Corrigendum to: Genetics of autoimmunity in plants: an evolutionary genetics perspective (New Phytologist, (2021), 229, 3, (1215-1233), 10.1111/nph.16947)

New Phytologist 229 (2021), 1215–1233, doi: 10.1111/nph.16947 Since its publication, the authors of Wan et al. (2021) have brought to our attention an error in their article. The allele labels in Fig. 1(b) were incorrectly presented. The correct Fig. 1 is shown below. 1 Fig. (Figure presented.) Simple genetics of hybrid necrosis conforming to the Bateson–Dobzhansky–Muller (BDM) model. (a) The BDM model of hybrid incompatibility with Dangerous Mix (DM) examples from hybrid necrosis cases in Arabidopsis thaliana. From an ancestral genotype, represented as aabb at the two loci, mutations arise and become fixed in the separate lineages. Derived alleles are represented with capital letters A and B. When individuals with the derived alleles hybridize, genetic incompatibility between A and B results in hybrid dysfunction. The first example of cloned DM genes, DM1 and DM2 encoding NLR receptors, are illustrated. Other examples of hybrid necrosis pairs are shown in the box: DM1/DM2, a TNL/TNL pair; DM2/DM3, a TNL/enzyme pair; DM6/DM7, a CNL/CC (RPW8) pair; DM8/DM8, a TNL/TNL pair. TIR, Toll/interleukin-1 receptor domain; CC, coiled-coil domain; NB-ARC, nucleotide-binding domain; TNL, NLR with TIR. CNL, NLR with CC. See also Table 1 for details and references of these hybrid necrosis pairs. (b) Punnett square demonstrates a phenotypic segregation with differing severity of autoimmunity in F₂ generation. The ratio of segregation reflects a degree of dominance and the number of interacting loci underlying autoimmunity. Photographs of A. thaliana are not scaled. We apologize to our readers for this mistake.