G Protein-Coupled Receptor Genes in the FANTOM2 Database

  1. Yuka Kawasawa1,6,
  2. Louise M. McKenzie2,
  3. David P. Hill2,
  4. Hidemasa Bono3,
  5. RIKEN GER Group3,
  6. GSL Members 4,5, and
  7. Masashi Yanagisawa1
  1. 1Howard Hughes Medical Institute, Department of Molecular Genetics, University of Texas Southwestern Medical Center at Dallas, Dallas, Texas 75390-9050, USA
  2. 2The Jackson Laboratory, Bar Harbor, Maine 04609, USA
  3. 3Laboratory for Genome Exploration Research Group, RIKEN Genomic Sciences Center (GSC), RIKEN Yokohama Institute, Suehiro-cho, Tsurumi-ku, Yokohama, Kanagawa 230-0045, Japan
  4. 4Genome Science Laboratory, RIKEN, Hirosawa, Wako, Saitama 351-0198, Japan

Abstract

G protein-coupled receptors (GPCRs) comprise the largest family of receptor proteins in mammals and play important roles in many physiological and pathological processes. Gene expression of GPCRs is temporally and spatially regulated, and many splicing variants are also described. In many instances, different expression profiles of GPCR gene are accountable for the changes of its biological function. Therefore, it is intriguing to assess the complexity of the transcriptome of GPCRs in various mammalian organs. In this study, we took advantage of the FANTOM2 (Functional Annotation Meeting of Mouse cDNA 2) project, which aimed to collect full-length cDNAs inclusively from mouse tissues, and found 410 candidate GPCR cDNAs. Clustering of these clones into transcriptional units (TUs) reduced this number to 213. Out of these, 165 genes were represented within the known 308 GPCRs in the Mouse Genome Informatics (MGI) resource. The remaining 48 genes were new to mouse, and 14 of them had no clear mammalian ortholog. To dissect the detailed characteristics of each transcript, tissue distribution pattern and alternative splicing were also ascertained. We found many splicing variants of GPCRs that may have a relevance to disease occurrence. In addition, the difficulty in cloning tissue-specific and infrequently transcribed GPCRs is discussed further.

Footnotes

  • [Supplemental material is available online at www.genome.org.]

  • Article and publication are at http://www.genome.org/cgi/doi/10.1101/gr.1087603.

  • 6 Corresponding author. E-MAIL Yuka.Kawasawa{at}UTSouthwestern.edu; FAX (214) 648-5068.

  • 5 Takahiro Arakawa, Piero Carninci, Jun Kawai, and Yoshihide Hayashizaki.

    • Accepted March 12, 2003.
    • Received December 17, 2002.
| Table of Contents

Preprint Server