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RNA editing of the serotonin 2C receptor and expression of Gα q protein: genetic mouse models do not support a role for regulation or compensation
Author(s) -
Canal Clinton E.,
Mahautmr Kontip C.,
Cao Chike,
SandersBush Elaine,
Airey David C.
Publication year - 2009
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.2008.05852.x
Subject(s) - biology , rna editing , gene isoform , messenger rna , receptor , rna , 5 ht5a receptor , microbiology and biotechnology , gene expression , transgene , gene , genetics
The serotonin 2C (5‐HT 2C ) receptor undergoes RNA editing at five bases in a region of the pre‐mRNA encoding the second intracellular loop, generating many unique 5‐HT 2C receptor isoforms. Mechanisms regulating in vivo expression of different edited 5‐HT 2C receptor isoforms are poorly understood, as are the adaptive consequences of variation in editing profiles. Recent findings suggest a putative relationship between expression levels of Gα q/11 protein and the degree of editing of 5‐HT 2C receptor transcripts. To elucidate the potential regulatory or adaptive role of Gα q/11 protein levels, we quantified editing of 5‐HT 2C receptor RNA transcripts in Gα q null mice and protein levels of Gα q and Gα 11 in transgenic male mice solely expressing either the non‐edited (INI) or the fully edited (VGV) isoforms of the 5‐HT 2C receptor. Pyrosequencing of RNA isolated from amygdaloid cortex in Gα q null and wild‐type mice revealed no significant differences in 5‐HT 2C receptor mRNA editing profiles. Cortical tissue from INI/y, VGV/y, and wild‐type mice was assayed for expression of Gα q and Gα 11 subunits by Western blotting. No differences in signal density between wild‐type and INI/y or VGV/y groups were found, indicating equivalent levels of Gα q and Gα 11 protein. Together, these data do not support a causal or compensatory relationship between 5‐HT 2C receptor RNA editing and G q protein levels.