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Identification of Lipoteichoic Acid as a Ligand for Draper in the Phagocytosis of Staphylococcus aureus by Drosophila Hemocytes¹

Yumi Hashimoto,^* Yukichika Tabuchi, Kenji Sakurai, Mayumi Kutsuna, Kenji Kurokawa, Takeshi Awasaki,^¶ Kazuhisa Sekimizu, Yoshinobu Nakanishi,^2* and Akiko Shiratsuchi^*

^*Graduate School of Medical Science, Graduate School of Natural Science and Technology, and Faculty of Pharmaceutical Sciences, Kanazawa University, Kanazawa, Ishikawa, Japan; Graduate School of Pharmaceutical Sciences, University of Tokyo, Bunkyo-ku, Tokyo, Japan; and ^¶Department of Neurobiology, University of Massachusetts Medical School, Worcester, MA 01605

Phagocytosis is central to cellular immunity against bacterial infections. As in mammals, both opsonin-dependent and -independent mechanisms of phagocytosis seemingly exist in Drosophila. Although candidate Drosophila receptors for phagocytosis have been reported, how they recognize bacteria, either directly or indirectly, remains to be elucidated. We searched for the Staphylococcus aureus genes required for phagocytosis by Drosophila hemocytes in a screening of mutant strains with defects in the structure of the cell wall. The genes identified included ltaS, which encodes an enzyme responsible for the synthesis of lipoteichoic acid. ltaS-dependent phagocytosis of S. aureus required the receptor Draper but not Eater or Nimrod C1, and Draper-lacking flies showed reduced resistance to a septic infection of S. aureus without a change in a humoral immune response. Finally, lipoteichoic acid bound to the extracellular region of Draper. We propose that lipoteichoic acid serves as a ligand for Draper in the phagocytosis of S. aureus by Drosophila hemocytes and that the phagocytic elimination of invading bacteria is required for flies to survive the infection.

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.

¹ This study was supported by Grants-in-Aid for Scientific Research from the Japan Society for the Promotion of Science (18570123 and 20570127 to A.S. and 19370051 to Y.N.) and from the Ministry of Education, Culture, Sports, Science and Technology-Japan (18057009 to A.S.), as well as a grant from the Mitani Foundation (to A.S.).

² Address correspondence and reprint requests to Dr. Yoshinobu Nakanishi, Graduate School of Medical Science, Kanazawa University, Shizenken, Kakuma-machi, Kanazawa, Ishikawa 920-1192, Japan. E-mail address: nakanaka{at}kenroku.kanazawa-u.ac.jp

³ Abbreviations used in this paper: LTA, lipoteichoic acid; EGF, epidermal growth factor; RNAi, RNA interference; WTA, wall teichoic acid.

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