Home News About Us Contact Contributors Disclaimer Privacy Policy Help FAQ

Home
Search
Quick Search
Advanced
Fulltext
Browse
Collections
Persons
My eDoc
Session History
Login
Name:
Password:
Documentation
Help
Support Wiki
Direct access to
document ID:


          Institute: MPI für molekulare Genetik     Collection: Department of Human Molecular Genetics     Display Documents



  history
ID: 472721.0, MPI für molekulare Genetik / Department of Human Molecular Genetics
Dicer is required for Sertoli cell function and survival
Authors:Kim, Gwang-Jin; Georg, Ina; Scherthan, Harry; Merkenschlager, Matthias; Guillou, Florian; Scherer, Gerd; Barrionuevo, Francisco
Language:English
Date of Publication (YYYY-MM-DD):2010
Title of Journal:International Journal of Developmental Biology
Journal Abbrev.:Int J Dev Biol
Volume:54
Start Page:867
End Page:875
Copyright:© UBC Press
Review Status:not specified
Audience:Experts Only
Abstract / Description:Dicer is a key enzyme that processes microRNA precursors into their mature form, enabling them to regulate gene expression. Dicer null mutants die before gastrulation. To study Dicer function in testis development, we crossed mice carrying a conditional Dicer allele with an AMH-Cre transgenic line, thereby inactivating Dicer in Sertoli cells around embryonic day 14.0 (E14.0). Dicer null Sertoli cells show normal embryonic development, and at postnatal day 0 (P0), testis tubules are normal in number and histologically undistinguishable from controls. Subsequently, Dicer-mutant testes show a progressively aberrant development, so that at P6, they contain a reduced number of disorganized testis tubules leading to primary sterility. Apoptosis and prophase I assays reveal a massive wave of apoptosis starting at P3, causing progressive loss of Sertoli cells, but also of germ cells, resulting in drastically reduced testis size. Expression of genes that play crucial roles in testis development, structural integrity and spermatogenesis is downregulated at P0, before morphological changes become apparent, indicating that Dicer-mutant testes are already transcriptionally compromised at this stage. Taken together, the results of this study show that Dicer is required for Sertoli cell function and survival and for spermatogenesis in mice.
Free Keywords:Dicer; miRNAs; Testis; Spermatogenesis; Sterility
Comment of the Author/Creator:email: francisco.barrionuevo@uniklinik-freiburg.de gerd.scherer@uniklinik-freiburg.de
External Publication Status:published
Document Type:Article
Communicated by:Hans-Hilger Ropers
Affiliations:MPI für molekulare Genetik
External Affiliations:Institute of Human Genetics, University of Freiburg, Germany
Faculty for Biology, University of Freiburg, Germany Bundeswehr Institute of Radiobiology, Munich, Germany Lymphocyte Development Group, MRC Clinical Sciences Centre, Imperial College London, UK
UMR 6175, Physiologie de la Reproduction, INRA-CNRS, Université de Tours, Nouzilly, France
Identifiers:DOI:10.1387/ijdb.092874gk
ISSN:0214-6282
Full Text:
You have privileges to view the following file(s):
Kim.pdf  [780,00 Kb]   
 
The scope and number of records on eDoc is subject to the collection policies defined by each institute - see "info" button in the collection browse view.