Skip to main content
ARS Home » Research » Publications at this Location » Publication #175320


item Chandra-shekar, A
item Navarre, Duroy - Roy
item Kachroo, A
item Klessig, D
item Kachroo, P

Submitted to: Plant Journal
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 8/24/2004
Publication Date: 12/1/2004
Citation: Chandra-Shekar, A., Navarre, D.A., Kachroo, A., Klessig, D.F., Cachroo, P. 2004. Signaling requirements and role of salicylic acid in hrt-mediated hypersensitive response and HRT- and rrt-mediated resistance to turnip crinkle viru. Plant Journal. 40(5):647-659.

Interpretive Summary: This research addresses the important question of how some plants resist infection by viruses and describes mechanisms that plants use to resist viruses. Plant resistance to viruses is particularly important because there is no pesticide or economical treatment available that is directly effective against crop viruses. The turnip crinkle virus (TCV) can cause lesions and induces plant defense genes. This work describes genes that regulate the plant response to TCV and suggests that salicylic acid is important for resistance to TCV. Interestingly, salicylic acid appears to cause an increase in the amount of the key gene that initiates the plant resistant response to TCV. Evidence for the involvement of a second gene in viral resistance is also presented and shows that in contrast to lesion formation, resistance requires two genes. This is important for several reasons, including that it shows that lesion formation and resistance are not the same thing, in contrast to what was believed for many years. Increased understanding of virus disease resistance mechanisms will facilitate the production of plants with superior disease resistance.

Technical Abstract: Inoculation of turnip crinkle virus (TCV) on the resistant Arabidopsis ecotype Di-17 elicits a hypersensitive response (HR), which is accompanied by increased expression of pathogenesis-related (PR) genes. Previous genetic analyses revealed that the HR to TCV is conferred by HRT, which encodes a coiled-coil (CC), nucleotide-binding site (NBS) and leucine-rich repeat (LRR) class resistance (R) protein. In contrast to the HR, resistance to TCV requires both HRT and a recessive allele at a second locus designated rrt. Here, we demonstrate that unlike most CC-NBS-LRR R genes, HRT/rrt-mediated resistance is dependent on EDS1 and independent of NDR1. Resistance is also independent of RAR1 and SGT1. HRT/rrt-mediated resistance is compromised in plants with reduced salicylic acid (SA) content as a consequence of mutations eds5, pad4, or sid2. By contrast, HR is not affected by mutations in eds1, eds5, pad4, sid2, ndr1, rar1, or sgt1b. Resistance to TCV is restored in both SA-deficient Di-17 plants expressing the nahG transgene and mutants containing the eds1, eds5, or sid2 mutations by exogenous application of SA or the SA analog benzo(1,2,3)thiadiazole-7-carbothioic acid (BTH). In contrast, SA/BTH treatment failed to enhance resistance in HRT pad4, Col-0, or hrt homozygous progeny of a cross between Di-17 and Col-0. Thus, HRT and PAD4 are required for SA-induced resistance. Exogenously supplied SA or high endogenous levels of SA, due to the ssi2 mutation, overcame the suppressive effects of RRT and enhanced resistance to TCV, provided the HRT allele was present. High levels of SA upregulate HRT expression via a PAD4-dependent pathway. As Col-0 transgenic lines expressing high levels of HRT were resistant to TCV, but lines expressing moderate to low levels of HRT were not, we conclude that SA enhances resistance in the RRT background by upregulating HRT expression. These data suggest that the HRT-TCV interaction is unable to generate sufficient amounts of SA required for a stable resistance phenotype, and the presence of rrt possibly corrects this deficiency.