Poster: Plant-pathogen interactions

Abs # 553: Control of defense-related gene expression in compatible host-virus interactions

Presenter:	huang, zhonglian , zhlhuang@iastate.edu
Authors	huang, zhonglian  (A)   whitham, steve A (A)
Affiliations:	(A): department of plant pathology, interdepartmental genetics program , iowa state university, ames, ia 50011

Positive-stranded RNA viruses elicit the expression of common sets of genes in susceptible Arabidopsis plants. About one-third of the genes induced in common by these viruses can be associated with plant defense and stress responses. We wanted to know if the expression of defense-related genes in compatible host-virus interactions is regulated through signaling pathways that normally control plant defense responses. To answer this question, pad4-1, eds5-1, NahG, npr1-1, jar1-1, ein2-1, and wild type Columbia-0 plants were infected with two different viruses, cucumber mosaic virus (CMV) and oilseed rape mosaic virus (ORMV). RNA was extracted from inoculated leaves at 2 and 5 days after inoculation, and we determined that virus accumulation was not altered in the mutants. Gene expression was assayed using a high-throughput fiber-optic bead array consisting of 388 genes. Bead array data clearly illustrated different patterns of gene expression after virus infection, and that expression of many defense-related genes is induced by a SA-dependent, NPR1-independent signaling pathway. These conclusions were confirmed by Northern blots probed with labeled DNA fragments corresponding to the beta-1, 3 glucanase 2 (BGL2), PR5-like, and PDF1.2 genes. The BGL2 and PR5-like genes were induced at 2 and 5 days after inoculation in Columbia-0, ein2-1, jar1-1, and npr1-1. However, their expression was reduced in pad4-1 and abolished in NahG transgenic plants. PDF1.2 was not expressed in response to any virus treatment as expected based on microarray data. Our experimental results indicated that expression of many SAR-related genes in compatible host plants might share a common signaling pathway with incompatible host-virus interactions but have no effect on viral infection.