Transgenic mice provide a powerful tool for elucidating the molecular
mechanisms of phototransduction. Mice expressing a phosphorylation-def
icient rhodopsin and mice deficient in arrestin are being used to stud
y shutoff of photoactivated rhodopsin. These in vivo mouse studies ind
icate that shutoff is partially mediated by rhodopsin phosphorylation
alone, but complete deactivation on a physiological time scale require
s arrestin. Work on other transgenic mutant mice to unravel the functi
on of recoverin and phosducin and to further define the role of the ga
mma subunit of phosphodiesterase is in progress. Transgenic mice are a
lso being used to investigate how mutant proteins give rise to retinal
disease and to develop therapeutic interventions.