The arabidopsis resistance-like gene SNC1 is activated by mutations in SRFR1 and contributes to resistance to the bacterial effector AvrRps4

The suppressor of rps4-rld1 (srfr1) gene was identified based on enhanced avrrps4-triggered resistance in the naturally susceptible arabidopsis accession rld. no other phenotypic effects were recorded,and the extent of srfr1 involvement in regulating effector-triggered immunity was unknown. here we show that mutations in srfr1 in the accession columbia-0 (col-0) lead to severe stunting and constitutive expression of the defense gene pr1. these phenotypes were temperaturedependent. a cross between srfr1-1 (rld background) and srfr1-4 (col-0) showed that stunting was caused by a recessive locus in col-0. mapping and targeted crosses identified the col-0-specific resistance gene snc1 as the locus that causes stunting. srfr1 was proposed to function as a transcriptional repressor,and snc1 is indeed overexpressed in srfr1-4. interestingly,co-regulated genes in the snc1 cluster are also upregulated in the srfr1-4 snc1-11 double mutant,indicating that the overexpression of snc1 is not a secondary effect of constitutive defense activation. in addition,a col-0 rps4 mutant showed full susceptibility to bacteria expressing avrrps4 at 24°c but not at 22°c,while rld susceptibility was not temperature-dependent. the rps4-2 snc1-11 double mutant showed increased,but not full,susceptibility at 22°c,indicating that additional cross-talk between resistance pathways may exist. intriguingly,when transiently expressed in nicotiana benthamiana,srfr1,rps4 and snc1 are in a common protein complex in a cytoplasmic microsomal compartment. our results highlight srfr1 as a convergence point in at least a subset of tir-nbs-lrr protein-mediated immunity in arabidopsis. based on the cross-talk evident from our results,they also suggest that reports of constitutive resistance phenotypes in col-0 need to consider the possible involvement of snc1. © 2010 kim et al.