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Altered G-protein coupling in an mGluR6 point mutant associated with congenital stationary night blindness.

Abstract：

:The highly specialized metabotropic glutamate receptor type 6 (mGluR6) is postsynaptically localized and expressed only in the dendrites of ON bipolar cells. Upon activation of mGluR6 by glutamate released from photoreceptors, a nonselective cation channel is inhibited, causing these cells to hyperpolarize. Mutations in this gene have been implicated in the development of congenital stationary night blindness type 1 (CSNB1). We investigated five known mGluR6 point mutants that lead to CSNB1 to determine the molecular mechanism of each phenotype. In agreement with other studies, four mutants demonstrated trafficking impairment. However, mGluR6 E775K (E781K in humans) suggested no trafficking or signaling deficiencies measured by our initial assays. Most importantly, our results indicate a switch in G-protein coupling, in which E775K loses G(o) coupling but retains coupling to G(i), which may explain the phenotype.

journal_name

Mol Pharmacol

journal_title

Molecular pharmacology

authors

Beqollari D,Betzenhauser MJ,Kammermeier PJ

doi

10.1124/mol.109.058628

subject

Has Abstract

pub_date

2009-11-01 00:00:00

pages

992-7

issue

5

eissn

0026-895X

issn

1521-0111

pii

mol.109.058628

journal_volume

76

pub_type

杂志文章

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