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ABSTRACT FROM PLANT CANADA 2005 - Reduced Expression of Eukaryotic Translation Initiation Factor 5A2 Imparts Strong Pathogen Resistance to Arabidopsis thaliana

PERRY, GE., HOPKINS, MT. AND

THOMPSON, JE.

Univ of Waterloo, Dept of Biology, Waterloo

Ontario, N2L 3G1

Previous studies in our laboratory have demonstrated that eukaryotic translation initiation Factor 5A (eIF5A) regulates programmed cell death (PCD). Specifically, eIF5A appears to act as a shuttle protein, translocating specific mRNAs encoding death proteins from the nucleus to the cytosol for subsequent translation. In Arabidopsis, there are two death isoforms of eIF5A. One of these, eIF5A1, regulates PCD accompanying senescence. In this study, we show that the second isoform, eIF5A2, regulates PCD accompanying infection by necrotrophic bacterial and fungal pathogens. Within 72 h of infection with virulent Pseudomonas syringae pv Tomato DC 3000, eIF5A2 protein is strongly up-regulated in the leaves of Arabidopsis wild-type plants. The upregulation coincides with visible symptoms of disease progression. Moreover, eIF5A2 is the only eIF5A isoform to show increased expression following infection. In addition, the up-regulation appears to be posttranscriptionally regulated. To further test the role of eIF5A2 in disease development, transgenic Arabidopsis plants with constitutively suppressed eIF5A2 expression were developed using antisense T-DNA insertions. The suppressed plants showed marked resistance to virulent Pseudomonas syringae pv Tomato DC 3000, with some lines exhibiting a 99 % decrease in bacterial load, relative to wild-type plants. This suppression of pathogen growth correlated with the absence of disease symptoms. The same lines also showed strong resistance to infection by the necrotrophic fungal pathogen, Sclerotinia sclerotiorum. The results have been interpreted as indicating that eIF5A2 regulates PCD induced by necrotrophic pathogens, and that suppression of eIF5A2 inhibits host cell death upon infection and the ensuing release of nutrients that normally support growth of the pathogen.