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Eukaryotic Cell, April 2007, p. 658-663, Vol. 6, No. 4
1535-9778/07/$08.00+0 doi:10.1128/EC.00346-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.
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Genetics Group, Biotechnology Research Institute, National Research Council, Montreal, Quebec H4P 2R2, Canada,1 Department of Biology, McGill University, Montreal, Quebec H3A 1B1, Canada,2 Department of Biochemistry, McGill University, Montreal, Quebec H3G 1Y6, Canada3
Received 31 October 2006/ Accepted 23 January 2007
We used Drosophila melanogaster macrophage-like Schneider 2 (S2) cells as a model to study cell-mediated innate immunity against infection by the opportunistic fungal pathogen Candida albicans. Transcriptional profiling of S2 cells coincubated with C. albicans cells revealed up-regulation of several genes. One of the most highly up-regulated genes during this interaction is the D. melanogaster translational regulator 4E-BP encoded by the Thor gene. Analysis of Drosophila 4E-BPnull mutant survival upon infection with C. albicans showed that 4E-BP plays an important role in host defense, suggesting a role for translational control in the D. melanogaster response to C. albicans infection.
Published ahead of print on 2 February 2007.
This is National Research Council publication 47513.
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