Plant immunity is the set of recognition and response mechanisms by which plants restrict harmful interactions with other organisms. Surface pattern recognition receptors detect characteristic molecular patterns; intracellular nucleotide-binding leucine-rich repeat receptors can detect pathogen-associated activity. These routes interact rather than forming independent, universally sufficient barriers.
An integrated decoy illustrates how recognition can exploit an attacker's own activity: an immune receptor incorporates a structure resembling a target, so modification of that structure can trigger defence. The RRS1-RPS4 receptor pair is an experimentally studied example.[ref]
Allocation and regulatory conflicts between growth and defence; the sign and magnitude of the relationship depend on environment and genotype.
PAD4, PHYTOALEXIN DEFICIENT 4, is a plant immunity signaling component that interacts with EDS1. Their coupled activity helps connect immune recognition to downstream responses; PAD4 is not itself the generic name of a pathogen-recognition receptor.
Comparative analyses found repeated joint losses of the EDS1-PAD4 pathway and associated genes in several plant lineages. This makes pathway composition an evolutionary question: absence of one component can be informative about the others.[ref]
EDS1 and PAD4 pathway-loss study by Erin L. Baggs and others. Abstract, lineage-associated losses
EDS1, ENHANCED Disease SUSCEPTIBILITY 1, is a plant immunity signaling component that forms complexes with partner proteins, including PAD4. Such interactions connect particular immune-recognition pathways to changes in defence activity.
The pathway is not present unchanged in every plant. Comparative genomic work identified convergent losses of EDS1, PAD4 and associated components, providing evidence for coevolution of an interacting molecular system.[ref]
EDS1 and PAD4 pathway-loss study by Erin L. Baggs and others. Abstract, convergent losses and pathway coevolution
A deleterious hybrid phenotype that can arise from incompatible immune-gene interactions and inappropriate defence activation.
A host resistance and pathogen avirulence specificity relationship; it is not the complete architecture of all plant disease resistance.
A nucleotide-binding leucine-rich repeat receptor, or NLR, is an intracellular immune-receptor protein characterized by a nucleotide-binding region and leucine-rich repeats. In plants, NLRs can detect pathogen-associated molecules or their effects and initiate defensive signaling.
An NLR can work as a sensor, a signaling helper or part of a paired NLR system. Different individuals can carry different receptor inventories, so one reference genome does not fully describe the species-wide pan-NLRome.[ref]
The species-wide collection of NLR genes and alleles across accessions, rather than the inventory in a single reference genome.
A genomic group of related receptor genes shaped by duplication, deletion and sequence exchange; not every NLR is clustered.
A domain incorporated into an immune receptor that mimics an effector target and links its perturbation to immune recognition.
Functionally coupled receptors whose sensor and signaling activities may be partitioned between two genes. Physical linkage can help preserve their compatible inheritance.
The RRS1-RPS4 receptor pair is a coupled immune-receptor system studied in Arabidopsis thaliana. RRS1 includes a WRKY domain resembling targets of pathogen activity, providing an integrated decoy linked to recognition and signaling by the pair.
The mechanism illustrates how a plant can monitor an attack on a host-like structure rather than recognizing only one isolated foreign pattern. It also explains why transferring or losing one receptor need not preserve the behavior of the complete paired NLR system.[ref]
A pattern recognition receptor detects characteristic molecular patterns associated with microbes or damaged tissue. In plant immunity, surface receptors connect extracellular recognition to intracellular signal transduction and defence.
Recognition of a widely shared pattern can provide broad surveillance, but the presence of that pattern does not by itself measure whether the interacting organism will cause disease. Pathogens can also interfere with signaling, which helps explain the additional surveillance provided by intracellular NLRs.
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