Thioredoxinh5 Is Required for Victorin Sensitivity Mediated by a CC-NBS-LRR Gene inArabidopsis

Abstract

The fungus Cochliobolus victoriae causes Victoria blight of oats (Avena sativa) and is pathogenic due to its production of victorin, which induces programmed cell death in sensitive plants. Victorin sensitivity has been identified in Arabidopsis thaliana and is conferred by the dominant gene LOCUS ORCHESTRATING VICTORIN EFFECTS1 (LOV1), which encodes a coiled-coil-nucleotide binding site-leucine-rich repeat protein. We isolated 63 victorin-insensitive mutants, including 59 lov1 mutants and four locus of insensitivity to victorin1 (liv1) mutants. The LIV1 gene encodes thioredoxin h5 (ATTRX5), a member of a large family of disulfide oxidoreductases. To date, very few plant thioredoxins have been assigned specific, nonredundant functions. We found that the victorin response was highly specific to ATTRX5, as the closely related ATTRX3 could only partially compensate for loss of ATTRX5, even when overexpressed. We also created chimeric ATTRX5/ATTRX3 proteins, which identified the central portion of the protein as important for conferring specificity to ATTRX5. Furthermore, we found that ATTRX5, but not ATTRX3, is highly induced in sensitive Arabidopsis following victorin treatment. Finally, we determined that only the first of the two active-site Cys residues in ATTRX5 is required for the response to victorin, suggesting that ATTRX5 function in the victorin pathway involves an atypical mechanism of action.

Plant disease susceptibility conferred by a “resistance” gene

“…LOV1-specified, victorin-induced PR-1 expression is SAdependent (Fig. 2), and victorin-induced expression of ATTRX5, a gene required for LOV1-conditioned C. victoriae susceptibility is also SA-dependent (36). Furthermore, ethylene involvement has been demonstrated in Vb-conditioned susceptibility of oats to C. victoriae (33), and a slight attenuation of LOV1-mediated victorin sensitivity occurs in ein2 Arabidopsis (Fig.…”

“…Novel pathways have been proposed for RPP7-and RPP8-mediated resistance (19), and known signaling pathways account for only a portion of the resistance mediated by RCY1 (21). Given the similarity of LOV1 to RPP8 and RCY1 and the finding that an extensive screen for suppressors of LOV1 did not reveal genes previously known to be required for defense (36), LOV1 could also function in an uncharacterized pathway, one that is sufficient for resistance to some pathogens (such as obligate biotrophs, as is the case for RPP8 and RCY1) but readily exploited for susceptibility by other pathogens such as C. victoriae. Such opposing functions in host response have been reported for MLO proteins, which are required for compatible interactions of powdery mildew pathogens with barley and Arabidopsis but contribute to resistance to necrotrophic and hemibiotrophic pathogens of Arabidopsis (8).…”

DNA Replication in Animal Systems Lacking Thioredoxin Reductase I

“…It is well established that the cytosolic and mitochondrial TrxR enzymes in Arabidopsis are cross-complementary. Thus, disruption of the gene encoding either of these E. coli-type TrxRs is compensated by a partial re-distribution of product from the other gene into the deficient sub-cellular compartment (Meyer et al, 2008;Reichheld et al, 2007;Sweat and Wolpert, 2007). To date, there is no in vivo evidence of similar crosscomplementation occurring in mammalian systems.…”

“…By contrast, yeast and plants deficient in TrxRs show slow-growth phenotypes (Koc et al, 2006;Reichheld et al, 2007;Sweat and Wolpert, 2007), suggesting Gsr-dependent routes are poor at supporting DNA replication in these eukaryotes. It was anticipated that all eukaryotic systems might depend primarily on the Trx system to supply electrons to RNR for DNA replication.…”

Synthesis of Redox-Active Molecules and Their Signaling Functions During the Expression of Plant Disease Resistance

“…Arabidopsis TRX-h5 (TRX5) has been shown to facilitate the reduction and subsequent monomerization of NPR1 oligomers upon SA-mediated plant defense activation leading to upregulation of defense genes (40). TRX5 has been implicated in plant immunity in response to victorin, produced by Victoria blight (39), and it is upregulated in response to avirulent bacterial pathogens (21). TRX proteins have recently emerged as enzymes with denitrosylating activity in human cells (2) and together with thioredoxin reductase (TRXreductase) can remove SNO groups from target proteins.…”