This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Reprints and Permissions Copyright Information Books from ASM Press MicrobeWorld Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Doi, Y. Articles by Seya, T. Search for Related Content PubMed PubMed Citation Articles by Doi, Y. Articles by Seya, T.

 Previous Article  |  Next Article 

J Virol, February 1998, p. 1586-1592, Vol. 72, No. 2
0022-538X/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.

Moesin Is Not a Receptor for Measles Virus Entry into Mouse Embryonic Stem Cells

Yoshinori Doi,^1,2 Mitsue Kurita,³ Misako Matsumoto,³ Takahisa Kondo,^1,4 Tetsuo Noda,⁵ Sachiko Tsukita,^1,6 Shoichiro Tsukita,¹ and Tsukasa Seya^3,7,*

Department of Cell Biology, Faculty of Medicine,¹ and College of Medical Technology,⁶ Kyoto University, Yoshida-Konoe, Sakyo-ku, Kyoto 606, Department of Immunology, Osaka Medical Center for Cancer and Cardiovascular Diseases, Higashinari-ku, Osaka 537,³ Second Department of Internal Medicine, Osaka University Medical School, Suita, Osaka 565,² First Department of Internal Medicine, Nagoya University School of Medicine, Showa-ku, Nagoya 466,⁴ Department of Cell Biology, Cancer Institute, Toshima-ku, Tokyo 170,⁵ and PROBRAIN, Tokyo 105,⁷ Japan

Received 2 September 1997/Accepted 28 October 1997

The involvement of moesin in measles virus (MV) entry was investigated with moesin-positive and -negative mouse embryonic stem (ES) cells. MV infection of these cells was very ineffective and was independent of moesin expression. Furthermore, when these cells were transfected to express human CD46, a 100-fold increase in syncytium formation was observed with these cells and was independent of the expression of moesin. The only obvious difference between moesin-positive and -negative ES cells was the shape of the syncytia formed. Moesin-negative ES cells expressing or not expressing human CD46 formed separate pieces of fragmented syncytia which were torn apart during spreading, whereas ES cells expressing moesin exhibited typical syncytia. In addition, moesin was not detected on the surface of any murine cells or cell lines that we have tested by a flow cytometric assay with moesin-specific antibodies. These findings indicate that murine moesin is neither a receptor nor a CD46 coreceptor for MV entry into mouse ES cells. Moesin is involved in actin filament-plasma membrane interactions as a cross-linker, and it affects only the spreading and shape of MV-mediated syncytia.

---

^* Corresponding author. Mailing address: Department of Immunology, Osaka Medical Center for Cancer and Cardiovascular Diseases, Higashinari-ku, Osaka 537, Japan. Phone: 81 6 972 1181. Fax: 81 6 981 3000. E-mail: tseya{at}takaipro.jst.go.jp.

This article has been cited by other articles:

• Takeuchi, K., Takeda, M., Miyajima, N., Kobune, F., Tanabayashi, K., Tashiro, M. (2002). Recombinant Wild-Type and Edmonston Strain Measles Viruses Bearing Heterologous H Proteins: Role of H Protein in Cell Fusion and Host Cell Specificity. J. Virol. 76: 4891-4900 [Abstract] [Full Text]  
• Kurita-Taniguchi, M., Fukui, A., Hazeki, K., Hirano, A., Tsuji, S., Matsumoto, M., Watanabe, M., Ueda, S., Seya, T. (2000). Functional Modulation of Human Macrophages Through CD46 (Measles Virus Receptor): Production of IL-12 p40 and Nitric Oxide in Association with Recruitment of Protein-Tyrosine Phosphatase SHP-1 to CD46. J. Immunol. 165: 5143-5152 [Abstract] [Full Text]