Abstract
Rpg1b and Rpg1r are soybean disease resistance (R) genes responsible for conferring resistance to Pseudomonas syringae strains expressing the effectors AvrB and AvrRpm1, respectively. The study of these cloned genes would be greatly facilitated by the availability of a suitable transient expression system. The commonly used Niciotiana benthamiana-based system is not suitable for studying Rpg1b and Rpg1r function, however, because expression of AvrB or AvrRpm1 alone induces a hypersensitive response (HR), indicating that N. benthamiana contains endogenous R genes that recognize these effectors. To identify a suitable alternative host for transient expression assays, we screened 13 species of Nicotiana along with 11 accessions of N. tabacum for lack of response to transient expression of AvrB and AvrRpm1. We found that N. glutinosa did not respond to either effector and was readily transformable as determined by transient expression of β-glucuronidase. Using this system, we determined that Rpg1b-mediated HR in N. glutinosa required co-expression of avrB and a soybean ortholog of the Arabidopsis RIN4 gene. All four soybean RIN4 orthologs tested worked in the assay. In contrast, Rpg1r did not require co-expression of a soybean RIN4 ortholog to recognize AvrRpm1, but recognition was suppressed by co-expression with AvrRpt2. These observations suggest that an endogenous RIN4 gene in N. glutinosa can substitute for the soybean RIN4 ortholog in the recognition of AvrRpm1 by Rpg1r.
Highlights
Effector-triggered immunity (ETI) depends on the expression of disease resistance (R) genes, the majority of which encode nucleotide binding-leucine rich repeat (NB-LRR) proteins
In Arabidopsis thaliana, the R gene RPM1 confers resistance to bacteria expressing both of these effectors, but only if a functional copy of RIN4 is present in the genome [5,6]
Phosphorylation of RIN4 is detected by RPM1, which initiates a signaling cascade that leads to a form of programmed cell death known as the hypersensitive response (HR) that inhibits the spread of the invading pathogen [9]
Summary
Effector-triggered immunity (ETI) depends on the expression of disease resistance (R) genes, the majority of which encode nucleotide binding-leucine rich repeat (NB-LRR) proteins. Indirect recognition requires an intermediate protein that serves as a substrate for the effector These intermediate proteins are targeted by effectors and can be modified in ways such as proteolytic cleavage or phosphorylation. In Arabidopsis thaliana, the R gene RPM1 confers resistance to bacteria expressing both of these effectors, but only if a functional copy of RIN4 is present in the genome [5,6]. This is considered a classic example of indirect recognition. The R protein (RPM1) guards the effector target (RIN4), which is modified in the presence of both AvrB and AvrRpm1 [6]. Phosphorylation of RIN4 is detected by RPM1, which initiates a signaling cascade that leads to a form of programmed cell death known as the hypersensitive response (HR) that inhibits the spread of the invading pathogen [9]
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