Effector-triggered immunity

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The host cell detects the presence of the pathogen directly from the molecular patterns on the pathogen and indirectly through the damage caused to the host cell by the toxins generated by the pathogen. Effector Triggered Immunity.tif
The host cell detects the presence of the pathogen directly from the molecular patterns on the pathogen and indirectly through the damage caused to the host cell by the toxins generated by the pathogen.

Effector-triggered immunity (ETI) is one of the pathways, along with the pattern-triggered immunity (PTI) pathway, by which the innate immune system recognises pathogenic organisms and elicits a protective immune response. ETI is elicited when an effector protein secreted by a pathogen into the host cell is successfully recognised by the host. 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 basis of the ETI model lies in the gene-for-gene resistance hypothesis proposed by Harold Henry Flor in 1942. [5] Flor proposed that plants may express resistance (R) proteins that recognise avirulence (Avr) proteins from pathogens, thus making them resistant to pathogen invasion. His hypothesis has since been confirmed by identifying multiple Avr-R gene pairs. [6] Some Avr proteins are direct ligands for receptors encoded by the R genes, such as the Leu-rich repeat receptors (LRRs). Other Avr proteins, called effectors, act to modify host proteins and those modifications are sensed by R proteins on the host plant side to initiate effector-triggered immunity. [7]

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<span class="mw-page-title-main">Effector (biology)</span> Small molecule affecting biological activity

In biology, an effector is a general term that can refer to several types of molecules or cells depending on the context:

<span class="mw-page-title-main">Toll-like receptor</span> Pain receptors and inflammation

Toll-like receptors (TLRs) are a class of proteins that play a key role in the innate immune system. They are single-spanning receptors usually expressed on sentinel cells such as macrophages and dendritic cells, that recognize structurally conserved molecules derived from microbes. Once these microbes have reached physical barriers such as the skin or intestinal tract mucosa, they are recognized by TLRs, which activate immune cell responses. The TLRs include TLR1, TLR2, TLR3, TLR4, TLR5, TLR6, TLR7, TLR8, TLR9, TLR10, TLR11, TLR12, and TLR13. Humans lack genes for TLR11, TLR12 and TLR13 and mice lack a functional gene for TLR10. The receptors TLR1, TLR2, TLR4, TLR5, TLR6, and TLR10 are located on the cell membrane, whereas TLR3, TLR7, TLR8, and TLR9 are located in intracellular vesicles.

<span class="mw-page-title-main">Adaptive immune system</span> Subsystem of the immune system

The adaptive immune system, also known as the acquired immune system, or specific immune system is a subsystem of the immune system that is composed of specialized, systemic cells and processes that eliminate pathogens or prevent their growth. The acquired immune system is one of the two main immunity strategies found in vertebrates.

Pathogen-associated molecular patterns (PAMPs) are small molecular motifs conserved within a class of microbes, but not present in the host. They are recognized by toll-like receptors (TLRs) and other pattern recognition receptors (PRRs) in both plants and animals. This allows the innate immune system to recognize pathogens and thus, protect the host from infection.

Pattern recognition receptors (PRRs) play a crucial role in the proper function of the innate immune system. PRRs are germline-encoded host sensors, which detect molecules typical for the pathogens. They are proteins expressed mainly by cells of the innate immune system, such as dendritic cells, macrophages, monocytes, neutrophils, as well as by epithelial cells, to identify two classes of molecules: pathogen-associated molecular patterns (PAMPs), which are associated with microbial pathogens, and damage-associated molecular patterns (DAMPs), which are associated with components of host's cells that are released during cell damage or death. They are also called primitive pattern recognition receptors because they evolved before other parts of the immune system, particularly before adaptive immunity. PRRs also mediate the initiation of antigen-specific adaptive immune response and release of inflammatory cytokines.

<span class="mw-page-title-main">Innate immune system</span> One of the two main immunity strategies

The innate, or nonspecific, immune system is one of the two main immunity strategies in vertebrates. The innate immune system is an alternate defense strategy and is the dominant immune system response found in plants, fungi, insects, and primitive multicellular organisms.

Systemic acquired resistance (SAR) is a "whole-plant" resistance response that occurs following an earlier localized exposure to a pathogen. SAR is analogous to the innate immune system found in animals, and although there are many shared aspects between the two systems, it is thought to be a result of convergent evolution. The systemic acquired resistance response is dependent on the plant hormone, salicylic acid.

<span class="mw-page-title-main">Hypersensitive response</span>

Hypersensitive response (HR) is a mechanism used by plants to prevent the spread of infection by microbial pathogens. HR is characterized by the rapid death of cells in the local region surrounding an infection and it serves to restrict the growth and spread of pathogens to other parts of the plant. It is analogous to the innate immune system found in animals, and commonly precedes a slower systemic response, which ultimately leads to systemic acquired resistance (SAR). HR can be observed in the vast majority of plant species and is induced by a wide range of plant pathogens such as oomycetes, viruses, fungi and even insects.

The gene-for-gene relationship is a concept in plant pathology that plants and their diseases each have single genes that interact with each other during an infection. It was proposed by Harold Henry Flor who was working with rust (Melampsora lini) of flax (Linum usitatissimum). Flor showed that the inheritance of both resistance in the host and parasite ability to cause disease is controlled by pairs of matching genes. One is a plant gene called the resistance (R) gene. The other is a parasite gene called the avirulence (Avr) gene. Plants producing a specific R gene product are resistant towards a pathogen that produces the corresponding Avr gene product. Gene-for-gene relationships are a widespread and very important aspect of plant disease resistance. Another example can be seen with Lactuca serriola versus Bremia lactucae.

Pyroptosis is a highly inflammatory form of lytic programmed cell death that occurs most frequently upon infection with intracellular pathogens and is likely to form part of the antimicrobial response. This process promotes the rapid clearance of various bacterial, viral, fungal and protozoan infections by removing intracellular replication niches and enhancing the host's defensive responses. Pyroptosis can take place in immune cells and is also reported to occur in keratinocytes and some epithelial cells.

<i>Pseudomonas syringae</i> Species of bacterium

Pseudomonas syringae is a rod-shaped, Gram-negative bacterium with polar flagella. As a plant pathogen, it can infect a wide range of species, and exists as over 50 different pathovars, all of which are available to researchers from international culture collections such as the NCPPB, ICMP, and others.

Damage-associated molecular patterns (DAMPs) are molecules within cells that are a component of the innate immune response released from damaged or dying cells due to trauma or an infection by a pathogen. They are also known as danger signals, and alarmins because they serve as warning signs to alert the organism to any damage or infection to its cells. DAMPs are endogenous danger signals that are discharged to the extracellular space in response to damage to the cell from mechanical trauma or a pathogen. Once a DAMP is released from the cell, it promotes a noninfectious inflammatory response by binding to a pattern recognition receptor. Inflammation is a key aspect of the innate immune response; it is used to help mitigate future damage to the organism by removing harmful invaders from the affected area and start the healing process. As an example, the cytokine IL-1α is a DAMP that originates within the nucleus of the cell which, once released to the extracellular space, binds to the PRR IL-1R, which in turn initiates an inflammatory response to the trauma or pathogen that initiated the release of IL-1α. In contrast to the noninfectious inflammatory response produced by DAMPs, pathogen-associated molecular patterns initiate and perpetuate the infectious pathogen-induced inflammatory response. Many DAMPs are nuclear or cytosolic proteins with defined intracellular function that are released outside the cell following tissue injury. This displacement from the intracellular space to the extracellular space moves the DAMPs from a reducing to an oxidizing environment, causing their functional denaturation, resulting in their loss of function. Outside of the aforementioned nuclear and cytosolic DAMPs, there are other DAMPs originated from different sources, such as mitochondria, granules, the extracellular matrix, the endoplasmic reticulum, and the plasma membrane.

Resistance genes (R-Genes) are genes in plant genomes that convey plant disease resistance against pathogens by producing R proteins. The main class of R-genes consist of a nucleotide binding domain (NB) and a leucine rich repeat (LRR) domain(s) and are often referred to as (NB-LRR) R-genes or NLRs. Generally, the NB domain binds either ATP/ADP or GTP/GDP. The LRR domain is often involved in protein-protein interactions as well as ligand binding. NB-LRR R-genes can be further subdivided into toll interleukin 1 receptor (TIR-NB-LRR) and coiled-coil (CC-NB-LRR).

Biotic stress is stress that occurs as a result of damage done to an organism by other living organisms, such as bacteria, viruses, fungi, parasites, beneficial and harmful insects, weeds, and cultivated or native plants. It is different from abiotic stress, which is the negative impact of non-living factors on the organisms such as temperature, sunlight, wind, salinity, flooding and drought. The types of biotic stresses imposed on an organism depend the climate where it lives as well as the species' ability to resist particular stresses. Biotic stress remains a broadly defined term and those who study it face many challenges, such as the greater difficulty in controlling biotic stresses in an experimental context compared to abiotic stress.

<span class="mw-page-title-main">Plant disease resistance</span> Ability of a plant to stand up to trouble

Plant disease resistance protects plants from pathogens in two ways: by pre-formed structures and chemicals, and by infection-induced responses of the immune system. Relative to a susceptible plant, disease resistance is the reduction of pathogen growth on or in the plant, while the term disease tolerance describes plants that exhibit little disease damage despite substantial pathogen levels. Disease outcome is determined by the three-way interaction of the pathogen, the plant and the environmental conditions.

In plant biology, elicitors are extrinsic or foreign molecules often associated with plant pests, diseases or synergistic organisms. Elicitor molecules can attach to special receptor proteins located on plant cell membranes. These receptors are able to recognize the molecular pattern of elicitors and trigger intracellular defence signalling via the octadecanoid pathway. This response results in the enhanced synthesis of metabolites which reduce damage and increase resistance to pest, disease or environmental stress. This is an immune response called pattern triggered immunity (PTI).

Guard theory is a branch of immunology which concerns the innate sensing of stereotypical consequences of a virulence factor or pathogen. This is in contrast to the classical understanding of recognition by the innate immune system, which involves recognition of distinct microbial structures- pathogen-associated molecular patterns (PAMPs)- with pattern recognition receptors (PRRs). Some of these stereotypical consequences of virulence factors and pathogens may include altered endosomal trafficking and changes in the cytoskeleton. These recognition mechanisms would work to complement classical pattern recognition mechanisms.

<span class="mw-page-title-main">EF-Tu receptor</span> Pattern-recognition receptor (PRR)

EF-Tu receptor, abbreviated as EFR, is a pattern-recognition receptor (PRR) that binds to the prokaryotic protein EF-Tu in Arabidopsis thaliana. This receptor is an important part of the plant immune system as it allows the plant cells to recognize and bind to EF-Tu, preventing genetic transformation and protein synthesis in pathogens such as Agrobacterium.

<span class="mw-page-title-main">Gene-for-gene interactions in rust fungi</span>

The study of gene-for-gene interactions uncovers genetic components, evolutionary impacts, and ecological/economic implications between rust fungi and plants. Rust fungi utilize the gene-for-gene interaction to invade host plants. Conversely, host plants utilize the gene-for-gene interaction to prevent invasion of rust fungi.

<span class="mw-page-title-main">Fungal effectors</span>

Fungal effectors are proteins or non-proteinaceous molecules secreted by pathogenic fungi into a host organism in order to modulate the host's immune response.

References

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