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Published 9 May 2005. doi:10.1083/jcb.200502122
The Rockefeller University Press, 0021-9525 $8.00
JCB, Volume 169, Number 3, 471-479
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Article

 Regulation of phototransduction responsiveness and retinal degeneration by a phospholipase D–generated signaling lipid

Mary M. LaLonde1,2, Hilde Janssens2, Erica Rosenbaum4,5, Seok-Yong Choi1,2, J. Peter Gergen3, Nansi J. Colley4,5, William S. Stark6, and Michael A. Frohman2

1 Program in Molecular and Cellular Biology, Center for Developmental Genetics, Stony Brook University, Stony Brook, NY 11794
2 Department of Pharmacology, Center for Developmental Genetics, Stony Brook University, Stony Brook, NY 11794
3 Department of Biochemistry, Center for Developmental Genetics, Stony Brook University, Stony Brook, NY 11794
4 Department of Ophthalmology and Visual Science, University of Wisconsin, Madison, WI 53706
5 Department of Genetics, University of Wisconsin, Madison, WI 53706
6 Department of Biology, Saint Louis University, St. Louis, MO 63103

Correspondence to Michael Frohman: michael{at}pharm.sunysb.edu

Drosophila melanogaster phototransduction proceeds via a phospholipase C (PLC)–triggered cascade of phosphatidylinositol (PI) lipid modifications, many steps of which remain undefined. We describe the involvement of the lipid phosphatidic acid and the enzyme that generates it, phospholipase D (Pld), in this process. Pldnull flies exhibit decreased light sensitivity as well as a heightened susceptibility to retinal degeneration. Pld overexpression rescues flies lacking PLC from light-induced, metarhodopsin-mediated degeneration and restores visual signaling in flies lacking the PI transfer protein, which is a key player in the replenishment of the PI 4,5-bisphosphate (PIP2) substrate used by PLC to transduce light stimuli into neurological signals. Altogether, these findings suggest that Pld facilitates phototransduction by maintaining adequate levels of PIP2 and by protecting the visual system from metarhodopsin-induced, low light degeneration.

M. LaLonde and H. Janssens contributed equally to this paper.

Abbreviations used in this paper: Arr2, arrestin2; ERG, electroretinogram; IP3, inositol 1,4,5-triphosphate; norpA, no receptor potential A; PA, phosphatidic acid; PAP, PA phosphatase; PI, phosphatidylinositol; PIP2, PI 4,5-bisphosphate; PI4P5K, PI 4-phosphate 5-kinase; Pld, phospholipase D; RdgB, retinal degeneration B; ROS, rod outer segments; SRC, subrhabdomeral cisternae; TRP, transient receptor potential.


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