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J. Biol. Chem., Vol. 283, Issue 39, 26302-26306, September 26, 2008

This Article Full Text Full Text (PDF) Supplemental Data All Versions of this Article: 283/39/26302    most recent C800117200v1 Submit a Letter to Editor Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Tsai, C.-Y. Articles by Tsai, T.-F. Search for Related Content PubMed PubMed Citation Articles by Tsai, C.-Y. Articles by Tsai, T.-F. Social Bookmarking                      What's this?

Hurp Deficiency in Mice Leads to Female Infertility Caused by an Implantation Defect^*

Ching-Yen Tsai, Chen-Kung Chou, Chu-Wen Yang^¶, Yi-Chen Lai, Chih-Chia Liang, Chun-Ming Chen, and Ting-Fen Tsai^||1

From the Department of Life Sciences and Institute of Genome Sciences, National Yang-Ming University, Taipei 112, Taiwan, the Department of Life Science, Chang Gung University, Tao-Yuan 333, Taiwan, the ^¶Department of Microbiology, Soochow University, Taipei 111, Taiwan, and the ^||Division of Molecular and Genomic Medicine, National Health Research Institutes, Zhunan 350, Taiwan

First revealed in cancer studies, HURP (hepatoma up-regulated protein) is a cell cycle-associated gene with elevated expression in the G₂/M phase. Cell culture studies have revealed that HURP is an essential factor required for spindle formation and chromosome congression during mitosis. However, the function of HURP in an in vivo context has not been explored. We generated a Hurp knock-out (Hurp^–/–) mouse to investigate the role of HURP in development under normal physiological conditions. Hurp^–/– mice develop normally and are indistinguishable from their wild-type littermates. Interestingly, breeding experiments revealed that Hurp^–/– females are completely infertile, whereas the males reproduce normally. Ovulation, fertilization, and pre-implantation embryo development are normal; however, the Hurp^–/– females are unable to form implantation sites due to an inability to undergo the decidual reaction. This is caused by a defect in endometrial stromal proliferation that leads to implantation failure. Additionally, HURP expression in the uterus coincides with the implantation stage and can be induced by estrogen treatment. Our results demonstrate for the first time that HURP affects endometrial stromal proliferation during implantation but is dispensable during normal development in mice; specifically, HURP has an essential function in uterine biology.

Received for publication, June 9, 2008 , and in revised form, August 1, 2008.

^* This work was supported by National Research Program for Genomic Medicine Grants 95HC007 and NSC96-2752-B-010-004-PAE (to T.-F. T.), CMRPD160471 (to C.-K. C.), and NSC96-2320-B-031-001-MY2 (to C.-W. Y.) from the National Science Council and by a grant from the Ministry of Education "Aim for the Top University Plan." Work performed in the Microarray and Gene Expression Analysis Core Facility of the National Yang-Ming University Genome Research Center was supported by the National Research Program for Genomic Medicine, National Science Council. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

The on-line version of this article (available at http://www.jbc.org) contains supplemental "Methods," Figs. S1–S5, Tables 1 and 2, and additional references.

¹ To whom correspondence should be addressed: National Yang-Ming University, 155 Li-Nong St., Sec. 2, Peitou, Taipei 112, Taiwan. Tel.: 886-2-2826-7293; Fax: 886-2-2828-0872; E-mail: tftsai{at}ym.edu.tw.

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