Abstract
Plants rely on multiple immune systems to protect themselves from pathogens. When pattern-triggered immunity (PTI)—the first layer of the immune response—is no longer effective as a result of pathogenic effectors, effector-triggered immunity (ETI) often provides resistance. In ETI, host plants directly or indirectly perceive pathogen effectors via resistance proteins and launch a more robust and rapid defense response. Resistance proteins are typically found in the form of nucleotide-binding and leucine-rich-repeat-containing receptors (NLRs). Upon effector recognition, an NLR undergoes structural change and associates with other NLRs. The dimerization or oligomerization of NLRs signals to downstream components, activates “helper” NLRs, and culminates in the ETI response. Originally, PTI was thought to contribute little to ETI. However, most recent studies revealed crosstalk and cooperation between ETI and PTI. Here, we summarize recent advancements in our understanding of the ETI response and its components, as well as how these components cooperate in the innate immune signaling pathways. Based on up-to-date accumulated knowledge, this review provides our current perspective of potential engineering strategies for crop protection.
Highlights
Plants and pathogens continually compete for supremacy as they coevolve
The first layer of the plant immune system is pattern-triggered immunity (PTI), which is activated by pathogen-associated molecular patterns (PAMPs), the conserved molecular structures of pathogens such as fungal chitin or bacterial flagellin, or damage-associated molecular patterns, which are molecules resulting from plant–pathogen interactions such as peptides and oligosaccharides (Figure 1)
These inducers can be recognized by pattern recognition receptors (PRRs), plasma membrane-localized plant immune receptors, which are mainly found in the forms of receptor-like protein kinases and receptor-like proteins [6,7,8]
Summary
Plants and pathogens continually compete for supremacy as they coevolve. In nature, many plants are resistant to most pathogens, but some pathogenic microbes are capable of causing severe diseases. The first layer of the plant immune system is pattern-triggered immunity (PTI), which is activated by pathogen-associated molecular patterns (PAMPs), the conserved molecular structures of pathogens such as fungal chitin or bacterial flagellin, or damage-associated molecular patterns, which are molecules resulting from plant–pathogen interactions such as peptides and oligosaccharides (Figure 1) These inducers can be recognized by pattern recognition receptors (PRRs), plasma membrane-localized plant immune receptors, which are mainly found in the forms of receptor-like protein kinases and receptor-like proteins [6,7,8]. To suppress PTI, the and pathogens deploy peat (LRR)-containing (NLRs), the second immune layer, ETI (indicated (LRR)by blue effectors. When they arereceptors recognized by nucleotide-binding andcalled leucine-rich-repeat arrows), takes place. NLRs directly or indirectly perceive pathogenic effectors, leading to a containing receptors (NLRs), the second immune layer, called ETI (indicated by blue arrows), confortakes mational togetherperceive with several intracellular signaling trigger the place. We summarize the current understanding and provide a perspective of crop engineering strategies based on this knowledge
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