Abstract
Parasites target the plant immune system for successful colonization. A new study in PLOS Biology reveals that unrelated parasites have evolved effectors that specifically suppress the function of helper nucleotide-binding leucine-rich repeats (NLRs), explaining the complex plant-parasite coevolutionary dynamics.
Highlights
Plants have evolved to recognize parasiteencoded effectors via the nucleotide-binding leucine-rich repeat (NLR) class of immune receptors and activate more robust effector-triggered immunity (ETI), which leads to cell death at the site of infection called the hypersensitive response (HR) [1] (Fig 1)
Using an effectoromics screen with a library consisting of a total of 165 effectors from bacteria, oomycete, nematode, and aphid, they have identified 5 effectors that can suppress the cell death induced by 2 NB-LRR protein required for HR-associated cell death (NRC)-dependent sensor NLRs, Prf or Rpi-blb2, in Nicotiana benthamiana plants
SS15, from the cyst nematode Globodera rostochiensis, and AVRcap1b, from the potato late blight oomycete pathogen P. infestans, showed strong suppression of the cell death triggered by autoimmune mutants of NRC2 and NRC3, but not NRC4
Summary
Plants have evolved to recognize parasiteencoded effectors via the nucleotide-binding leucine-rich repeat (NLR) class of immune receptors and activate more robust effector-triggered immunity (ETI), which leads to cell death at the site of infection called the hypersensitive response (HR) [1] (Fig 1). Accumulating evidence indicates that some sensor NLRs require the function of other NLRs, referred to as helper NLRs, to activate downstream immune signaling and cell death induction [4,5] (Fig 1).
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