Identification of two novel, alternatively spliced mRNA transcripts of the human follicle‐stimulating hormone receptor. Issue 11 (5th September 2013)

• Record Type: Journal Article
• Authors: Zhou, Jun; Huang, Yiting; Li, Lili; Zhu, Liang; Zhang, Dan; Zhang, Suzhan; Chen, Yiding
• Is Part Of: Molecular reproduction and development. Volume 80:Issue 11(2013:Nov.)
• Page Start: 916
• Page End: 923
• Publication Date: 2013-09-05
• Subjects: Reproduction -- Periodicals; Molecular biology -- Periodicals; Molecular genetics -- Periodicals; Embryology -- Periodicals; 571.8
• DOI: 10.1002/mrd.22227
• Languages: English
• ISSNs: 1040-452X

Abstract

<abstract abstract-type="main" xml:lang="en"> <title>SUMMARY</title> <sec id="mrd22227-sec-0001" sec-type="section"> <p>Glycoprotein hormone receptors contain large extracellular domains encoded by multiple exons that can be alternatively spliced. Using human ovarian surface epithelium, we cloned two new splice variants of the human follicle‐stimulating hormone receptor (<italic>FSH‐R</italic>) gene, <italic>hFSH‐R2</italic> and <italic>hFSH‐R3</italic>. The <italic>hFSH‐R2</italic> splice variant differed from the full‐length <italic>FSH‐R</italic> mRNA by the deletion of exon 10 and inclusion of two small exons after exon 9 whereas the <italic>hFSH‐R3</italic> splice variant retained only exons 1–6 of the full‐length transcript. Both variants were expressed at low levels, but were detected in cells from follicular fluid derived from 30 different subjects. Transfection of these two variants individually into KGN cells, an ovarian cancer cell line that expresses wild‐type FSH‐R, reduced FSH‐mediated phosphorylation of ERK_1/2, Akt, and p38/MAPK. Furthermore, in vitro co‐expression of either <italic>hFSH‐R2</italic> or <italic>hFSH‐R3</italic> and full‐length FSH‐R in HEK293T cells reduced signal transduction through full‐length FSH‐R. Further studies are needed to fully elucidate the functions of these receptor isoforms. <italic>Mol. Reprod. Dev. 80: 916–923, 2013. © 2013 Wiley Periodicals, Inc</italic>.</p> </sec> </abstract>