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Originally published In Press as doi:10.1074/jbc.M406865200 on July 29, 2004

J. Biol. Chem., Vol. 279, Issue 40, 41580-41585, October 1, 2004
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A Novel Venom Peptide from an Endoparasitoid Wasp Is Required for Expression of Polydnavirus Genes in Host Hemocytes*

Guangmei Zhang{ddagger}, Otto Schmidt{ddagger}, and Sassan Asgari§

From the {ddagger}Insect Molecular Biology Laboratory, Department of Plant and Pest Science, Waite Campus, University of Adelaide, Glen Osmond SA 5064, Australia and §Department of Zoology and Entomology, School of Life Sciences, University of Queensland, St. Lucia QLD 4072, Australia

Maternal factors introduced into host insects by endoparasitoid wasps are usually essential for successful parasitism. This includes polydnaviruses (PDVs) that are produced in the reproductive organ of female hymenopteran endoparasitoids and are injected, together with venom proteins, into the host hemocoel at oviposition. Inside the host, PDVs enter various tissue cells and hemocytes where viral genes are expressed, leading to developmental and physiological alterations in the host, including the suppression of the host immune system. Although several studies have shown that some PDVs are only effective when accompanied by venom proteins, there is no report of an active venom ingredient(s) facilitating PDV infection and/or gene expression. In this study, we describe a novel peptide (Vn1.5) isolated from Cotesia rubecula venom that is required for the expression of C. rubecula bracoviruses (CrBVs) in host hemocytes (Pieris rapae), although it is not essential for CrBV entry into host cells. The peptide consists of 14 amino acids with a molecular mass of 1598 Da. In the absence of Vn1.5 or total venom proteins, CrBV genes are not expressed in host cells and did not cause inactivation of host hemocytes.


Received for publication, June 21, 2004 , and in revised form, July 22, 2004.

* This project was funded by a University of Adelaide small grant scheme, a University of Queensland grant (to S. A.), and a University of Adelaide scholarship (to G. Z.). 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.

To whom correspondence should be addressed. Tel.: 617-3365-2043; Fax: 617-3365-1655; E-mail: s.asgari{at}uq.edu.au.


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