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General Information
Symbol
Dmel\ninaE17
Species
D. melanogaster
Name
FlyBase ID
FBal0013022
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
ninaEI17, ninaEl17, ninaEoI17, ninaEOl17, ninaE117, rh1I17, Df(3R)oI17, ninaE0117, ninaE17ol
Mutagen
Nature of the Allele
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Cytology
Nature of the lesion
Statement
Reference

Large deletion of the 5' region of ninaE.

Deletion of ninaE.

Deletion of the 5' flanking and 5' coding regions.

Small deletion within ninaE.

Large deletion encompassing most of the transcription unit and a large upstream region.

Deletion in the ninaE gene.

Internal deletion in ninaE.

Intragenic deletion.

1.6kb deletion.

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
Modifiers Based on Experimental Evidence ( 1 )
Disease
Interaction
References
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In

rhabdomere & actin filament

Detailed Description
Statement
Reference

ninaE17 third instar larvae exhibit greatly diminished mechanically evoked spiking increase in abdominal lateral pentascolopidial chordotonal organ (lch5) compared to controls. Spiking responses of the mutants remain uncompromised by nutrient carotenoid depletion for six generations.

Electroretinogram recordings indicate that ninaE17 adults lack prolonged depolarization afterpotential when compared to controls.

ninaE17 homozygous adults exhibit a severe decrease in retinal response to light in electro-retinograms, as compared to controls.

The electroretinogram response of light-adapted ninaEΔ356;ninaE17,rdgC306 flies to oscillating light of gradually increasing frequencies is comparable to controls at both lower and higher frequencies. 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, no defects are observed in light-adapted flies at high frequency either.

ninaE17 mutants exhibit rhabdomeres that are highly reduced in size at eclosion, as compared to wild type.

ninaE17 homozygous mutant larvae are impaired in temperature selection at 72 and 96 hr AEL (after egg laying) and prefer higher temperatures compared to controls, however at late third instar (120 hr AEL) their temperature preferences (larvae distribution across a temperature gradient) are indistinguishable from wild-type.

ninaE17 mutants exhibit normal light-dependent temperature preference. Similarly to wild-type, they prefer higher temperature in the light than in the dark.

The R1-6 and R7 rhabdomeres of freshly eclosed ninaE17 are well formed however the R1-6 rhabdomeres degenerate within 7 days while R7 rhabdomere remains in the ommatidia compared to controls.

Retinal ultrastructure of transgenic ninaEP37H flies in a ninaE17 genetic background is similar to that of wild-type, as evidenced by a normal complement of photoreceptor neurons. However, numerous rhabdomeres exhibit structural abnormalities suggesting rhabdomere structural defects in the mutant. Compared with controls, a marked expansion of the endoplasmic reticulum network is observed in mutant photoreceptor neurons. There is also a significant increase in the number of mitochondria in the mutants relative to wild-type. High-resolution images reveal that numerous mitochondria in the mutant flies display structural abnormalities, such as absent or poorly patterned cristae. Compared with wild-type, a strong increase in the number of autophagic vacuoles, multivesicular bodies, and lysosomes is detected in the mutants.

30-day old transgenic ninaEP37H flies in a ninaE17 genetic background, unlike control flies, exhibit a blunted electrical response to light stimulation.

Heterozygous ninaE17 flies exhibit a normal ERG response.

The first rhabdomere development defects are observed at approximately 85% pupal development in mutant animals; short intrusions of closely apposed membranes emanating from the base of the rhabdomere microvilli are readily detected in the cytoplasm, disrupting the normally well-defined boundary between the base of the rhabdomere and the cytosol. These short intrusions develop further over time to eventually represent a significant proportion of the rhabdomeric membrane collapsing inside the cell.

Mutant larvae show a reduced preference for 18[o]C over 24[o]C in a binary choice thermotaxis assay compared to controls. The mutant larvae also show impaired discrimination between 18[o]C and other temperatures in the comfortable range (20 or 22[o]C), but do not show defects in selection of 18[o]C over cooler (14 or 16[o]C) or warmer temperatures (26 to 32[o]C).

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).

Photoreceptors of 3 day old mutant adults have largely disorganized rhabdomeres.

ninaE17 flies show no detectable optomotor responses and largely compromised phototaxis to blue and UV light. However, they show normal phototaxic responses to green light.

ninaE17 flies do not exhibit motion-elicited landing reflexes, although they are capable of spontaneous leg extension.

In response to a striped pattern that rotates around the anterior-posterior body axis, ninaE17 flies do not exhibit the normal head-roll response.

The light-triggered translocation of trplninaE.T:Avic\GFP-EGFP is abolished in ninaE17 flies.

In ninaE17 mutants, the rhabdomeres of R1-R6 degenerate, whereas expression of opsins Rh3-Rh6 is unaffected. Phototaxis is retained in these mutants.

ninaE17 mutants do not exhibit a response to colour contrast (when moving green and blue stripes are presented).

The R1-R6 rhabdomeres are severely reduced in 3 day old mutant flies. The R7 rhabdomere is unaffected.

Mutant flies show normal escape jump behaviour in response to a mechanical shock.

Mutant flies do not show an escape jump in response to sudden darkness, in contrast to wild-type flies.

The presence of ninaEP37H.+t2747 rescues the ERG phenotype of ninaE17 mutants at day 1 after eclosion. Compared to wild-type transgenes (such as ninaEWT.+t2747), however, ninaEP37H.+t2747-ninaE17 flies display significantly reduced ERG amplitude.

The climbing initiation and gap-crossing success of ninaE17 flies is impaired compared to wild-type flies.

Three day old mutant flies have ill-formed rhabdomeres, and remnant rhabdomeres are seen as long contiguous elements of plasma membrane involuting into the cell body in R1-R6 photoreceptors.

In newly eclosed mutant flies, the R1-6 rhabdomeres degenerate. The Myosin-II system in mutant photoreceptors is disorganised, this disorganisation becomes more pronounced with age. At the retinal floor of mutant flies, however, no change in the Myosin-II is seen.

The electroretinogram light responses from ninaE17/ninaE17 flies that are 12 hr after eclosion lack a prolonged depolarizing afterpotential in response to blue light and show small light response amplitudes in comparison to ERGs from wild-type flies. ninaEpp100/ninaE17 transheterozygotes also lack the prolonged depolarizing afterpotential.

ninaEpp100/ninaE17 transheterozygotes show a retinal degeneration phenotype that is similar to that of ninaEpp100/ninaEpp100 homozygotes.

Flies that express ninaEt.G299R in a ninaE17/+ background exhibit a retinal degeneration phenotype, that is indistinguishable from that seen in ninaEpp100/+ flies.

ninaE17 flies are significantly impaired in the ability to maintain their orientation towards a landmark when walking in the Buridan's paradigm assay. Their average and maximum walking speed are reduced to about one-half of the corresponding speed observed under identical conditions in wild-type flies. ninaE17 flies retain about 12% of the normal course control and about 58% of the object fixation of normal flies when tested in fixed flying and freely walking assays.

The rhabdomere terminal web (RTW) of mutant photoreceptors appear normal before the time when ninaE expression would normally commence. However, the RTW growth and bundling that normally follow ninaE expression fails in mutant photoreceptors. Unlike wild-type rhabdomeres, the smaller, flattened mutant rhabdomeres of cells R1-R6 collapse into the photoreceptor cytoplasm in convoluted sheets of apposed membranes during the first day after eclosion. The actin cytoskeleton becomes thoroughly disorganised.

Mutant flies lack the electroretinogram 'on' and 'off' transients.

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

Mutant flies have a dramatically reduced electroretinogram (ERG).

Some rhabdomeres are completely degenerated while others appear intact in mutant R1-R6 photoreceptor cells.

ninaE17 larvae reduce their path lengths and show increased head swinging when exposed to light. This response is indistinguishable from wild-type 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. The change of direction at the L to D transition in ninaE17 larvae is reduced to levels indistinguishable from that seen in the absence of a light transition (D to D). These larvae do show a D to L change of direction that is greater than both the L to D change of direction and the direction change in the absence of a light transition (D to D).

The electroretinograms of homozygous ninaE17 flies have no on- or off-transients and the magnitude of depolarisation is dramatically reduced compared to wild-type.

The on- and off-transients are absent in the electroretinogram of ninaE17 flies.

Curtains of rhabdomere membrane invade photoreceptor cytoplasm. ERG recordings demonstrate response amplitudes are reduced and off-transients are absent.

rdgE1/Df(2R)vg135; ninaE17/ninaE17 double mutants exhibit small and abnormally shaped R1-6 rhabdomeres, lacking the microvillar unpacking and vesiculation of the rhabdomere associated with rdgE1. Some of the rdgE1/Df(2R)vg135; ninaE17/ninaE+ mutant photoreceptors exhibit unpacking and vesiculation of the rhabdomeres.

One day post-eclosion individuals exhibit rhabdomere degeneration in the outer photoreceptors and the intrusion of the rhabdomere membranes into the cell body. In the rhabdomere base microvilli terminate in irregular loops and hairpin turns disrupting the smooth plane of the normal base. ninaE17; ninaC5 double mutants exhibit degeneration of the outer and inner photoreceptor rhabdomeres and the intrusion of the rhabdomere membranes into the cell body.

Heterozygotes retain the deep pseudopupil for greater than 35 days, homozygotes exhibit rapid loss of the pseudopupil.

Microspectrophotometry (MSP) reveals minimal photopigment within a week after eclosion. Small rhabdomeres.

Whole cell patch clamp recordings of UV sensitive rhodopsin transgene, P{Rh1+4}; ninaE17, photoreceptors demonstrates light-dependent changes in intracellular calcium result from the influx of external calcium. Application of thapsigargin results in a steady increase of intracellular calcium (demonstrating the existance of IP3-sensitive stores of calcium). Even after complete depletion of calcium the light response is not abolished. Instead the rise in intracellular calcium is associated with a partial desensitisation (adaptation) of the electrical response. There is no functional link between average intracellular calcium and adaptation recovery mechanisms. Localised intracellular calcium drives aspects of photoreceptor cell regulation.

Degeneration of the outer photoreceptor cells prior to eclosion, R7 is the only cell remaining and sometimes this is split. Ommatidia contain more than one rhabdomere in double mutants with ttk1.

Rapid rate (more rapid than for ninaE8 of degeneration of R1-6 rhabdomeres: by three weeks post-eclosion none remain.

Degeneration of outer photoreceptor cells R1 to R6. In ommatidia of double mutants with Gap1sxt-BJ61 the extra receptor cells do not degenerate, this implies the extra cells have an R7 or R8 identity.

The outer rhabdomeres of the ommatidia are nearly absent. R7 is normal. ERG is abnormal.

Double mutants, for ninaA3 and ninaE17, which also contain Rh2ninaE.P still display dramatic accumulations of ER membranes in photoreceptors R1-R6.

Disarray of membrane in the area of rhabdomere's normal location in the R1 cell.

Rhodopsin levels very low in R1--R6 photoreceptors: respond poorly or not at all to light stimulus.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhanced by
Statement
Reference
Suppressed by
Statement
Reference

ninaE17, ninaEP37H has neuroanatomy defective phenotype, suppressible by DriceΔ1/Ice[+]

ninaE17, ninaEP37H has neuroanatomy defective phenotype, suppressible by Ark[+]/Dark82

ninaE17, ninaEP37H has neurophysiology defective phenotype, suppressible by Traf4[+]/Traf4ex1

ninaE17, ninaEP37H has neuroanatomy defective phenotype, suppressible by Traf4[+]/Traf4ex1

ninaE17, ninaEP37H has neurophysiology defective phenotype, suppressible by bsk1/bsk[+]

ninaE17, ninaEP37H has neuroanatomy defective phenotype, suppressible by bsk1/bsk[+]

NOT suppressed by
Statement
Reference

ninaE17 has thermotaxis defective | larval stage | temperature conditional phenotype, non-suppressible by 5-HT2ADCIII.UAS/Scer\GAL4ninaE.PT

Enhancer of
Statement
Reference
NOT Enhancer of
Suppressor of
Statement
Reference
NOT Suppressor of
Statement
Reference

ninaE17 is a non-suppressor of paralytic | adult stage | progressive | conditional phenotype of CpesKO

ninaE17 is a non-suppressor of locomotor behavior defective | adult stage | progressive | conditional phenotype of CpesKO

ninaE17/Rh3Rh1+3 is a non-suppressor of neurophysiology defective phenotype of Arr25

ninaE17 is a non-suppressor of neurophysiology defective phenotype of Rh3Rh1+3

Other
Phenotype Manifest In
Enhanced by
Suppressed by
Statement
Reference

ninaE17 has rhabdomere phenotype, suppressible by ninaD1

ninaE17 has rhabdomere & actin filament phenotype, suppressible by Scer\GAL4hs.PB/Rac1V12.C.UAS

ninaE17 has phenotype, suppressible by Sgre\Ops2ninaE.PE

ninaE17 has phenotype, suppressible by Rh6ninaE.PS

ninaE17 has phenotype, suppressible by Rh3Rh1+3

ninaE17 has phenotype, suppressible by Rh4ninaE.P

NOT suppressed by
Statement
Reference
NOT Enhancer of
Statement
Reference
Suppressor of
Statement
Reference
NOT Suppressor of
Statement
Reference

ninaE17 is a non-suppressor of ommatidium phenotype of Rh3Rh1+3

ninaE17/Rh3Rh1+3 is a non-suppressor of ommatidium phenotype of Arr25

ninaE17 is a non-suppressor of rhabdomere phenotype of rdgA1

Other
Additional Comments
Genetic Interactions
Statement
Reference

The loss of retinal response to light displayed by ninaE17 homozygotes and by ninaE17, norpA36 double homozygotes that also contain a copy of norpAninaE.PW is suppressed by the expression of Rh7Scer\UAS.cNa under the control of Scer\GAL4ninaE.PT.

Flies expressing norpAninaE.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.

Retinal degeneration and light-response defects are strongly suppressed in ninaEP37H, ninaE17, bsk1/+ flies.

Retinal degeneration and light-response defects are strongly suppressed in ninaEP37H, ninaE17, Traf4ex1/+ flies.

Retinal degeneration and light-response defects are strongly suppressed in ninaEP37H, ninaE17, Ark82/+ flies.

Retinal degeneration and light-response defects are strongly suppressed in ninaEP37H, ninaE17, Nc51/+ flies.

ninaEP37H, ninaE17, Whid-A206/+ flies exhibit strong recovery of visual response to light stimulation.

ninaEP37H, ninaE17, IceΔ1/+ flies show dramatic suppression of retinal degeneration and strong recovery of visual response to light stimulation.

Vps261 ninaE17 double mutants display significant suppression of the ERG and photoreceptor cell defects seen in Vps261 single mutant flies that have been kept in a 12-hour Light/Dark cycle for 4 days.

The presence of ninaE17/+ rescues the photoreceptor degeneration phenotype seen in Fatpk10307 clones in the retina.

The progression of retinal degeneration seen in mosaic animals containing homozygous Dbp21E21 eyes is not altered if the flies are also homozygous for ninaE17.

Expression of Gα49BQ203L.Scer\UAS.cPa under the control of Scer\GAL4unspecified does not rescue the rhabdomere morphogenesis defects of ninaE17 flies.

Expression of 5-HT2DCIII.Scer\UAS under the control of Scer\GAL4ninaE.PT does not rescue the ability of ninaE17 larvae to strongly discriminate between 18[o]C and 24[o]C in a binary choice thermotaxis assay.

Rh3ninaE.P fails to rescue the impaired ability of ninaE17 larvae to discriminate between 18[o]C and 24[o]C in a binary choice thermotaxis assay.

Expression of either Rh2ninaE.P, Rh4ninaE.P, Rh5ninaE.PC or Rh5ninaE.PC rescues the ability of ninaE17 larvae to strongly discriminate between 18[o]C and 24[o]C in a binary choice thermotaxis assay.

The degeneration of the rhabdomeres that is seen in 3 day old ninaE17 adults is suppressed if they are doubly mutant with ninaD1.

ninaE17 cryb double mutants need more days to adapt to a new phase of green light (472-603nm) and Y-FL (475-724nm) compared to cryb single mutants.

The retrainment of ninaE17 Rh61 cryb to 6 hour delayed green light (472-603nm) and Y-FL (475-724nm) is significantly slower than that of ninaE17 cryb mutants. Indeed some flies do not adapt to the new photoperiod within 7 days.

Reduced ninaE dosage in ninaE17 heterozygotes fails to protect the outer photoreceptor cells from Scer\GAL4ninaE.PT-p53Scer\UAS.cJa-induced killing.

Reduced ninaE dosage in ninaE17 heterozygotes suppresses the ninaAE110V/+ protective effect in photoreceptor cells submitted to Scer\GAL4ninaE.PT-p53Scer\UAS.cJa-induced killing.

Expression of CDaseScer\UAS.cAa under the control of Scer\GAL4unspecified in the fat body enhances the turnover of involuting rhabdomeric elements in ninaE17 mutants.

Rh3Rh1+3, ninaE17 flies exhibit a shift in the point of equiluminance such that, compared with wild-type flies much less blue light is required to balace the standard green intensity, giving a blue/green ratio of 0.017 compared with 0.40 for wild-type flies.

The retinal degeneration phenotype of rdgA1 flies is not suppressed by ninaE17.

CDaseScer\UAS.cAa (driven by Scer\GAL4GMR.PF) enhances the rhabdomere phenotype seen in ninaE17 animals. Very few rhabdomeric elements remain at the apical surface of the photoreceptors in three day old animals of this genotype. Most of the rhabdomeric membranes are internalised and are in the process of being cleared. When CDaseScer\UAS.cAa is driven by Scer\GAL4hs.PB and expressed in ninaE17 flies (under heat shock) just after eclosion, most of the rhabdomere is cleared from the apical region, unlike the phenotype seen in ninaE17 animals alone.

norpA36 ; ninaE17/+ flies that carry norpAninaE.PM have a robust response to light at both 350nm and 520nm (measured using an electroretinogram (ERG) recording). norpA36 ; ninaE17/ninaE17 flies that carry norpAninaE.PM have no response to light at both 350nm and 520nm (measured using an ERG recording). Introduction of Lpol\Ops1ninaE.PK or Lpol\Ops1ninaE.T:Btau\1D4 into a norpA36 ; ninaE17/ninaE17 ; norpAninaE.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\Ops1ninaE.PK in a ninaE17 Gα49B1 background show no response to light (measured using an ERG recording). Flies expressing Lpol\Ops1ninaE.T:Btau\1D4 in a ninaE17 Gα49B1 background show no response to light (measured using an ERG recording). Flies expressing Lpol\Ops1ninaE.PK in a ninaE17 norpA36 background show no response to light (measured using an ERG recording). Flies expressing Lpol\Ops1ninaE.T:Btau\1D4 in a ninaE17 norpA36 background show no response to light (measured using an ERG recording).

Expression of Rac1V12.C.Scer\UAS under the control of Scer\GAL4hs.PB during rhabdomere morphogenesis substantially rescues rhabdomere morphogenesis in ninaE17 mutants. Occasional loops of rhabdomere membrane are seen intruded into the photoreceptor, but most terminate at a well-defined base. The rhabdomere terminal web (RTW) is more tightly organised. Substantial rescue is seen 5 days after eclosion. About 18% of R1-R6 rhabdomeres are rescued in non-heat shocked animals, rising to 90% in animals heat shocked at 80% of pupal development.

The light response in the ERG is completely restored if the flies are carrying either Rh5ninaE.PC or Rh6ninaE.PS.

Expression of Rh5ninaE.PC restores normal light response, ERGs display a robust response to light with normal on and off transients and a maintained depolarisation with a large amplitude.

Double mutants, for ninaA3 and ninaE17, which also contain Rh2ninaE.P, still display dramatic accumulations of ER membranes in photoreceptors R1-R6.

Xenogenetic Interactions
Statement
Reference

Expression of Mmus\Opn4ninaE.PS partially suppresses the reduced rhabdomere size observed in ninaE17 mutants, although the rhabdomeres also show deformed structure, and abnormal actin localization, as compared to wild type. Flies expressing Mmus\Opn4ninaE.PS in a ninaE17 background also exhibit defects in photoreceptor light induced currents, with reduced sensitivity to light stimuli, and abnormal continuous production of quantum bump-like unitary currents, as compared to wild type.

Expression of Amel\VP-blueninaE.PT, Btau\RHOninaE.PA or Lpol\Ops1ninaE.PK rescues the rhabdomere morphogenesis defects of ninaE17 flies.

Expression of Hsap\OPN4Scer\UAS.T:Zzzz\His6 partially rescues the rhabdomere morphogenesis defects of ninaE17 flies.

Expression of Mmus\Opn4ninaE.PS rescues the ability of ninaE17 larvae to strongly discriminate between 18[o]C and 24[o]C in a binary choice thermotaxis assay.

Btau\RHOninaE.PA is able to partially rescue the rhabdomere defects of ninaE17 flies. At 3 days of age, rhabdomere size is largely rescued, although they are smaller and slightly irregular in shape compared to wild type. At 7 days, more substantial defects in rhabdomere packing are seen in the rescued flies, and at 14 days the rhabdomere membranes are extensively unraveled. The unraveling phenotype is seen in 14 day old rescued flies raised both under light-dark conditions and raised under constant darkness.

Expression of either ninaE::Btau\RHORHOC2.ninaE or ninaE::Btau\RHORHOC3.ninaErescues the rhabdomere defects of ninaE17 flies. The rescued flies show excellent rhabdomere morphology at 7 days after eclosion and ommatidial structure remains intact in 14 day old flies.

7 day old ninaE17 flies expressing ninaE::Btau\RHORHOCt.ninaE have reduced rhabdomeres that are irregular in shape compared to wild type. At 14 days after eclosion, some photoreceptors lacking a visible rhabdomere are observed.

Rhabdomere structure is improved in 7 and 14 day old ninaE17 flies expressing ninaE::Btau\RHORh1Ct.ninaE compared to 7 and 14 day old ninaE17 flies expressing Btau\RHOninaE.PA.

Sgre\Ops2ninaE.PE suppresses the electroretinogram defects of ninaE17 flies; 'on' and 'off' transients are restored.

Visual defect can be rescued by expression of Amel\VP-blueninaE.PT or Amel\VP-UVninaE.PT.

Complementation and Rescue Data
Partially rescued by

ninaE17 is partially rescued by ninaED96N

ninaE17 is partially rescued by ninaEAAXXA

Not rescued by
Partially rescues
Comments

ninaEninaE.T:Zzzz\SBP largely rescues the electroretinogram defects of ninaE17 flies; the on and off transients are restored.

ninaEAAXXA significantly rescues the collapsing of the closely apposed membrane inside the cells that is seen in ninaE17 photoreceptors. However, there are numerous vesicles occupying the sub-rhabdomeric space.

Expression of ninaEScer\UAS.cSa under the control of either Scer\GAL4ninaE.PT or Scer\GAL4TrpA1.PR rescues the thermotaxis behaviour of ninaE17 larvae, such that the rescued larvae strongly prefer 18[o]C over 24[o]C in a binary choice thermotaxis assay.

ninaE17/+ or ninaE17/ninaE17 largely rescues the retinal degeneration and photoreceptor loss, and partially rescues the phototaxis defects seen in flies expressing ninaEP37H.

Expression of ninaET:Zzzz\His6 in ninaE17 flies restores normal visual physiology.

Images (0)
Mutant
Wild-type
Stocks (12)
Notes on Origin
Discoverer

O'Tousa.

Comments
Comments

The basic expression and daily oscillation pattern of per protein in light-dark cycles is normal in ninaE17 mutant flies.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (25)
Reported As
Symbol Synonym
Df(3R)I17e
Df(3R)oraI17
NinaEI17
ninaEEl17
ninaEO117
Name Synonyms
Secondary FlyBase IDs
    References (117)