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Plant nucleotide-binding domain and leucine-rich repeat-containing (NLR) proteins function as intracellular receptors in response to pathogens and activate effector-triggered immune responses (ETI). The activation of some sensor NLRs (sNLR) by their corresponding pathogen effector is well studied. However, the mechanisms by which the recently defined helper NLRs (hNLR) function to transduce sNLR activation into ETI-associated cell death and disease resistance remains poorly understood. We briefly summarize recent examples of sNLR activation and we then focus on hNLR requirements in sNLR-initiated immune responses. We further discuss how shared sequence homology with fungal self-incompatibility proteins and the mammalian mixed lineage kinase domain like pseudokinase (MLKL) proteins informs a plausible model for the structure and function of an ancient clade of plant hNLRs, called RNLs., (Copyright © 2019. Published by Elsevier Ltd.)

Phytopathogenic microbes multiply in the apoplast-a plant's intercellular spaces-of infected plants, and hence their success relies on the conditions in this habitat. Despite being extracellular parasites, most microbes translocate effectors into host cells that promote disease by acting inside cells. Initial studies suggested that effectors act predominantly as suppressors of plant immunity. These pioneering studies were trend-setting, causing a strong bias in the functional investigation of effectors. Yet, recent studies on bacterial model pathogens have identified effectors that promote disease by causing either increased sugar or water levels in the apoplast. These studies are likely to initiate a new era of effector research that will clarify the disease-promoting rather than defense-suppressing function of effectors, a molecular rather than genetic distinction., (Copyright © 2018 Elsevier Ltd. All rights reserved.)