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Abstract

Hybrid necrosis in plants refers to a genetic autoimmunity syndrome in the progeny of interspecific or intraspecific crosses. Although the phenomenon was first documented in 1920, it has been unequivocally linked to autoimmunity only recently, with the discovery of the underlying genetic and biochemical mechanisms. The most common causal loci encode immune receptors, which are known to differ within and between species. One mechanism can be explained by the guard hypothesis, in which a guard protein, often a nucleotide-binding site-leucine-rich repeat protein, is activated by interaction with a plant protein that mimics standard guardees modified by pathogen effector proteins. Another surprising mechanism is the formation of inappropriately active immune receptor complexes. In this review, we summarize our current knowledge of hybrid necrosis and discuss how its study is not only informing the understanding of immune gene evolution but also revealing new aspects of plant immune signaling.