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Alternatively, effector-triggered susceptibility (ETS) can occur if an effector protein can block the immune response triggered by pattern recognition receptors (PRR) and evade immunity, allowing the pathogen to propagate in the host. [1] ETI was first identified in plants [2] [3] but has also been identified in animal cells. [4]
The system is known as PAMP-triggered immunity or as pattern-triggered immunity (PTI). [7] [6] [8] The second tier, primarily governed by R gene products, is often termed effector-triggered immunity (ETI). ETI is typically activated by the presence of specific pathogen "effectors" and then triggers strong antimicrobial responses (see R gene ...
The remaining immunity is called basal defense [4] which can limit the spread of virulent pathogens in their hosts but it is typically insufficient to prevent disease. [1] In response to this threat, plant's have evolved effector recognition protein receptors to recognise, or monitor, effectors and initiate effector-triggered immunity (ETI). [5]
Some pathogens carry effectors that suppress PTI in the plant and induce effector triggered susceptibility (ETS). In response, plants evolve resistance (R) genes that encode for proteins capable of recognizing the newly developed pathogen effectors, resulting in what is called effector triggered immunity (ETI).
To protect themselves from the actions of effector proteins, plants have evolved resistance proteins (R proteins), which may in turn recognise an effector and trigger a second tier of immune responses, known as effector-triggered immunity (ETI).
To make up for this lack of defense, plants use the pattern-triggered immunity (PTI) and effector-triggered immunity (ETI) pathways to combat trauma and pathogens. PTI is the first line of defense in plants and is triggered by PAMPs to initiate signaling throughout the plant that damage has occurred to a cell. Along with the PTI, DAMPs are also ...
Upon ligand recognition, the plant PRRs transduce "PAMP-triggered immunity" (PTI). [42] Plant immune systems also encode resistance proteins that resemble NOD-like receptors (see above), that feature NBS and LRR domains and can also carry other conserved interaction domains such as the TIR cytoplasmic domain found in Toll and interleukin ...
The induction of plant-induced resistance to pathogen protection was identified in 1901 and was described as the "system of acquired resistance." Subsequently, several different terms have been used, namely, "acquired physiological immunity", "resistance displacement", "plant immune function" and "induced system resistance."