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BOR - Papers in Press, published online ahead of print April 9, 2008.
Biol Reprod 2008, 10.1095/biolreprod.108.068072
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BIOLOGY OF REPRODUCTION 79, 51–57 (2008)
DOI: 10.1095/biolreprod.108.068072
© 2008 by the Society for the Study of Reproduction, Inc.

research-article

Mice Deficient for a Small Cluster of Piwi-Interacting RNAs Implicate Piwi-Interacting RNAs in Transposon Control1

Mingang Xu 3, Yun You 4, Patricia Hunsicker 4, Tamaki Hori 3, Chris Small 5, Michael D Griswold 5, and Norman B Hecht 2 3

Center for Research on Reproduction and Women's Health,3 University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104-6080 Life Sciences Division,4 Oak Ridge National Laboratory, Oak Ridge, Tennessee 37830-6942 Department of Molecular Biosciences,5 Washington State University, Pullman, Washington 99164-4660

ABSTRACT

The mammalian testis expresses a class of small noncoding RNAs that interact with mammalian PIWI proteins. In mice, the PIWI-interacting RNAs (piRNAs) partner with mammalian PIWI proteins, PIWIL1 and PIWIL2, also known as MIWI and MILI, to maintain transposon silencing in the germline genome. Here, we demonstrate that inactivation of Nct1/2, two noncoding RNAs encoding piRNAs, leads to derepression of LINE-1 (L1) but does not affect mouse viability, spermatogenesis, testicular gene expression, or fertility. These findings indicate that piRNAs from a cluster on chromosome 2 are necessary to maintain transposon silencing.

gametogenesis, gene regulation, male reproductive tract, piRNA, spermatogenesis, testis, transposon

FOOTNOTES

1Supported by National Institutes of Health grant HD 28832.

Correspondence: 2Norman B. Hecht, Center for Research on Reproduction and Women's Health, University of Pennsylvania School of Medicine, 1310 Biomedical Research Building, 421 Curie Blvd., Philadelphia, PA 19104-6080. FAX: 215 573 7627; e-mail: nhecht{at}mail.med.upenn.edu






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Copyright © 2008 by the Society for the Study of Reproduction.