Plant Immune System

Last update: Sep 2020

Plants have several ways of protecting themselves against pathogens. One basic immunity type, similar to innate immunity in animals, is called Pathogen-Associated Molecular Pattern-Triggered Immunity (PAMP-Triggered Immunity, PTI). PAMPs are structural elements of pathogenic microorganisms and are characterized by large diversity. PAMPs are recognized by Pattern Recognition Receptors (PRR), which relay the signal downstream via MAPK (MAP kinase) cascade. This results in the induction of the plant's immune response, such as the production of antimicrobial molecules or the formation of physical barriers against the invading pathogens (Fig.1.a). PAMP-triggered immunity is characterized by low specificity. One example of PAMP is flagellar protein flg22, which is recognized by the FLS2 protein (PRR). PRRs are similar in structure to Toll-like receptors, which mediate innate immunity in animals. For example, FLS2 consists of a leucine-rich repeat and a kinase domain.

Figure 1. PAMP-triggered immunity, Effector-Triggered Susceptibility and Effector-Triggered Immunity

In order to counteract the plant's PAMP-triggered immunity, pathogenic microbe​s produce molecules called effectors, which are secreted inside of the plant cells, impeding the immune responses through, for example, inhibiting the PPRs (Fig.1.b). Effectors have very high diversity and are often species-specific, which makes them very effective against the low-specificity PAMP-triggered immunity. As a response to effectors, plants have developed Effector-triggered immunity (ETI), which is characterized by high specificity. ETI takes advantage of R (Resistance) proteins, which can specifically recognize effectors and induce a potent immune response, such as hypersensitive response (HR) characterized by rapid plant cell death (Fig.1.c).

Plant immune system constantly evolves as the result of the arms race between pathogens and plants. The evolution of plant immunity in response to pathogens and their effectors, and the PTI and ETI immune response levels are illustrated in Figure 2. Note that once defense reaches a certain amplitude, programmed cell death (PCD) occurs as part of the hypersensitive response.

Figure 2. Zig-zag model illustrating the fluctuating plant defense levels as pathogens and plants evolve.

Systemic Acquired Resistance (SAR) is another defense mechanism used by plants in order to gain long-term (weeks-month, sometimes season) protection against a variety of pathogens. When a plant is infected, necrotic lesions form on its leaves, often as a result of the hypersensitive response. This leads to an increase in the concentration of salicylic acid, which acts as a signal molecule. Next, SAR genes, including genes encoding pathogenesis-related (PR) proteins, become upregulated. Several PR proteins were confirmed to exhibit antimicrobial activity, thus conferring long-lasting pathogen resistance during subsequent infections. Notably, though SAR is induced locally (leaves), the defense signal is relayed throughout the plant, which can contribute to the resistance of the entire organism.

Figure 3. Systemic Acquired Resistance induces PR protein production in tissues distant to the attacked site

Lastly, plants exhibit resistance against viruses via the RNA silencing mechanism. After a virus infects a plant, it begins to replicate, using RNA-dependent RNA polymerases (RDRs) to make dsRNA. A plant can cleave this dsRNA with Dicer-like (DCL) proteins and produce a 21-22 nucleotide long double-stranded siRNA. This ds-siRNA binds to Argonaute (AGO) protein and forms an RNA-induced silencing complex (RISC) that can cleave and degrade the target (complementary to siRNA guide strand) viral RNA (Fig.4). Moreover, the silencing signal can move to the surrounding plant cells through channels called plasmodesmata or phloem tissue, spreading the RNA silencing signal. Thus, the plant gains antiviral resistance.

However, viruses have developed virus suppressor proteins, which act as suppressors of RNA silencing in several ways. For example, they inhibit DCL proteins, hinder the RNA-cleaving activity of AGO, or prevent the RNA silencing signal from spreading to surrounding plant cells.

Figure 4. Viral RNA silencing mechanism



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