One of two major response pathways is initiated when plants are attacked by microbial pathogens. One major difference difference between these two pathways is the specificity with which the plant identifies the pathogen. In one pathway, the plant recognizes general signals common to a broad array of pathogens. These signals are known as pathogen-associated molecular patterns (PAMPs), thus this pathway is called PAMP-triggered immunity (PTI). In the second kind of signaling pathway, the plant responds to highly specific molecules secreted by the pathogen. These molecules are called effectors, hence this pathway is known as effector-triggered immunity (ETI).
PAMP-triggered immunity (PTI)
The hallmark of PTI is the ability of the plant to detect the molecular signature of pathogens. These signatures may take many different forms, including peptides derived from bacterial flagellum proteins, chitin (which makes up the cell wall of fungi), double-stranded RNA, and certain sequences of DNA common to microbes. Each of these presents a specific molecular pattern recognizable by the plant as indicating the presence of a potentially pathogenic organism.
These molecular signatures are detected by the cell through a class of proteins known as pattern recognition receptors (PRRs) that are specific for certain molecules. For example, the flagellum peptide known as flg22 is perceived by a PRR called FLS2. It is important to note that the flg22 peptide is a common motif found in all bacterial flagella as they are hydrolyzed. Upon perceiving flg22, FLS2 interacts with and phosphorylates the first member in a kinase cascade called MEKK1. MEKK1 phosphorylates one or more of several kinases (MEK4/5), which target several other kinases (MPK3/6). This series of events is known as a mitogen-activated protein kinase cascade, a signal transduction pathway common across all organisms. This kind of signaling system is modular and achieves the amplification of a single signal. The end result of all of this kinase activity is the activation of several transcription factors (WRKY22/29) that control defense-regulated genes. One example of these genes is those involved in synthesis of salicylic acid and jasmonic acid. There is also evidence that the kinase cascade can modify chromatin structure through acetylation and methylation, both of which can have a strong effect on genome-wide gene expression. All of this signaling has the overall result of “priming” the plant defense response.
Effector-triggered immunity (ETI)
The fundamental difference between PTI and ETI is the degree of specificity, with ETI representing a highly-specific, gene-for-gene defense response. The high specificity makes this pathway less durable than PTI and more targeted against an individual pathogen.
The ETI response is initiated by the secretion of effector molecules by the secretory system of bacterial cells. These effector molecules, called Avr (avirulence) proteins, are detected by the plant through recognitional resistance genes, or R-genes. The R genes encode Ser/Thr protein kinases, which interact with partners called nucleotide binding leucine-rich repeat proteins (NB-LRRs). This signaling complex also touches of a kinase cascade, but the overall result is the activation of the hypersensitive response and rapid cell death around the site of infection.
The avirulence (Avr) proteins represent an interesting evolutionary riddle: how is it adaptive for the bacteria to secrete a molecule that signals its presence to the plant? In at least one case, the answer seems to be related to the function of the Avr protein. AvrAC, secreted by a strain of Xanthomonas, acts as a uridyl transferase that modifies a component of the signal cascade such that its phosphorylation site is masked. Unable to be phosphorylated, the kinase cascade is interrupted and the plant fails to activate the hypersensitive response.