a flanking gene problem leads to the discovery of a gprc5b splice variant predominantly expressed in c57bl6j mouse brain and in maturing neurons侧翼基因问题导致的发现gprc5b拼接变异主要表现在c57bl6j老鼠大脑和成熟神经元.pdfVIP

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2017-09-04 发布于上海
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a flanking gene problem leads to the discovery of a gprc5b splice variant predominantly expressed in c57bl6j mouse brain and in maturing neurons侧翼基因问题导致的发现gprc5b拼接变异主要表现在c57bl6j老鼠大脑和成熟神经元.pdf

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a flanking gene problem leads to the discovery of a gprc5b splice variant predominantly expressed in c57bl6j mouse brain and in maturing neurons侧翼基因问题导致的发现gprc5b拼接变异主要表现在c57bl6j老鼠大脑和成熟神经元

A Flanking Gene Problem Leads to the Discovery of a Gprc5b Splice Variant Predominantly Expressed in C57Bl/ 6J Mouse Brain and in Maturing Neurons 1 2 1 1 1 1 Bethany H. Cool , Guy C-K. Chan , Lin Lee , Junko Oshima , George M. Martin *, Qubai Hu * 1 Department of Pathology, University of Washington, Seattle, Washington, United States of America, 2 Department of Pharmacology, University of Washington, Seattle, Washington, United States of America Abstract Background: Gprc5b, a retinoic acid-inducible orphan G protein–coupled receptor (GPCR), is a member of the group C metabotropic glutamate receptor family proteins possibly involved in non-canonical Wnt signaling. Many GPCR transcripts are alternatively spliced, which diversifies this class of proteins in their cell- and tissue-specific signaling, regulatory and/or pharmacological properties. We previously generated p97FE65 isoform-specific knockout mice that showed learning/ memory deficits. In this study, we further characterized the 97FE65 null mice using cDNA microarray and RT-PCR analyses. Methodology/Principal Findings: We discovered a novel brain-specific C-terminal splice variant of Gprc5b, Gprc5b_v2, which was differentially expressed in p97FE65 wild type and null mouse brains. The null mice were generated in 129/Sv ES cells, and backcrossed to C57Bl/6J for ten generations. We found that expression of Gprc5b_v2 mRNA in the brains of p97FE65 null mice was dramatically down-regulated (more than 20 fold) compared to their wild type littermates. However, expression profiles of Gprc5b variants and SNP analysis surrounding the FE65 locus suggest that the down-regulation is unlikely due to the altered FE65 function, but