Vol 444j16 November 2006jdoi:10.1038/nature05286
The plant immune system
Jonathan D. G. Jones1 & Jeffery L. Dangl2
Many plant-associated microbes are pathogens that impair plant growth and reproduction. Plants respond to infection using
a two-branched innate immune system. The first branch recognizes and responds to molecules common to many classes of
microbes, includingnon-pathogens. The second responds to pathogen virulence factors, either directly or through their
effects on host targets. These plant immune systems, and the pathogen molecules to which they respond, provide
extraordinary insights into molecular recognition, cell biology and evolution across biological kingdoms. A detailed
understanding of plant immune function will underpin crop improvement forfood, fibre and biofuels production.
Plant pathogens use diverse life strategies. Pathogenic bacteria proliferate in intercellular spaces (the apoplast) after entering through
gas or water pores (stomata and hydathodes, respectively), or gain
access via wounds. Nematodes and aphids feed by inserting a stylet
directly into a plant cell. Fungi can directly enter plant epidermal
cells, or extendhyphae on top of, between, or through plant cells.
Pathogenic and symbiotic fungi and oomycetes can invaginate feeding structures (haustoria), into the host cell plasma membrane.
Haustorial plasma membranes, the extracellular matrix, and host
plasma membranes form an intimate interface at which the outcome
of the interaction is determined. These diverse pathogen classes all
deliver effectormolecules (virulence factors) into the plant cell to
enhance microbial fitness.
Plants, unlike mammals, lack mobile defender cells and a somatic
adaptive immune system. Instead, they rely on the innate immunity
of each cell and on systemic signals emanating from infection sites1–3.
We previously reviewed disease resistance (R) protein diversity, polymorphism at R loci in wild plants and lackthereof in crops, and
the suite of cellular responses that follow R protein activation1. We
hypothesized that many plant R proteins might be activated indirectly by pathogen-encoded effectors, and not by direct recognition.
This ‘guard hypothesis’ implies that R proteins indirectly recognize
pathogen effectors by monitoring the integrity of host cellular targets
of effector action1,4. Theconcept that R proteins recognize ‘pathogen-induced modified self’ is similar to the recognition of ‘modified
self’ in ‘danger signal’ models of the mammalian immune system5.
It is now clear that there are, in essence, two branches of the plant
immune system. One uses transmembrane pattern recognition
receptors (PRRs) that respond to slowly evolving microbial- or
pathogen-associated molecularpatterns (MAMPS or PAMPs), such
as flagellin6. The second acts largely inside the cell, using the polymorphic NB-LRR protein products encoded by most R genes1. They
are named after their characteristic nucleotide binding (NB) and
leucine rich repeat (LRR) domains. NB-LRR proteins are broadly
related to animal CATERPILLER/NOD/NLR proteins7 and STAND
ATPases8. Pathogen effectors from diversekingdoms are recognized
by NB-LRR proteins, and activate similar defence responses. NBLRR-mediated disease resistance is effective against pathogens that
can grow only on living host tissue (obligate biotrophs), or hemibiotrophic pathogens, but not against pathogens that kill host tissue
during colonization (necrotrophs)9.
Our current view of the plant immune system can be represented
as a fourphased ‘zigzag’ model (Fig. 1), in which we introduce several
important abbreviations. In phase 1, PAMPs (or MAMPs) are recognized by PRRs, resulting in PAMP-triggered immunity (PTI) that can
halt further colonization. In phase 2, successful pathogens deploy
effectors that contribute to pathogen virulence. Effectors can interfere with PTI. This results in effector-triggered susceptibility...
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