The plant immune system is well equipped to ward off the attacks of different types of phytopathogens. It primarily relies on two types of immune sensors - plasma membrane-resident receptor-like kinases (RLKs) and intracellular nucleotide-binding domain leucine-rich repeat receptors (NLRs) that engage preferentially in pattern- and effector-triggered immunity, respectively. Delicate fine-tuning, in particular of the NLR-governed branch of immunity, is key to prevent inappropriate and deleterious activation of plant immune responses. Inadequate NLR allele constellations, such as in the case of hybrid incompatibility, and the mis-activation of NLRs or the absence or modification of proteins guarded by these NLRs can result in the spontaneous initiation of plant defense responses and cell death – a phenomenon referred to as plant autoimmunity. Here we review recent insights augmenting our mechanistic comprehension of plant autoimmunity. The recent findings broaden our understanding regarding hybrid incompatibility, unravel candidates for proteins likely guarded by NLRs and underline the necessity for the fine-tuning of NLR expression at various levels to avoid autoimmunity. We further present recently emerged tools to study plant autoimmunity and draw a cross-kingdom comparison to the role of NLRs in animal autoimmune conditions.

Barley mlo mutants are well known for their profound resistance against powdery mildew disease. Recently, mlo mutant plants were generated in hexaploid bread wheat (Triticum aestivum) with the help of transgenic (transcription-activator-like nuclease, TALEN) and non-transgenic (targeted induced local lesions in genomes, TILLING) biotechnological approaches. While full-gene knockouts in the three wheat Mlo (TaMlo) homoeologs, created via TALEN, confer full resistance to the wheat powdery mildew pathogen (Blumeria graminis f.sp. tritici), the currently available TILLING-derived Tamlo missense mutants provide only partial protection against powdery mildew attack. Here, we studied the infection phenotypes of TALEN- and TILLING-derived Tamlo plants to the two hemibiotrophic pathogens Zymoseptoria tritici, causing Septoria leaf blotch in wheat, and Magnaporthe oryzae pv. Triticum (MoT), the causal agent of wheat blast disease. While Tamlo plants showed unaltered outcomes upon challenge with Z. tritici, we found evidence for allele-specific levels of enhanced susceptibility to MoT, with stronger powdery mildew resistance correlated with more invasive growth by the blast pathogen. Surprisingly, unlike barley mlo mutants, young wheat mlo mutant plants do not show undesired pleiotropic phenotypes such as spontaneous callose deposits in leaf mesophyll cells or signs of early leaf senescence. In conclusion, our study provides evidence for allele-specific levels of enhanced susceptibility of Tamlo plants to the hemibiotrophic wheat pathogen MoT.

Loss-of-function alleles of plant MLO genes confer broad-spectrum resistance to powdery mildews in many eudicot and monocot species. Although barley (Hordeum vulgare) mlo mutants have been used in agriculture for more than 40 years, understanding of the molecular principles underlying this type of disease resistance remains fragmentary. Forward genetic screens in barley have revealed mutations in two Required for mlo resistance (Ror) genes that partially impair immunity conferred by mlo mutants. While Ror2 encodes a soluble N-ethylmaleimide-sensitive factor-attached protein receptor (SNARE), the identity of Ror1, located at the pericentromeric region of barley chromosome 1H, remained elusive. We report the identification of Ror1 based on combined barley genomic sequence information and transcriptomic data from ror1 mutant plants. Ror1 encodes the barley class XI myosin Myo11A (HORVU.MOREX.r3.1HG0046420). Single amino acid substitutions of this myosin, deduced from non-functional ror1 mutant alleles, map to the nucleotidebinding region and the interface between the relay-helix and the converter domain of the motor protein.Ror1 myosin accumulates transiently in the course of powdery mildew infection. Functional fluorophorelabeled Ror1 variants associate with mobile intracellular compartments that partially colocalize with peroxisomes. Single-cell expression of the Ror1 tail region causes a dominant-negative effect that phenocopies ror1 loss-of-function mutants. We define a myosin motor for the establishment of mlo-mediated resistance, suggesting that motor protein-driven intracellular transport processes are critical for extracellular immunity, possibly through the targeted transfer of antifungal and/or cell wall cargoes to pathogen contact sites.

Barley mlo mutants are well known for their profound resistance against powdery mildew disease. Recently, mlo mutant plants were generated in hexaploid bread wheat (Triticum aestivum) with the help of transgenic (transcription-activator-like nuclease, TALEN) and non-transgenic (targeted induced local lesions in genomes, TILLING) biotechnological approaches. While full gene knockouts in the three wheat Mlo (TaMlo) homoeologs, created via TALEN, confer full resistance to the wheat powdery mildew pathogen (Blumeria graminis f.sp. tritici), the currently available TILLING-derived Tamlo missense mutants provide only partial protection against powdery mildew attack. Here we studied the infection phenotypes of TALEN- and TILLING-derived Tamlo plants to the two hemibiotrophic pathogens Zymoseptoria tritici, causing Septoria leaf blotch in wheat, and Magnaporthe oryzae pv. Triticum (MoT), the causal agent of wheat blast disease. While Tamlo plants showed unaltered outcomes upon challenge with Z. tritici, we found allele-specific levels of enhanced susceptibility to MoT, with stronger powdery mildew resistance correlated with more invasive growth by the blast pathogen. Surprisingly, unlike barley mlo mutants, young wheat mlo mutant plants do not show undesired pleiotropic phenotypes such as spontaneous callose deposits in leaf mesophyll cells or signs of early leaf senescence. In conclusion, our study provides evidence for allele-specific levels of enhanced susceptibility of Tamlo plants to the hemibiotrophic wheat pathogen MoT.