L De Moerlooze, J Williamson, F Liners, J Perret, M Parmentier
{"title":"Cloning and chromosomal mapping of the mouse and human genes encoding the orphan glucocorticoid-induced receptor (GPR83).","authors":"L De Moerlooze, J Williamson, F Liners, J Perret, M Parmentier","doi":"10.1159/000015650","DOIUrl":null,"url":null,"abstract":"<p><p>The mouse glucocorticoid-induced receptor (GIR) is an orphan G protein-coupled receptor highly expressed in brain and thymus (Harrigan et al., 1989; 1991). We have cloned the mouse GIR gene (Gpr83), determined its genomic organization and compared it with the human gene. The genomic organization of the gene is similar in both species although differences leading to specific splicing variants in the mouse have been found. Three introns interrupting the coding sequence are common to both mouse and human. A short sequence in the second intron of the mouse gene can be alternatively spliced in, leading to an insertion in the second intracellular loop of the receptor. This insertion constitutes an additional exon which is not present in the human genome. The human GIR polypeptide shares 89.5% and 91.5% identity with its mouse and dog orthologs respectively. Splice variants lacking the first extracellular loop and the third transmembrane domain have been found in human and mouse species. The receptor variants resulting from these minor transcripts are likely to be non functional. Comparative genetic mapping of the Gpr83 gene showed that it maps to regions of conserved synteny on mouse chromosome 9 (A2-3 region) and human chromosome 11 (q21 region).</p>","PeriodicalId":10982,"journal":{"name":"Cytogenetics and cell genetics","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"2000-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000015650","citationCount":"22","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Cytogenetics and cell genetics","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1159/000015650","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 22
Abstract
The mouse glucocorticoid-induced receptor (GIR) is an orphan G protein-coupled receptor highly expressed in brain and thymus (Harrigan et al., 1989; 1991). We have cloned the mouse GIR gene (Gpr83), determined its genomic organization and compared it with the human gene. The genomic organization of the gene is similar in both species although differences leading to specific splicing variants in the mouse have been found. Three introns interrupting the coding sequence are common to both mouse and human. A short sequence in the second intron of the mouse gene can be alternatively spliced in, leading to an insertion in the second intracellular loop of the receptor. This insertion constitutes an additional exon which is not present in the human genome. The human GIR polypeptide shares 89.5% and 91.5% identity with its mouse and dog orthologs respectively. Splice variants lacking the first extracellular loop and the third transmembrane domain have been found in human and mouse species. The receptor variants resulting from these minor transcripts are likely to be non functional. Comparative genetic mapping of the Gpr83 gene showed that it maps to regions of conserved synteny on mouse chromosome 9 (A2-3 region) and human chromosome 11 (q21 region).
小鼠糖皮质激素诱导受体(GIR)是一种在大脑和胸腺中高度表达的孤儿G蛋白偶联受体(Harrigan et al., 1989;1991)。我们克隆了小鼠GIR基因(Gpr83),确定了其基因组结构,并与人类基因进行了比较。该基因的基因组组织在两个物种中是相似的,尽管在小鼠中发现了导致特定剪接变异的差异。中断编码序列的三个内含子在小鼠和人类中都是常见的。小鼠基因的第二个内含子中的一个短序列可以被选择性地剪接,从而插入受体的第二个细胞内环。这种插入构成了人类基因组中不存在的额外外显子。人GIR多肽与其小鼠和狗的同源物分别具有89.5%和91.5%的同源性。在人类和小鼠物种中发现了缺乏第一细胞外环和第三跨膜结构域的剪接变异体。由这些次要转录物产生的受体变异可能是无功能的。Gpr83基因定位于小鼠9号染色体(A2-3区)和人类11号染色体(q21区)的保守共聚区域。