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Blood, 1 September 2005, Vol. 106, No. 5, pp. 1612-1620. Prepublished online as a Blood First Edition Paper on May 17, 2005; DOI 10.1182/blood-2004-08-3367. This Article Full Text (PDF) All Versions of this Article: 2004-08-3367v1 106/5/1612    most recent Alert me when this article is cited Alert me if a correction is posted 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 Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Katoh-Fukui, Y. Articles by Morohashi, K.-i. Search for Related Content PubMed PubMed Citation Articles by Katoh-Fukui, Y. Articles by Morohashi, K.-i. Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted September 1, 2004 Accepted April 29, 2005 Mouse Polycombm M33 is required for splenic vascular and adrenal gland formation through regulating Ad4BP/SF-1 expression Yuko Katoh-Fukui*, Akiko Owaki, Yoshiro Toyama, Masatomo Kusaka, Yuko Shinohara, Mamiko Maekawa, Kiyotaka Toshimori, and Ken-ichirou Morohashi Division for Sex Differentiation, National Institute for Basic Biology, National Institutes of Natural Sciences, Okazaki, Aichi, Japan; Core Research for Evolutional Science and Technology (CREST), Japan Science and Technology Corporation, Kawaguchi, Saitama, Japan Department of Anatomy, Graduate School of Medicine, Chiba University, Chiba, Japan Division for Sex Differentiation, National Institute for Basic Biology, National Institutes of Natural Sciences, Okazaki, Aichi, Japan; Department of Molecular Biomechanism, School of Life Sciences, Graduate University for Advanced Studies, Okazaki, Aichi, Japan * Corresponding author; email: yfukui{at}nibb.ac.jp. Mice with disrupted mammalian PcG (Polycomb Group) genes commonly show skeletal transformation of anterior-posterior identities. Disruption of the murine M33 gene, a PcG member, displayed posterior transformation of the vertebral columns and sternal ribs. In addition, failure of T-cell expansion and hypoplasia and sex-reversal of the gonads, have been observed. In the present study, we identified defects in the splenic and adrenal formation of M33-knockout (KO) mice on a C57BL/6 genetic background. The spleen in these animals was smaller than in the wild-type and was spotted red due to non-uniform distribution of blood cells. Histological examination revealed disorganization of the vascular endothelium and its surrounding structures, and immunohistochemistry demonstrated disturbances in vascular formation and colonization of immature hematopoietic cells. These splenic phenotypes observed in the M33-KO mice were quite similar to those seen in Ad4BP/SF-1 (Nr5a1) knockouts. Moreover, the adrenal glands of M33-KO and Ad4BP/SF-1 heterozygous KO mice were smaller than those of the wild-type. Western-blot, immunohistochemistry and RT-PCR analyses of the M33 knockouts all indicated significantly low expression of Ad4BP/SF-1, indicating that M33 is an essential upstream regulator of Ad4BP/SF-1. In agreement with these observations, chromatin immunoprecipitation assays with adrenocortical Y-1 cells revealed direct binding of the M33-containing PcG to the Ad4BP/SF-1 gene locus. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: M. A. Edson, A. K. Nagaraja, and M. M. Matzuk The Mammalian Ovary from Genesis to Revelation Endocr. Rev., October 1, 2009; 30(6): 624 - 712. [Abstract] [Full Text] [PDF] M. Zubair, S. Oka, K. L. Parker, and K.-i. Morohashi Transgenic Expression of Ad4BP/SF-1 in Fetal Adrenal Progenitor Cells Leads to Ectopic Adrenal Formation Mol. 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