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Modulating sphingolipid biosynthetic pathway rescues photoreceptor degeneration

  1. Author:
    Acharya, U.
    Patel, S.
    Koundakjian, E.
    Nagashima, K.
    Han, X.
    Acharya, J. K.

  2. Author Address

    NCI, Regulat Cell Growth Lab, Frederick, MD 21702 USA NCI, Regulat Cell Growth Lab, Frederick, MD 21702 USA Univ Calif San Diego, Howard Hughes Med Inst, La Jolla, CA 92093 USA Sci Applicat Int Corp, Electron Microscopy Facil Image Anal Lab, Frederick, MD 21702 USA Washington Univ, Sch Med, Dept Med, Div Bioorgan Chem & Mol Pharmacol, St Louis, MO 63110 USA Acharya JK NCI, Regulat Cell Growth Lab, Frederick, MD 21702 USA
    1. Year: 2003
  2. Journal: Science
    1. 299
    2. 5613
    3. Pages: 1740-1743
  4. Type of Article: Article
  1. Abstract:

    Mutations in proteins of the Drosophila phototransduction cascade, a prototypic guanine nucleotide-binding protein- coupled receptor signaling system, lead to retinal degeneration and have been used as models to understand human degenerative disorders. Here, modulating the sphingolipid biosynthetic pathway rescued retinal degeneration in Drosophila mutants. Targeted expression of Drosophila neutral ceramidase rescued retinal degeneration in arrestin and phospholipase C mutants. Decreasing flux through the de novo sphingolipid biosynthetic pathway also suppressed degeneration in these mutants. Both genetic backgrounds modulated the endocytic machinery because they suppressed defects in a dynamin mutant. Suppression of degeneration in arrestin mutant flies expressing ceramidase correlated with a decrease in ceramide levels. Thus, enzymes of sphingolipid metabolism may be suitable targets in the therapeutic management of retinal degeneration.

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