- THIS ARTICLE
- Full Text (PDF)
- Alert me when this article is cited
- Alert me if a correction is posted
- SERVICES
- Similar articles in this journal
- Similar articles in PubMed
- Alert me to new issues of the journal
- Download to citation manager
- Reprints & Permissions
- CITING ARTICLES
- Citing Articles via HighWire
- Citing Articles via Google Scholar
- GOOGLE SCHOLAR
- Articles by Zars, T.
- Articles by Hyde, D. R.
- Search for Related Content
- PUBMED
- PubMed Citation
- Articles by Zars, T.
- Articles by Hyde, D. R.
Genetics, Vol 144, 127-138, Copyright © 1996
INVESTIGATIONS |
rdgE: A Novel Retinal Degeneration Mutation in Drosophila melanogaster
T. Zars and D. R. Hyde
Department of Biological Sciences, University of Notre Dame, Notre Dame, Indiana 46556
We report isolating the Drosophila retinal degeneration E (rdgE) mutation. The hypomorphic rdgE(1) allele causes rapid photoreceptor degeneration in light and a slower rate of degeneration when the flies are raised in constant darkness. The rdgE(1) flies exhibited an electrophysiological light response that decreased with age, coinciding with the degeneration. This suggests that degeneration caused the loss of the light response. We determined that the ninaE (rhodopsin) mutation, but not norpA [phospholipase C (PLC)], slowed the rdgE-dependent degeneration. This was consistent with the light-enhanced degeneration, but revealed that the degeneration is independent of the PLC-mediated phototransduction cascade. Transmission electron microscopy revealed that rdgE(1) photoreceptors exhibited a number of vesicular transport defects including unpacking/vesiculation of rhabdomeres, endocytosis of novel vesicles by photoreceptors, a buildup of very large multivesicular bodies, and an increased amount of rough endoplasmic reticulum. We determined that the rdgE null phenotype is a late embryonic lethality. Therefore, rdgE(+) is required in cells outside of the retina, quite possibly in a large number of neurons. Thus, rdgE may define a mutational class that exhibits both light-enhanced retinal degeneration and a recessive null lethality by perturbing neuronal membrane biosynthesis and/or recycling.
This article has been cited by other articles:
 |
|
 |
|
  C. Lu, T. S. Vihtelic, D. R. Hyde, and T. Li A Neuronal-specific Mammalian Homolog of the Drosophila Retinal Degeneration B Gene with Expression Restricted to the Retina and Dentate Gyrus J. Neurosci., September 1, 1999; 19(17): 7317 - 7325. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 D. W. Paetkau, V. A. Elagin, L. M. Sendi, and D. R. Hyde Isolation and Characterization of Drosophila retinal degeneration B Suppressors Genetics, February 1, 1999; 151(2): 713 - 724. [Abstract] [Full Text]
|
|
|
|
 |
|
 S. C. Milligan, J. G. Alb Jr., R. B. Elagina, V. A. Bankaitis, and D. R. Hyde The Phosphatidylinositol Transfer Protein Domain of Drosophila Retinal Degeneration B Protein Is Essential for Photoreceptor Cell Survival and Recovery from Light Stimulation J. Cell Biol., October 20, 1997; 139(2): 351 - 363. [Abstract] [Full Text] [PDF]
|
|