Abstract
The neuronal Ca2+-binding protein Recoverin has been shown to regulate phototransduction termination in mammalian rods. Here we identify four recoverin genes in the zebrafish genome, rcv1a, rcv1b, rcv2a and rcv2b, and investigate their role in modulating the cone phototransduction cascade. While Recoverin-1b is only found in the adult retina, the other Recoverins are expressed throughout development in all four cone types, except Recoverin-1a, which is expressed only in rods and UV cones. Applying a double flash electroretinogram (ERG) paradigm, downregulation of Recoverin-2a or 2b accelerates cone photoresponse recovery, albeit at different light intensities. Exclusive recording from UV cones via spectral ERG reveals that knockdown of Recoverin-1a alone has no effect, but Recoverin-1a/2a double-knockdowns showed an even shorter recovery time than Recoverin-2a-deficient larvae. We also showed that UV cone photoresponse kinetics depend on Recoverin-2a function via cone-specific kinase Grk7a. This is the first in vivo study demonstrating that cone opsin deactivation kinetics determine overall photoresponse shut off kinetics.
Highlights
The vertebrate retina contains two classes of photoreceptors, rods and cones, which function at low and bright light conditions, respectively
In order to explore the role of Recoverins (Rcvs) in the termination of the visual transduction cascade, we cloned four zebrafish recoverin orthologues, namely rcv1a, rcv1b, rcv2a and rcv2b
Rhodopsin quenching requires the phosphorylation by rhodopsin kinase [6,32] and subsequent binding of Arrestin [33]
Summary
The vertebrate retina contains two classes of photoreceptors, rods and cones, which function at low and bright light conditions, respectively Both share a similar G-protein-coupled phototransduction pathway, the cone photoresponse is characterized by lower sensitivity and faster kinetics, which allows cones to function over almost 9 orders of illumination magnitude [1]. The Transducin a-subunit in turn binds to phosphodiesterase (PDE), causing a decrease in the second messenger cGMP This drop in cGMP levels leads to the closure of CNG cation channels, hyperpolarizing the photoreceptor and lowering [Ca2þ]i [5]. The deactivation of both Rh* and the PDE–Transducin complex is required to terminate the phototransduction cascade. The final deactivation of Rh* is achieved by the binding of Arrestin [12], while intrinsic GTPase activity ends the ability of PDE–Transducin complex to hydrolyse cGMP [13]
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