Home  |   Archive  |   Online Submission  |   News & Events  |   Subscribe  |   APFA  |   Society  |   Contact Us  |   中文版
Search   
 
Journal

Ahead of print
Authors' Accepted
    Manuscripts
new!
Current Issue
Archive
Acknowledgments
Special Issues
Browse by Category

Manuscript Submission

Online Submission
Online Review
Instruction for Authors
Instruction for Reviewers
English Corner new!

About AJA

About AJA
Editorial Board
Contact Us
News

Resources & Services

Advertisement
Subscription
Email alert
Proceedings
Reprints

Download area

Copyright licence
EndNote style file
Manuscript word template
Guidance for AJA figures
    preparation (in English)

Guidance for AJA figures
    preparation (in Chinese)

Proof-reading for the
    authors

AJA Club (in English)
AJA Club (in Chinese)

 
Abstract

Volume 5, Issue 4 (December 2003) 5, 267–275;

Targeted expression of human FSH receptor Asp567Gly mutant mRNA in testis of transgenic mice: role of human FSH receptor promoter

V. Nordhoff, J. Gromoll, L. Foppiani, C.M. Luetjens, S. Schlatt, E. Kostova, I. Huhtaniemi, E. Nieschlag, M. Simoni

1.Institute of Reproductive Medicine, University of Mnster, D-48149 Mnster, Germany
    2.Department of Physiology, University of Turku, Kiinamyllynkatu 10, FIN-20520 Turku, Finland
    
    

Advance online publication 1 December 2003

Abstract

Aim: To specifically express the Asp567Gly human follicle-stimulating hormone receptor (FSHR) under the control of its promoter to evaluate the phenotypic consequences in the presence of normal pituitary function. Methods: We produced transgenic mice overexpressing the Asp567Gly human FSHR under the control of a 1.5kb 5'-flanking region fragment of its promoter. Results: Mice were phenotypically normal and fertile. In males, mRNA could be detected in the testis and the brain, indicating that the 1.5kb promoter fragment drives expression not only in the gonads. The testis weight/body weight ratio and the testosterone levels in transgenic and non-transgenic littermates were similar. By in situ hybridisation we found that the transgenic FSHR was highly expressed in Sertoli cells, spermatocytes and round spermatids. However, a radioligand receptor assay failed to show a significant difference in total FSHR binding sites in testis homogenates of transgenic and wild type animals, suggesting that the transgenic FSHR is probably not translated into functional receptor protein. Conclusion: A 1.5kb 5'-region of the human FSHR drives mRNA expression of the transgene in the testis but leads to ectopic expression in germ cells and in the brain. No phenotypic consequences could be documented due to the lack of protein expression
    
    

Full Text |

 
Browse:  2268
 
Asian Journal of Andrology CN 31-1795/R ISSN 1008-682X  Copyright © 2023  Shanghai Materia Medica, Chinese Academy of Sciences.  All rights reserved.