

(Kurada and O'Tousa, 1995)

norpA^P24 has phenotype, suppressible by ninaE⁷

(Kurada and O'Tousa, 1995)

norpA^P24 has phenotype, suppressible by ninaE⁸

(Kurada and O'Tousa, 1995)

norpA^P24 has phenotype, suppressible by ninaE⁹

(Kurada and O'Tousa, 1995)

norpA^P24 has phenotype, suppressible by ninaE^D1

(Kurada and O'Tousa, 1995)

norpA^P24 has phenotype, suppressible by ninaE^G168D

(Kurada and O'Tousa, 1995)

norpA^P24 has phenotype, suppressible by ninaE^G67E

(Kurada and O'Tousa, 1995)

norpA^P24 has phenotype, suppressible by ninaE^G69D

(Kurada and O'Tousa, 1995)

norpA^P24 has phenotype, suppressible by ninaE¹

(Kurada and O'Tousa, 1995)

norpA^P24 has phenotype, suppressible by ninaE^L205W

(Kurada and O'Tousa, 1995)

norpA^P24 has phenotype, suppressible by ninaE^L309W

(Kurada and O'Tousa, 1995)

norpA^P24 has phenotype, suppressible by ninaE^P350

(Kurada and O'Tousa, 1995)

norpA^P24 has phenotype, suppressible by ninaE^P84A

(Kurada and O'Tousa, 1995)

norpA^P24 has phenotype, suppressible by ninaE^RH27

(Kurada and O'Tousa, 1995)

norpA^P24 has phenotype, suppressible by ninaE^S233F

(Kurada and O'Tousa, 1995)

norpA^P24 has phenotype, suppressible by ninaE^S95F

(Kurada and O'Tousa, 1995)

norpA^P24 has phenotype, suppressible by ninaE^US6275

(Kurada and O'Tousa, 1995)

NOT suppressed by

Statement

Reference

norpA^P24 has retina | conditional phenotype, non-suppressible by PIP5K59B¹⁸

(Chakrabarti et al., 2015)

norpA^P24 has retina phenotype, non-suppressible by su(rdgA)40⁴⁰

(Georgiev et al., 2012)

norpA^P24 has retina phenotype, non-suppressible by Df(3L)H99

(Hsu et al., 2004)

norpA^P24 has retina phenotype, non-suppressible by Diap1^GMR.PH

(Hsu et al., 2004)

Enhancer of

Statement

Reference

norpA^P24 is an enhancer of rhabdomere | adult stage | decreased number phenotype of Pkc53E^HMC04134, Scer\GAL4^GMR.PF

(Shieh et al., 2023)

NOT Enhancer of

Statement

Reference

norpA^P24 is a non-enhancer of eye photoreceptor cell | somatic clone | decreased number phenotype of Pect²⁹, Scer\FLP1^ey.PU

(Zhao and Wang, 2020)

norpA^P24 is a non-enhancer of rhabdomere | somatic clone | decreased number phenotype of Pect²⁹, Scer\FLP1^ey.PU

(Zhao and Wang, 2020)

Suppressor of

Statement

Reference

norpA^P24 is a suppressor of endoplasmic reticulum-plasma membrane contact site phenotype of Esyt2^KO

(Nath et al., 2020)

norpA^P24 is a suppressor of outer photoreceptor cell phenotype of Esyt2^KO

(Nath et al., 2020)

norpA^P24 is a suppressor of eye photoreceptor cell | somatic clone | adult stage phenotype of alc^Δ12.125

(Spasić et al., 2008)

norpA^P24 is a suppressor of retina | somatic clone | adult stage phenotype of alc^Δ12.125

(Spasić et al., 2008)

norpA^P24 is a suppressor of retina | conditional phenotype of Cnx99A¹

(Rosenbaum et al., 2006)

norpA^P24 is a suppressor | partially of rhabdomere | somatic clone phenotype of Nmnat²

(Zhai et al., 2006)

norpA^P24 is a suppressor | partially of ommatidium | somatic clone phenotype of Nmnat²

(Zhai et al., 2006)

norpA^P24 is a suppressor of rhabdomere phenotype of rdgA¹

(Georgiev et al., 2005)

norpA^P24 is a suppressor of rhabdomere phenotype of rdgA³

(Georgiev et al., 2005)

norpA^P24 is a suppressor | partially of retina phenotype of ninaE^pp100

(Iakhine et al., 2004)

NOT Suppressor of

Statement

Reference

norpA^P24 is a non-suppressor of eye photoreceptor cell | somatic clone | decreased number phenotype of Pect²⁹, Scer\FLP1^ey.PU

(Zhao and Wang, 2020)

norpA^P24 is a non-suppressor of rhabdomere | somatic clone | decreased number phenotype of Pect²⁹, Scer\FLP1^ey.PU

(Zhao and Wang, 2020)

norpA^P24 is a non-suppressor of adult brain phenotype of Cpes^KO

(Kunduri et al., 2018)

Other

Statement

Reference

Osi21^+tLa, Osi21^MB01450/Osi21^die4, norpA^P24 has retina | conditional phenotype

(Lee et al., 2013)

Additional Comments

Genetic Interactions

Statement

Reference

norpA³⁶, cry⁰¹ double homozygous adults previously trained under 12h:12h light:dark cycles present slightly increased circadian rhythmicity defects under constant darkness conditions, which are rescued by additional homozygosity for either as trp^MB03672 or trpl^MB10553, compared to each single homozygotes.

norpA³⁶, ninaE¹⁷ double homozygotes that also contain a copy of norpA^ninaE.PW display a complete loss of retinal response to light in electro-retinograms, which is suppressed by the expression of Rh7^Scer\UAS.cNa under the control of Scer\GAL4^ninaE.PT, as compared to controls.

(Ni et al., 2017)

The light-dependent retinal degeneration as well as the elevated number of rhodopsin1-containing vesicles per ommatidium characteristic for norpA³⁶ homozygous adults can be partially suppressed by expression of Pld^Scer\UAS.cRa under the control of Scer\GAL4^ninaE.PU in the mutant background.

(Thakur et al., 2016)

Light-dependent retinal degeneration seen in norpA³⁶ mutants is not suppressed in norpA³⁶ PIP5K59B¹⁸ animals.

(Chakrabarti et al., 2015)

Flies expressing norpA^ninaE.PM in norpA³⁶ ninaE¹⁷/ninaE¹⁷ background exhibit a dramatically reduced response to light (lack of a light induced depolarization and on and off transients) than controls in electroretinogram readings although they are stimulated with higher light intensity than controls.

(Zheng et al., 2015)

Overexpression of Vps35^{Scer\UAS.T:Ivir\HA1} in a Scer\GAL4^Act5C.PU w^JF01901 background, significantly restores rhabdomere number in norpA³⁶ mutants that have been continuously exposed to white light for 6 days.

Overexpression of Vps26^{Scer\UAS.T:SV5\V5} in a Scer\GAL4^Act5C.PU w^JF01901 background, significantly restores rhabdomere number in norpA³⁶ mutants that have been continuously exposed to white light for 6 days.

(Wang et al., 2014)

Osi21^die4/Osi21^die4, Osi21^die4/Df(2L)Exel6028, Osi21^die4/Osi21^MB01450 or Osi21^VDRC.cUa driven by Scer\GAL4^ninaE.PTa (but not Osi21^die4/Osi21^MB01450;Osi21^+tLa) partially suppresses the progressive retinal degeneration seen under constant light exposure in norpA³⁶/norpA³⁶ flies.

(Lee et al., 2013)

Twenty-day old norpA³⁶ flies expressing ninaE^Δ356 or ninaE^StoA exhibit the full complement of R1-R6 rhabdomeres and display no sign of retinal degeneration. Rhabdomere degeneration is delayed in norpA³⁶ flies expressing one copy of ninaE^Δ356 or ninaE^StoA in a ninaE¹⁷ mutant background, as rhabdomeres retain wild-type morphology for at least 3 weeks post-eclosion. At 4 weeks, some ommatidia exhibit signs of deterioration as characterised by missing and/or reduced rhabdomeres in norpA³⁶ flies co-expressing ninaE^Δ356 or ninaE^StoA (in a ninaE¹⁷ background), but degeneration is greatly delayed compared to norpA³⁶ flies.

(Kristaponyte et al., 2012)

The retinal degeneration (loss of deep pseudopupil) seen in norpA³⁶ flies after 5 days in constant light is suppressed if the eyes are homozygous for diehard1^diehard1 (partial suppression), diehard3^diehard3 or diehard4^diehard4.

(Lee, 2012)

norpA³⁶ -mediated photoreceptor degeneration is significantly suppressed by overexpression of either Tsc1^Scer\UAS.cGa and gig^Scer\UAS.cTa under the control of Scer\GAL4^GMR.PU, or Atg1^{ninaE.T:Hsap\MYC}.

(Wang et al., 2009)

The ability of norpA³⁶ to select 18[o]C is eliminated in a rdgC³⁰⁶ background.

(Kwon et al., 2008)

Consistent with the hypothesis that neurodegeneration in adults with alc^Δ12.125 homozygous eyes and antennae (inducing homozygous somatic clones in the eye and antenna with Scer\GAL4^ey.PH; Scer\FLP1^Scer\UAS.cDa and killing non-mutant cells in the eye with W^GMR.PG) is dependent on neuronal activity, this phenotype is suppressed when phototransduction is blocked using a norpA³⁶/norpA³⁶ background.

(Spasić et al., 2008)

norpA³⁶ cry⁰¹, norpA³⁶ cry⁰² and norpA³⁶ cry⁰³ double mutant flies generally fail to resynchronise to the new light regime when they are entrained to 12 hour light: 12 hour dark cycles and then exposed to 8 hour delayed light-dark (LD) cycles; their daily peaks of locomotion continue to occur at the time of the photic transitions that that were in operation before the 8 hour shift. Some of the double mutant flies are "partially entrained"; six says after the photic shift, daily peaks of locomotion fall between the phases expected for continuing entrainment to the old LD regime versus re-entrainment to the new one.

norpA³⁶ cry⁰¹ and norpA³⁶ cry⁰² double mutant flies are impaired in their ability to re-entrain with novel non-24 hour light:dark (LD) cycles (compared to single mutant flies) when they are entrained to 12:12 LD and are then shifted to 9:9 , 13:13 or 14:14 LD cycles.

norpA³⁶ cry⁰³ double mutant flies are impaired in their ability to re-entrain with novel non-24 hour light:dark (LD) cycles (compared to single mutant flies) when they are entrained to 12:12 LD and are then shifted to 9:9 or 14:14 LD cycles.

(Dolezelova et al., 2007)

When CG11426^{Scer\UAS.T:Avic\GFP} is expressed under the control of Scer\GAL4^ninaE.PT in rdgA³ norpA³⁶ flies, the rhabdomeres are normal and do not show degeneration over time.

(Garcia-Murillas et al., 2006)

Inclusion of norpA³⁶ slows down the onset and progression of retinal degeneration in Cnx99A¹ mutants.

(Rosenbaum et al., 2006)

In norpA³⁶; Nmnat² double mutant photoreceptors, the neurodegeneration seen in Nmnat² single mutant receptors is partially suppressed; the overall ommatidial structure is better organized, the vacuoles in the ommatidia are smaller and the loss of rhabdomeres is reduced.

(Zhai et al., 2006)

norpA³⁶ completely suppresses the retinal degeneration seen in rdgA³ flies.

norpA³⁶ almost completely suppresses the retinal degeneration seen in rdgA¹ flies.

(Georgiev et al., 2005)

Homozygous norpA³⁶; Df(3L)H99 clones in the retina show the same course of degeneration as norpA³⁶ single mutants.

Expression of th^GMR.PH does not alter the degeneration of norpA³⁶ rhabdomeres, while expression of Nc^GMR.PH slows down degeneration but does not prevent it.

(Hsu et al., 2004)

In norpA³⁶; ninaE^pp100 double mutants, retinal degeneration is delayed but not prevented, relative to ninaE^pp100 single mutants.

(Iakhine et al., 2004)

In recordings of norpA³⁶ rdgA¹ double mutant photoreceptors, with a standard electrode solution containing nucleotide additives, the constitutive inward currents recorded immediately on establishing the whole-cell configuration are greatly enhanced compared with norpA³⁶ single mutant photoreceptors. The spontaneous currents in the double mutant photoreceptors slowly decay, reaching a quiet base line after about 20 minutes. Towards the end of this decay, large (about 8pA) slowly terminating quantum bumps can be resolved, similar in both amplitude and kinetics to those seen in norpA³⁶ single mutant photoreceptors without ATP. Sensitivity to light is enhanced in the double mutant photoreceptors, with bright flashes eliciting responses of up to about 200pA in amplitude before the decay of the spontaneous current and responses of up to about 400pA that decay with the slow kinetics characteristic of norpA³⁶ after decay to base line. Spontaneous currents are abolished in norpA³⁶ Gα49B¹ double mutant and Gα49B¹ norpA³⁶ rdgA¹ triple mutant photoreceptors. Responses to light are greatly reduced in norpA³⁶ Gα49B¹ double mutant photoreceptors compared to norpA³⁶ single mutant photoreceptors.

(Hardie et al., 2003)

norpA³⁶ ; ninaE¹⁷/+ flies that carry norpA^ninaE.PM have a robust response to light at both 350nm and 520nm (measured using an electroretinogram recording). norpA³⁶ ; ninaE¹⁷/ninaE¹⁷ flies that carry norpA^ninaE.PM have no response to light at both 350nm and 520nm (measured using an ERG recording). Introduction of Lpol\Ops1^ninaE.PK or Lpol\Ops1^{ninaE.T:Btau\1D4} into a norpA³⁶ ; ninaE¹⁷/ninaE¹⁷ ; norpA^ninaE.PM background restores the response to light (measured using an ERG recording), although the response at 520nm is much great than that at 350nm. Flies expressing Lpol\Ops1^ninaE.PK in a ninaE¹⁷ norpA³⁶ background show no response to light (measured using an ERG recording). Flies expressing Lpol\Ops1^{ninaE.T:Btau\1D4} in a ninaE¹⁷ norpA³⁶ background show no response to light (measured using an ERG recording).

(Knox et al., 2003)

Retinal degeneration phenotype can be suppressed by ninaE mutations.

(Kurada and O'Tousa, 1995)

Xenogenetic Interactions

Statement

Reference

norpA³⁶ partially suppresses the navigation of adults with optogenetic activation (using Cnoc\ChR1::Csub\ChR^{CsChrimson.IVS.20xUAS.Venus} with 624 nm (red) light) of Scer\GAL4^0273-G4 cells to areas associated with illumination only when the assay is performed in an arena lacking tactile features.

(Stern et al., 2019)

A norpA³⁶ background blocks phototaxis in Crei\ChR2^Scer\UAS.cSa-Scer\GAL4^{Or83b.2.642.T:Hsim\VP22} mutants.

A norpA³⁶ background blocks phototaxis in Zzzz\PACα^{Scer\UAS.cSLa}-Scer\GAL4^{Or83b.2.642.T:Hsim\VP22} mutants.

(Bellmann et al., 2010)

Expression of BacA\p35^GMR.PH delays the retinal degeneration of norpA³⁶ flies, but does not prevent it.

Expression of either BacA\p35^GMR.PH and Nc^GMR.PH together, or BacA\p35^GMR.PH and th^GMR.PH together, provide no better suppression of the retinal degeneration of norpA³⁶ flies, than BacA\p35^GMR.PH alone.

(Hsu et al., 2004)

Complementation and Rescue Data

Rescued by

norpA^P24 is rescued by norpA^ninaE.PW

(Ni et al., 2017)

norpA^P24 is rescued by norpA^UAS.ckb/Scer\GAL4^TrpA1-AB-G4

(Kim et al., 2010)

norpA^P24 is rescued by norpA^UAS.ckb/Scer\GAL4^TrpA1.PR

(Kwon et al., 2010)

norpA^P24 is rescued by norpA^UAS.ckb/Scer\GAL4^{Orco.2.642.Hsim\VP22}

(Kwon et al., 2010)

norpA^P24 is rescued by norpA^UAS.ckb/Scer\GAL4^TrpA1.PR

(Kwon et al., 2008)

norpA^P24 is rescued by norpA^hs.PW

(Wang et al., 2008)

norpA^P24 is rescued by norpA^ninaE.PM

(Kim et al., 2003)

norpA^P24 is rescued by norpA^ninaE.PM

(van Huizen et al., 1998)

norpA^P24 is rescued by norpA^hs.PS

(Shieh et al., 1997)

Partially rescued by

norpA^P24 is partially rescued by norpA^ninaE.PK

(Kim et al., 2003)

norpA^P24 is partially rescued by norpA^CDI.ninaE

(van Huizen et al., 1998)

norpA^P24 is partially rescued by norpA^ninaE.PM

(Pearn et al., 1996)

norpA^P24 is partially rescued by norpA^ninaE.PM

(McKay et al., 1995)

Not rescued by

norpA^P24 is not rescued by norpA^S559A.ninaE

(Wang et al., 2008)

norpA^P24 is not rescued by norpA^CDII.ninaE

(van Huizen et al., 1998)

Comments

The complete loss of retinal response to light displayed by norpA³⁶ homozygotes is rescued by the presence of a copy of norpA^ninaE.PW.

(Ni et al., 2017)

Expression of norpA^Scer\UAS.ckb using Scer\GAL4^TrpA1-GAL4 rescues the reduced avoidance to aristolochic acid and the reduced aristolochic acid-induced action potentials shown by norpA³⁶ mutants.

(Kim et al., 2010)

Expression of norpA^Scer\UAS.ckb under the control of either Scer\GAL4^TrpA1.PR or Scer\GAL4^{Orco.2.642.T:Hsim\VP22} rescues the reduced avoidance to citronellal which is seen in norpA³⁶ flies in a direct airborne repellent test (DART) assay.

(Kwon et al., 2010)

The presence of norpA^Scer\UAS.ckb, under the control of Scer\GAL4^TrpA1.PR iresotred 18[o]C selection in norpA³⁶ mutants.

(Kwon et al., 2008)

Expression of norpA^hs.PW using heat shock in a norpA³⁶ background results in a rescue of the electroretinogram (ERG) response, depending on the level of norpA protein expression. After a 15 minute heat shock, the flies express approximately 3.8% of the normal protein level and show a severe slow termination of the light response. As the duration of the heat shock is increased, the termination of the photoresponse becomes faster, and expression of approximately 20% of the normal protein level restores a wild-type ERG.

(Wang et al., 2008)

Light evoked responses are restored in homozygotes carrying norpA^ninaE.PM. Light evoked responses are partially rescued by norpA^CDI.ninaE. Light evoked responses are not rescued by norpA^CDII.ninaE.

(van Huizen et al., 1998)

Expression of norpA^hs.PS rescues the light response. Expression of norpA^C1094S.hs causes an ERG with slower kinetics.

(Shieh et al., 1997)

norpA^ninaE.PM rescues the electrophysiological phenotype of norpA³⁶ flies in photoreceptor cells R1 to R6, but not in R7 and R8. The degeneration phenotype of the R1 to R6 photoreceptors is also rescued by norpA^ninaE.PM.

(Pearn et al., 1996)

The reduction in phospholipase C activity seen in the heads of norpA³⁶ flies is partially rescued by norpA^ninaE.PM.

(McKay et al., 1995)

Images (0)

Mutant

Wild-type

Stocks (2)

Bloomington

9048

w^* norpA^P24

52276

w^* norpA^P24; P{ninaE-norpA.W}2

Notes on Origin

Discoverer

Pak.

Comments

The basic expression and daily oscillation pattern of per protein in light-dark cycles is normal in norpA³⁶ mutant flies.

(Zerr et al., 1990)

norpA RNA and protein expression, and phospholipase C activity have been studied in norpA³⁶ flies.

(Zhu et al., 1993)

Photolysis of the caged Ca²⁺ compounds DM-nitrophen and nitr-5 induces a small inward current with no detectable latency in norpA³⁶ photoreceptor cells.

(Hardie, 1995)

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (7)

Reported As

Symbol Synonym

NorpA

(Gao et al., 2008)

NorpA³⁶

(Clarembaux-Badell et al., 2022, Fujiwara et al., 2022, Deutsch et al., 2020, Gao et al., 2008, Gao et al., 2008)

NorpA^P24

(Li et al., 2018)

norpA³⁶

(Cornean et al., 2024, Gorko et al., 2024, Ikeda et al., 2022, Hu et al., 2020, Leung et al., 2020, Tanaka and Clark, 2020, Akin et al., 2019, Stern et al., 2019, Suver et al., 2019, Yang and Edery, 2019, Duistermars et al., 2018, Wu et al., 2016, Guntur et al., 2015, Melnattur et al., 2014, Holbrook et al., 2012, Vasiliauskas et al., 2011, Yuan et al., 2011, Frohman, 2007.1.29)

norpA^P24

(Shieh et al., 2023, Gu et al., 2022, Omelchenko et al., 2022, Shieh et al., 2021, Chen and Montell, 2020, Li et al., 2020, Liu et al., 2020, Nath et al., 2020, Zhao and Wang, 2020, Liang et al., 2019, Mu et al., 2019, Schopf et al., 2019, Cao et al., 2018, Kim et al., 2018, Panda et al., 2018, Ahn et al., 2017, Asteriti et al., 2017, Ni et al., 2017, Saint-Charles et al., 2016, Sokabe et al., 2016, Thakur et al., 2016, Chakrabarti et al., 2015, Hardie et al., 2015, Jaiswal et al., 2015, Delgado et al., 2014, Wang et al., 2014, Sengupta et al., 2013, Zhang et al., 2013, Georgiev et al., 2012, Lee, 2012, Szular et al., 2012, Oberegelsbacher et al., 2011, Rosenbaum et al., 2011, Shen et al., 2011, Bellmann et al., 2010, Elsaesser et al., 2010, Kim et al., 2010, Kwon et al., 2010, Kwon et al., 2010, Kwon et al., 2010, Mecklenburg et al., 2010, Dasgupta et al., 2009, Kain et al., 2009, Wang et al., 2009, Kain et al., 2008, Krause et al., 2008, Kwon et al., 2008, Spasić et al., 2008, Wang et al., 2008, Dolezelova et al., 2007, Frohman, 2007.1.29, Baumann and Lutz, 2006, Garcia-Murillas et al., 2006, Meyer et al., 2006, Rosenbaum et al., 2006, Ueno et al., 2006, Zhai et al., 2006, Chorna-Ornan et al., 2005, Georgiev et al., 2005, Glaser and Stanewsky, 2005, Satoh and Ready, 2005, Baumann, 2004, Hardie et al., 2004, Hsu et al., 2004, Hardie et al., 2003, Kim et al., 2003, Knox et al., 2003, Kosloff et al., 2003, Baehner et al., 2002, Hardie et al., 2002, Agam et al., 2000, Bahner et al., 2000, Cook et al., 2000, Hassan et al., 2000, Li and Montell, 2000, Liu et al., 2000, Busto et al., 1999, Chyb et al., 1999, Salcedo et al., 1999, Bubis et al., 1998, Smith et al., 1998, Stanewsky et al., 1998, Barth et al., 1997, Chevesich et al., 1997, Gu and Singh, 1997, Hekmat-Scafe and Carlson, 1996, Pearn et al., 1996, Hardie, 1995, Hevers and Hardie, 1995, Kurada and O'Tousa, 1995, McKay et al., 1995, Riesgo-Escovar et al., 1995, Lee et al., 1994, McKay et al., 1994, Peretz et al., 1994, Sahly et al., 1994, Stark et al., 1993, Zhu et al., 1993, Hamblen-Coyle et al., 1992, Garen-Fazio et al., 1991, Newby and Jackson, 1991, Pearn et al., 1991, Schneuwly et al., 1991, Guillen et al., 1990, Zerr et al., 1990, Kulkarni et al., 1988, Banga et al., 1986)

norpA^P29

(Bubis et al., 1998)

Name Synonyms

Secondary FlyBase IDs

References (156)

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