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Abstract
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.
Highlights
Plants rely on a sophisticated immune system to defend themselves against pathogens
We discovered that there are variants at other genetic loci that can mask the effects of an overly active ACCELERATED CELL DEATH 6 (ACD6) gene
The SNC1 variant that attenuates ACD6 activity is rather common in A. thaliana populations, suggesting that new combinations of the hyperactive ACD6 variant and this antagonistic SNC1 variant will often arise by natural crosses
Summary
Plants rely on a sophisticated immune system to defend themselves against pathogens. A central challenge for plants is how to achieve a fast, effective response upon pathogen attack, while at the same time preventing spontaneous firing of the signaling machinery in the absence of danger [1]. Inappropriate activation of immune signaling can reduce growth or even damage the plant’s own cells, while an inefficient immune response makes plants more likely to succumb to pathogen attack [2,3,4,5,6]. Highly effective immune alleles may have background activity, they will be favored when pathogen pressure is high. If differently active alleles exist at the same locus, such temporal or spatial variation in pathogen pressure will maintain both types of alleles at ratios that reflect the prevalence of the different environments; this is one example of the phenomenon of balancing selection [8,9,10]. NLR immune receptors detect the presence of so-called pathogen effector molecules, leading to effector-triggered immunity (ETI). Variation in NLR immune receptors is linked to the fact that effectors are rarely essential for pathogen survival, and that even closely related pathogens can greatly vary in effector content [16,18]
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