Open AccessThe putative RxLR effector protein SpHtp1 from the fish pathogenic oomycete Saprolegnia parasitica is translocated into fish cells
Author(s) -
Van West Pieter,
De Bruijn Irene,
Minor Kirsty L.,
Phillips Andrew J.,
Robertson Emma J.,
Wawra Stephan,
Bain Judith,
Anderson Victoria L.,
Secombes Chris J.
Publication year - 2010
Publication title -
fems microbiology letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.899
H-Index - 151
eISSN - 1574-6968
pISSN - 0378-1097
DOI - 10.1111/j.1574-6968.2010.02055.x
Subject(s) - oomycete , biology , zoospore , saprolegnia , effector , rainbow trout , microbiology and biotechnology , trout , fish proteins , fish <actinopterygii> , pathogen , fishery , spore
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.