BIOL 4380 Lecture Notes - Lecture 8: Rhodopsin Kinase, Transducin, Rhodopsin
Feb 15th
• Recap: unusual feature in the responses of the photoreceptors to signals, namely the response
is ot like the typial AP. rather, it’s graded. Ulike i euros, istead of depol, e hae hypol.
• In the dark, conc of GMP is high, GMP haels o the surfae of the rod is ope → depol. I
light these haels are losed → hyperpol.
• Which ion flow acts to depolarize and hyperpolarize the cell?
o Na+ (cGMP channels) causes depolarization, K+ channels responsible for
hyperpolarization. The two are antagonizing one another.
• In light, hyperpolarization K+ channel becomes dominant.
• Molecular steps in the cGMP concentration changes: the mechanism determines the extreme
sensitivity of our rod cell based vision.
o Double bod i the is retial → asors photo → tras oforatio → oforatio
of rhodopsin channel which results in activation of transducin. Transducin is a GPCR,
activated when rhodopsin has changed conformation.
o Trasdui → atiates PDE hih is a ezyme that hydrolyzes cGMP), the more
active PDE the more it will hydrolyze cGMP< theless cGMP available in the rod. The less
active the cGMP gated Ca2+ will become.
o One single photon of light, will change conformation in a single rhodopsin molecule and
that single photon will activate 800 transducins (1/10th of the entire transducins in a
gie rod ell → trasdui atiates PDE : → eery sigle PDE a hydrolyze 6
GMP 6 GMP/PDE, hydrolyzatio = deatiatio → deatiates io haels
(which is 2% of total) and is = to reducing potential by 1 mV.
• What is the mechanism behind terminating the phototransduction chain?
o Activated rhodopsin is phosphorylated by rhodopsin kinase, and this phosphorylated
rhodopsin can now bind arrestin, phosphorylated rhodopsin with arrestin can no longer
activate transducin, and therefore, no longer activate PDE.
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