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Plants defend themselves against pathogens by activating an array of immune responses. Unfortunately, immunity programs may also cause unintended collateral damage to the plant itself. The quantitative disease resistance gene  ACCELERATED CELL DEATH 6  ( ACD6 ) serves to balance growth and pathogen resistance in natural populations of  Arabidopsis thaliana . An autoimmune allele,  ACD6- Est, which strongly reduces growth under specific laboratory conditions, is found in over 10% of wild strains. There is, however, extensive variation in the strength of the autoimmune phenotype expressed by strains with an  ACD6 -Est allele, indicative of genetic modifiers. Quantitative genetic analysis suggests that  ACD6  activity can be modulated in diverse ways, with different strains often carrying different large-effect modifiers. One modifier is  SUPPRESSOR OF NPR1-1 ,  CONSTITUTIVE 1  ( SNC1 ), located in a highly polymorphic cluster of nucleotide-binding domain and leucine-rich repeat (NLR) immune receptor genes, which are prototypes for qualitative disease resistance genes. Allelic variation at  SNC1  correlates with  ACD6 -Est activity in multiple accessions, and a common structural variant affecting the NL linker sequence can explain differences in SNC1 activity. Taken together, we find that an NLR gene can mask the activity of an  ACD6  autoimmune allele in natural  A .  thaliana  populations, thereby linking different arms of the plant immune system.

Modulation of ACD6 dependent hyperimmunity by natural alleles of an Arabidopsis thaliana NLR resistance gene