TY - JOUR
T1 - Background light produces a recoverin-dependent modulation of activated-rhodopsin lifetime in mouse rods
AU - Chen, Ching Kang
AU - Woodruff, Michael L.
AU - Chen, Frank S.
AU - Chen, Desheng
AU - Fain, Gordon L.
PY - 2010/1/27
Y1 - 2010/1/27
N2 - The Ca2+-binding protein recoverin is thought to regulate rhodopsin kinase and to modulate the lifetime of the photoexcited state of rhodopsin (Rh*), the visual pigment of vertebrate rods. Recoverin has been postulated to inhibit the kinase in darkness, when Ca2+ is high, and to be released from the disk membrane in light when Ca2+ is low, accelerating rhodopsin phosphorylation and shortening the lifetime of Rh*. This proposal has remained controversial, in part because the normally rapid turnoff of Rh* has made Rh* modulation difficult to study in an intact rod. To circumvent this problem, we have made mice that underexpress rhodopsin kinase so that Rh* turnoff is rate limiting for the decay of the rod light response. We show that background light speeds the decay of Rh* turnoff, and that this no longer occurs in mice that have had recoverin knocked out. This is the first demonstration in an intact rod that light accelerates Rh* inactivation and that the Ca2+-binding protein recoverin may be required for the light-dependent modulation of Rh* lifetime. Copyright
AB - The Ca2+-binding protein recoverin is thought to regulate rhodopsin kinase and to modulate the lifetime of the photoexcited state of rhodopsin (Rh*), the visual pigment of vertebrate rods. Recoverin has been postulated to inhibit the kinase in darkness, when Ca2+ is high, and to be released from the disk membrane in light when Ca2+ is low, accelerating rhodopsin phosphorylation and shortening the lifetime of Rh*. This proposal has remained controversial, in part because the normally rapid turnoff of Rh* has made Rh* modulation difficult to study in an intact rod. To circumvent this problem, we have made mice that underexpress rhodopsin kinase so that Rh* turnoff is rate limiting for the decay of the rod light response. We show that background light speeds the decay of Rh* turnoff, and that this no longer occurs in mice that have had recoverin knocked out. This is the first demonstration in an intact rod that light accelerates Rh* inactivation and that the Ca2+-binding protein recoverin may be required for the light-dependent modulation of Rh* lifetime. Copyright
UR - https://www.scopus.com/pages/publications/75349111124
UR - https://www.scopus.com/pages/publications/75349111124#tab=citedBy
U2 - 10.1523/JNEUROSCI.4353-09.2010
DO - 10.1523/JNEUROSCI.4353-09.2010
M3 - Article
C2 - 20107049
AN - SCOPUS:75349111124
SN - 0270-6474
VL - 30
SP - 1213
EP - 1220
JO - Journal of Neuroscience
JF - Journal of Neuroscience
IS - 4
ER -