Author: Chaudhari, Prateek; Ahmed, Bulbul; Joly, David L; Germain, Hugo
Title: Effector biology during biotrophic invasion of plant cells Document date: 2014_10_1
ID: 7g8st5cz_1
Snippet: Being sessile organisms, plants are constantly challenged by their environment, and their situation is compounded by biotic stresses. A number of plant pathogens, such as fungi, oomycetes, bacteria, viruses, nematodes, etc., pose serious threats to the plant well-being. Nonetheless, over the course of evolution, plants have acquired a refined, two-layered immune system to respond to pathogen attack. 1 The first line of plant immunity, thought to .....
Document: Being sessile organisms, plants are constantly challenged by their environment, and their situation is compounded by biotic stresses. A number of plant pathogens, such as fungi, oomycetes, bacteria, viruses, nematodes, etc., pose serious threats to the plant well-being. Nonetheless, over the course of evolution, plants have acquired a refined, two-layered immune system to respond to pathogen attack. 1 The first line of plant immunity, thought to be the most ancient, relies on the recognition of evolutionarilyconserved pathogen molecules known as PAMPs (pathogenassociated molecular patterns), and is therefore referred to as PAMP-triggered immunity (PTI). [2] [3] [4] Pattern recognition receptors (PRRs) are plant components responsible for the detection of PAMPs 5 and for activating the immune machinery of plants. One of the best characterized PRRs in plants is FLAGELLIN SENSITIVE 2 (FLS2), a receptor kinase that activates PTI upon perception of flagellin, a conserved protein found in bacterial flagellum. 6, 7 To gain greater access to plant resources for subsequent colonization, plant pathogens, just like their animal equivalents, deploy an arsenal of highly-sophisticated molecules known as effectors. These molecules greatly augment the pathogen's capacity to propagate on its host by interfering with various cellular processes, including PTI. Fortunately, plants monitor the presence of some effectors through their resistance (R)-proteins, which constitutes the second line of defense, also known as effector-triggered immunity (ETI). 1 ETI typically results in a strong hypersensitive response, characterized by cell death, which shows some mechanistical similarities with apoptosis in animals. 8 It is regulated by direct physical interaction between a R-protein and its corresponding effector (ligand-receptor model) or between a R-protein and a host-protein modified by an effector (guard model). Resistance thus depends on the presence of both the R-protein and its corresponding effector, a situation depicted by Flor's gene-for-gene model. 9, 10 For pathogens to succeed, proper delivery of these effectors is as crucial as the molecule itself. The bacterial type three secretion system (T3SS), one of many secretion systems deployed by Pseudomonas syringae, is well-characterized and has been studied in great detail. The syringe-like T3SS provides bacteria with a robust mechanical structure which enables it to inject key molecules involved in pathogenicity directly into host cells. 11 Obligate biotrophic, filamentous pathogens, such as many fungi and oomycetes, are devoid of such secretion systems. Instead, they invaginate within host cells to form particular infection structures called haustoria. 12, 13 To accommodate haustoria, host cells are forced to greatly expand their plasma membrane, and it is plausible that pathogens drive this process for their own benefit.
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