Journal
FEBS JOURNAL
Volume 283, Issue 8, Pages 1385-1391Publisher
WILEY
DOI: 10.1111/febs.13613
Keywords
autoimmunity; cell death; innate immunity; negative regulators; resistance proteins
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Genetics studies the structure/function of genes via the characterization of their mutant phenotypes. In plants, a readily scorable mutant phenotype comprises macroscopic lesions symptomatic of disease in the absence of pathogens. Such mutants therefore exhibit autoimmune phenotypes. Many of these mutants are considered to be associated with immunity and the corresponding genes have been described as negative regulators' of immunity and/or cell death. Pathogens deliver effectors into host cells to increase infectivity by modifying or removing host proteins. Plants detect effectors via nucleotide-binding, leucine-rich repeat (NLR) immune receptors, which monitor host effector targets. In response to effector-mediated target tampering, NLR proteins potentiate immunity. The guard hypothesis proposes that NLRs guard' host guardees' targeted by pathogen effectors. An obvious corollary to this guard model is that forms of plant autoimmunity are a result of inappropriate NLR protein activation. In this review, we discuss what is known about some of the negative regulators' of immunity, and propose simple strategies that may help to characterize autoimmune mutants.
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