Editor: Craig Shoemaker
The putative RxLR effector protein SpHtp1 from the fish pathogenic oomycete Saprolegnia parasitica is translocated into fish cells
Version of Record online: 9 JUL 2010
© 2010 Federation of European Microbiological Societies. Published by Blackwell Publishing Ltd. All rights reserved
FEMS Microbiology Letters
Volume 310, Issue 2, pages 127–137, September 2010
How to Cite
Van West, P., De Bruijn, I., Minor, K. L., Phillips, A. J., Robertson, E. J., Wawra, S., Bain, J., Anderson, V. L. and Secombes, C. J. (2010), The putative RxLR effector protein SpHtp1 from the fish pathogenic oomycete Saprolegnia parasitica is translocated into fish cells. FEMS Microbiology Letters, 310: 127–137. doi: 10.1111/j.1574-6968.2010.02055.x
Present address: Emma J. Robertson, Department of Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, NY 10461, USA.
- Issue online: 23 AUG 2010
- Version of Record online: 9 JUL 2010
- Received 18 May 2010; revised 25 June 2010; accepted 30 June 2010.Final version published online 26 July 2010.
- protein translocation
The fish pathogenic oomycete Saprolegnia parasitica causes the disease Saprolegniosis in salmonids and other freshwater fish, resulting in considerable economic losses in aquaculture. Very little is known about the molecular and cellular mechanisms underlying the infection process of fish pathogenic oomycetes. In order to investigate the interaction in detail, an in vitro infection assay using an Oncorhynchus mykiss (rainbow trout) cell line (RTG-2) was developed. In a zoospore/cyst cDNA library, we identified the ORF SpHtp1, which encodes a secreted protein containing an RxLR motif. Detailed expression analysis indicated that SpHtp1 is highly expressed in zoospores/cysts from S. parasitica and in the very early stages of infection on RTG-2 cells, when compared with in vitro-grown mycelium. Moreover, the protein, SpHtp1, was found to translocate into the RTG-2 trout cells, during the interaction with S. parasitica, and also when the RTG-2 cells were treated with recombinant SpHtp1 fused to a C-terminal His-tag. These findings suggest that protein translocation could play an important role in Saprolegniosis.