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Gene Review

ninaE  -  neither inactivation nor afterpotential E

Drosophila melanogaster

Synonyms: 143283_at, 1F9, BEST:GH11778, CG4550, DMELRH1, ...
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Disease relevance of ninaE

  • The Drosophila Rh1 rhodopsin gene was the first gene shown to cause retinal degeneration when mutated [1].
  • Rhodopsin formation in Drosophila is dependent on the PINTA retinoid-binding protein [2].
  • Some of these dominant rod opsin mutant proteins, which desensitize transgenic Xenopus rods, provide an animal model for congenital night blindness [3].
  • Expression of the E. coli genes was then used to assay the ability of various sequences from the ninaE gene to confer the ninaE pattern of expression [4].
  • rhodopsin mutations result in autosomal dominant retinitis pigmentosa (ADRP), the most frequent being Proline-23 substitution by histidine (RhoP23H) [5].

High impact information on ninaE

  • Homothorax increases rhabdomere size and uncouples R7-R8 communication to allow both cells to express the same opsin rather than different ones as required for color vision [6].
  • The Rhesus blood-group antigens are defined by a complex association of membrane polypeptides that includes the non-glycosylated Rh proteins (RhD and RhCE) and the RHag glycoprotein, which is strictly required for cell surface expression of these antigens [7].
  • Despite their importance in transfusion medicine, the function of RhAG and Rh proteins remains unknown, except that their absence in Rh(null) individuals leads to morphological and functional abnormalities of erythrocytes, known as the Rh-deficiency syndrome [7].
  • The theory quantitatively describes the inactivation kinetics of activated rhodopsin in vivo and can be independently tested with molecular and spectroscopic data [8].
  • We now show that mutations in the ninaA gene severely inhibit opsin transport from the ER, leading to dramatic accumulations of ER cisternae in the photoreceptor cells [9].

Chemical compound and disease context of ninaE


Biological context of ninaE

  • We have used P-element-mediated transformation to introduce the cloned Rh1 rhodopsin gene into the germ line of Drosophila and fully rescue the visual phenotype of mutant ninaE flies [11].
  • This opsin gene contains no introns and encodes a 383 amino acid polypeptide that is approximately 35% homologous to the blue absorbing ninaE and Rh2 opsins, which are expressed in photoreceptor cells R1-6 and R8, respectively [12].
  • We have determined the DNA sequence of the Rh2 promoter from -448 to +32 and have found an 11-bp sequence which is also present in the upstream flanking sequences of two other photoreceptor-specific genes (ninaE and ninaC) [13].
  • In Drosophila, the major rhodopsin Rh1 is synthesized in endoplasmic reticulum (ER)-bound ribosomes of the R1-R6 photoreceptor cells and is then transported to the rhabdomeres where it functions in phototransduction [9].
  • Arrestin1 mediates light-dependent rhodopsin endocytosis and cell survival [14].

Anatomical context of ninaE

  • Null mutations of the Drosophila Rh1 rhodopsin gene, ninaE, result in developmental defects in the photosensitive membranes, the rhabdomeres, of compound eye photoreceptors R1-R6 [15].
  • In ninaE null mutants, these catacombs do not form and developing rhabdomere membrane involutes into the cell as curtains of apposed plasma membrane [15].
  • Intriguingly, we have found a third isoform, dgqC, which is specifically and abundantly expressed in male gonads, and shares the divergent rhodopsin-binding exon of dgqA [16].
  • Rh1 rhodopsin localizes to and is essential for the development and maintenance of the rhabdomere, the specialized membrane-rich organelle that serves as the site of phototransduction [17].
  • It is hypothesized that (1) this accumulation of membranes may be caused by the failure of newly synthesized membranes that are inserted into the base of microvilli to be assembled into R1-6 rhabdomeres and (2) this failure may be caused by the extremely low concentration of normal R1-6 rhodopsin in the ninaE mutants [18].

Associations of ninaE with chemical compounds


Physical interactions of ninaE

  • These results establish a role for Rab11 in the post-Golgi transport of rhodopsin and of other proteins to the rhabdomeric membranes of photoreceptors, and in analogous transport processes in other cells [23].

Co-localisations of ninaE


Regulatory relationships of ninaE


Other interactions of ninaE

  • We found that, in contrast, opsin Rh2 is the predominant opsin expressed in the ocelli [25].
  • Moreover, a detailed noise analysis shows that photoreceptor responses of both a ninaE mutant and a ninaD mutant follow the adapting bump model [26].
  • Numerous changes have occurred in these genes since the duplications, including the loss and/or gain of introns in the different genes and even within the Rh1 and Rh4 clades [27].
  • In addition, we show that two mutants that specifically affect the R1-R6 cells, ninaA and rdgB, do not directly affect expression of the ninaE gene [11].
  • RESULTS: We show, for the first time, that visual pigment appears pink in white light, especially for Rh1 and Rh6 [28].

Analytical, diagnostic and therapeutic context of ninaE

  • We have used in situ hybridization to study the messenger RNAs expressed by these four opsin genes in all three visual organs [25].
  • Novel Gq alpha isoform is a candidate transducer of rhodopsin signaling in a Drosophila testes-autonomous pacemaker [16].
  • The sequence alignment of Lo1 reveals significant homology to mantid opsin [29].
  • Recovery of Rh1 protein upon such carotenoid replacement followed, barely detectable on Western blots at 4 hr but conspicuous by 8 hr [30].
  • Northern blots on Drosophila heads showed that mRNA of Rh1 (the predominant rhodopsin) was high in vitamin A replete controls, very low in deprived flies, and increased upon feeding carrot juice to deprived flies as early as 1 hr [30].


  1. Rhodopsin mutations as the cause of retinal degeneration. Classification of degeneration phenotypes in the model system Drosophila melanogaster. Bentrop, J. Acta anatomica. (1998) [Pubmed]
  2. Rhodopsin formation in Drosophila is dependent on the PINTA retinoid-binding protein. Wang, T., Montell, C. J. Neurosci. (2005) [Pubmed]
  3. Novel dominant rhodopsin mutation triggers two mechanisms of retinal degeneration and photoreceptor desensitization. Iakhine, R., Chorna-Ornan, I., Zars, T., Elia, N., Cheng, Y., Selinger, Z., Minke, B., Hyde, D.R. J. Neurosci. (2004) [Pubmed]
  4. Analysis of the promoter of the ninaE opsin gene in Drosophila melanogaster. Mismer, D., Rubin, G.M. Genetics (1987) [Pubmed]
  5. Rhodopsin maturation defects induce photoreceptor death by apoptosis: a fly model for RhodopsinPro23His human retinitis pigmentosa. Galy, A., Roux, M.J., Sahel, J.A., Léveillard, T., Giangrande, A. Hum. Mol. Genet. (2005) [Pubmed]
  6. Homothorax switches function of Drosophila photoreceptors from color to polarized light sensors. Wernet, M.F., Labhart, T., Baumann, F., Mazzoni, E.O., Pichaud, F., Desplan, C. Cell (2003) [Pubmed]
  7. The human Rhesus-associated RhAG protein and a kidney homologue promote ammonium transport in yeast. Marini, A.M., Matassi, G., Raynal, V., André, B., Cartron, J.P., Chérif-Zahar, B. Nat. Genet. (2000) [Pubmed]
  8. Arrestin binding determines the rate of inactivation of the G protein-coupled receptor rhodopsin in vivo. Ranganathan, R., Stevens, C.F. Cell (1995) [Pubmed]
  9. The cyclophilin homolog ninaA is required in the secretory pathway. Colley, N.J., Baker, E.K., Stamnes, M.A., Zuker, C.S. Cell (1991) [Pubmed]
  10. Cellular effects of olomoucine, an inhibitor of cyclin-dependent kinases. Abraham, R.T., Acquarone, M., Andersen, A., Asensi, A., Bellé, R., Berger, F., Bergounioux, C., Brunn, G., Buquet-Fagot, C., Fagot, D. Biol. Cell (1995) [Pubmed]
  11. Ectopic expression of a minor Drosophila opsin in the major photoreceptor cell class: distinguishing the role of primary receptor and cellular context. Zuker, C.S., Mismer, D., Hardy, R., Rubin, G.M. Cell (1988) [Pubmed]
  12. A rhodopsin gene expressed in photoreceptor cell R7 of the Drosophila eye: homologies with other signal-transducing molecules. Zuker, C.S., Montell, C., Jones, K., Laverty, T., Rubin, G.M. J. Neurosci. (1987) [Pubmed]
  13. Analysis of the promoter of the Rh2 opsin gene in Drosophila melanogaster. Mismer, D., Michael, W.M., Laverty, T.R., Rubin, G.M. Genetics (1988) [Pubmed]
  14. Arrestin1 mediates light-dependent rhodopsin endocytosis and cell survival. Satoh, A.K., Ready, D.F. Curr. Biol. (2005) [Pubmed]
  15. Rhodopsin plays an essential structural role in Drosophila photoreceptor development. Kumar, J.P., Ready, D.F. Development (1995) [Pubmed]
  16. Novel Gq alpha isoform is a candidate transducer of rhodopsin signaling in a Drosophila testes-autonomous pacemaker. Alvarez, C.E., Robison, K., Gilbert, W. Proc. Natl. Acad. Sci. U.S.A. (1996) [Pubmed]
  17. The Drosophila rhodopsin cytoplasmic tail domain is required for maintenance of rhabdomere structure. Ahmad, S.T., Natochin, M., Artemyev, N.O., O'Tousa, J.E. FASEB J. (2007) [Pubmed]
  18. Degeneration of photoreceptors in rhodopsin mutants of Drosophila. Leonard, D.S., Bowman, V.D., Ready, D.F., Pak, W.L. J. Neurobiol. (1992) [Pubmed]
  19. Receptor demise from alteration of glycosylation site in Drosophila opsin: electrophysiology, microspectrophotometry, and electron microscopy. Brown, G., Chen, D.M., Christianson, J.S., Lee, R., Stark, W.S. Vis. Neurosci. (1994) [Pubmed]
  20. Nonsense suppression of the major rhodopsin gene of Drosophila. Washburn, T., O'Tousa, J.E. Genetics (1992) [Pubmed]
  21. Rescue of photoreceptor degeneration in rhodopsin-null Drosophila mutants by activated Rac1. Chang, H.Y., Ready, D.F. Science (2000) [Pubmed]
  22. Maturation of major Drosophila rhodopsin, ninaE, requires chromophore 3-hydroxyretinal. Ozaki, K., Nagatani, H., Ozaki, M., Tokunaga, F. Neuron (1993) [Pubmed]
  23. Rab11 mediates post-Golgi trafficking of rhodopsin to the photosensitive apical membrane of Drosophila photoreceptors. Satoh, A.K., O'Tousa, J.E., Ozaki, K., Ready, D.F. Development (2005) [Pubmed]
  24. Direct regulation of rhodopsin 1 by Pax-6/eyeless in Drosophila: evidence for a conserved function in photoreceptors. Sheng, G., Thouvenot, E., Schmucker, D., Wilson, D.S., Desplan, C. Genes Dev. (1997) [Pubmed]
  25. Transcript localization of four opsin genes in the three visual organs of Drosophila; RH2 is ocellus specific. Pollock, J.A., Benzer, S. Nature (1988) [Pubmed]
  26. Electrophysiological study of Drosophila rhodopsin mutants. Johnson, E.C., Pak, W.L. J. Gen. Physiol. (1986) [Pubmed]
  27. Phylogeny and physiology of Drosophila opsins. Carulli, J.P., Chen, D.M., Stark, W.S., Hartl, D.L. J. Mol. Evol. (1994) [Pubmed]
  28. Microscopy of multiple visual receptor types in Drosophila. Stark, W.S., Thomas, C.F. Mol. Vis. (2004) [Pubmed]
  29. Primary structure of locust opsins: a speculative model which may account for ultraviolet wavelength light detection. Towner, P., Harris, P., Wolstenholme, A.J., Hill, C., Worm, K., Gärtner, W. Vision Res. (1997) [Pubmed]
  30. Control of Drosophila opsin gene expression by carotenoids and retinoic acid: northern and western analyses. Picking, W.L., Chen, D.M., Lee, R.D., Vogt, M.E., Polizzi, J.L., Marietta, R.G., Stark, W.S. Exp. Eye Res. (1996) [Pubmed]
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