期刊
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
卷 114, 期 45, 页码 E9675-E9684出版社
NATL ACAD SCIENCES
DOI: 10.1073/pnas.1712405114
关键词
PP2A; photoreceptors; GPCRs; visual cycle; dark adaptation
资金
- NIH [EY026675, EY019312, EY02687]
- Research to Prevent Blindness
- Swiss National Science Foundation Doc.Mobility Fellowship [P1SKP3_158634]
- Swiss National Science Foundation (SNF) [P1SKP3_158634] Funding Source: Swiss National Science Foundation (SNF)
Resetting of G-protein-coupled receptors (GPCRs) from their active state back to their biologically inert ground state is an integral part of GPCR signaling. This on-off GPCR cycle is regulated by reversible phosphorylation. Retinal rod and cone photoreceptors arguably represent the best-understood example of such GPCR signaling. Their visual pigments (opsins) are activated by light, transduce the signal, and are then inactivated by a GPCR kinase and arrestin. Although pigment inactivation by phosphorylation is well understood, the enzyme(s) responsible for pigment dephosphorylation and the functional significance of this reaction remain unknown. Here, we show that protein phosphatase 2A (PP2A) acts as opsin phosphatase in both rods and cones. Elimination of PP2A substantially slows pigment dephosphorylation, visual chromophore recycling, and ultimately photoreceptor dark adaptation. These findings demonstrate that visual pigment dephosphorylation regulates the dark adaptation of photoreceptors and provide insights into the role of this reaction in GPCR signaling.
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