PAMPs/MAMPs

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Plants are constantly exposed to microbes that, to be pathogenic,(in most cases) must access the plant interior, either by penetrating the leaf or root surface directly or by entering through wounds or natural openings such as stomata. Once entered, microbes must overcome the rigid plant cell wall to access to the host plasma membrane where they encounter extracellular surface receptors that recognize pathogen-associated molecular patterns (PAMPs).

(Chisholm ST, Coaker G, Day B, Staskawicz BJ. Host-microbe interactions: shaping the evolution of the plant immune response. Cell. 2006 Feb 24;124(4):803-14 PMID: 16497589)

Resistance and susceptibility to pathogens.
Microbial- or pathogen-associated molecular patterns (MAMPS or PAMPs)are recognized by plants through pattern recognition receptors (PRRs) present at the plant’s cell surface, inducing PAMP-triggered immunity (PTI).

Successful pathogens produce effectors able to inhibit PTI; as a response, plants can perceive such effectors through additional receptors (typically NB-LRR proteins) and promote effector-triggered immunity (ETI; formerly known as gene-for-gene resistance).

PRR response is carachterized by sensitivity and specificity: it allows plants expressing the right receptor to perceive the corresponding MAMP or PAMP also at subnanomolar concentrations, through the recognition of a conserved epitope.

(Boller T, He SY. Innate immunity in plants: an arms race between pattern recognition receptors in plants and effectors in microbial pathogens. Science. 2009 May 8;324(5928):742-4. PMID: 19423812) An adapted pathogen must effectively overcome host resistance to enable its infection of a given plant.

(Zhang J, Lu H, Li X, Li Y, Cui H, Wen CK, Tang X, Su Z, Zhou JM. Effector-triggered and pathogen-associated molecular pattern-triggered immunity differentially contribute to basal resistance to Pseudomonas syringae. Mol Plant Microbe Interact. 2010 Jul;23(7):940-8. PMID: 20521956)


Pathogenic microbes evolved mechanisms to avoid plant recognition or to suppress defense responses through secreted virulence effectors. In turn, plants evolved R proteins able to recognize these effectors or their action, which results in effector-triggered immunity. This model is referred to as the zig-zag model and PAMP perception acts as an evolutionary driving force.

(Zipfel C, Robatzek S. Pathogen-associated molecular pattern-triggered immunity: veni, vidi...? Plant Physiol. 2010 Oct;154(2):551-4. PMID: 20921183)

It is thought that PTI and ETI are sequentially evolved to counter the co-evolving pathogens and modern pathogens have acquired effectors to collectively overcome PTI and ETI in their host plants.

(Zhang J, Lu H, Li X, Li Y, Cui H, Wen CK, Tang X, Su Z, Zhou JM. Effector-triggered and pathogen-associated molecular pattern-triggered immunity differentially contribute to basal resistance to Pseudomonas syringae. Mol Plant Microbe Interact. 2010 Jul;23(7):940-8.PMID: 20521956)

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