title: Phototransduction in transgenic mice.
abstract: Transgenic mice provide a powerful tool for elucidating the molecular mechanisms of phototransduction. Mice expressing a phosphorylation-deficient rhodopsin and mice deficient in arrestin are being used to study shutoff of photoactivated rhodopsin. These in vivo mouse studies indicate that shutoff is partially mediated by rhodopsin phosphorylation alone, but complete deactivation on a physiological time scale requires arrestin. Work on other transgenic mutant mice to unravel the function of recoverin and phosducin and to further define the role of the gamma subunit of phosphodiesterase is in progress. Transgenic mice are also being used to investigate how mutant proteins give rise to retinal disease and to develop therapeutic interventions.
authors.affiliation: Department of Ophthalmology, New England Eye Center, Tufts Medical School, 750 Washington Street, Box 450, Boston, Massachusetts 02111, USA. jlem@opal.tufts.edu
authors.forename: J
authors.initials: J
authors.lastname: Lem
authors.forename: C L
authors.initials: CL
authors.lastname: Makino
mesh_terms: D000222:Adaptation, Physiological; D000818:Animals; D015870:Gene Expression; D018014:Gene Transfer Techniques; D006801:Humans; D008027:Light; D051379:Mice; D008822:Mice, Transgenic / Q000235:genetics; D008845:Microinjections; D009154:Mutation; D012162:Retinal Degeneration / Q000235:genetics; D015398:Signal Transduction; D019076:Transgenes