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Danger signals - damaged-self recognition across the tree of life.

Heil M, Land WG - Front Plant Sci (2014)

Bottom Line: Danger signals are "damage-associated molecular patterns" (DAMPs) that are released from the disrupted host tissue or exposed on stressed cells.Ca(2+)-fluxes, membrane depolarization, the liberation of reactive oxygen species and mitogen-activated protein kinase (MAPK) signaling cascades are the ubiquitous molecular mechanisms that act downstream of the PRRs in organisms across the tree of life.Damaged-self recognition contains both homologous and analogous elements and is likely to have evolved in all eukaryotic kingdoms, because all organisms found the same solutions for the same problem: damage must be recognized without depending on enemy-derived molecules and responses to the non-self must be directed specifically against detrimental invaders.

View Article: PubMed Central - PubMed

Affiliation: Departamento de Ingeniería Genética, Centro de Investigación y de Estudios Avanzados del Instituto Politécnico Nacional-Irapuato Irapuato, México.

ABSTRACT
Multicellular organisms suffer injury and serve as hosts for microorganisms. Therefore, they require mechanisms to detect injury and to distinguish the self from the non-self and the harmless non-self (microbial mutualists and commensals) from the detrimental non-self (pathogens). Danger signals are "damage-associated molecular patterns" (DAMPs) that are released from the disrupted host tissue or exposed on stressed cells. Seemingly ubiquitous DAMPs are extracellular ATP or extracellular DNA, fragmented cell walls or extracellular matrices, and many other types of delocalized molecules and fragments of macromolecules that are released when pre-existing precursors come into contact with enzymes from which they are separated in the intact cell. Any kind of these DAMPs enable damaged-self recognition, inform the host on tissue disruption, initiate processes aimed at restoring homeostasis, such as sealing the wound, and prepare the adjacent tissues for the perception of invaders. In mammals, antigen-processing and -presenting cells such as dendritic cells mature to immunostimulatory cells after the perception of DAMPs, prime naïve T-cells and elicit a specific adaptive T-/B-cell immune response. We discuss molecules that serve as DAMPs in multiple organisms and their perception by pattern recognition receptors (PRRs). Ca(2+)-fluxes, membrane depolarization, the liberation of reactive oxygen species and mitogen-activated protein kinase (MAPK) signaling cascades are the ubiquitous molecular mechanisms that act downstream of the PRRs in organisms across the tree of life. Damaged-self recognition contains both homologous and analogous elements and is likely to have evolved in all eukaryotic kingdoms, because all organisms found the same solutions for the same problem: damage must be recognized without depending on enemy-derived molecules and responses to the non-self must be directed specifically against detrimental invaders.

No MeSH data available.


Related in: MedlinePlus

Putative mechanisms for DAMP perception in plants. Wounding activates the MAPKs, WIPK, and SIPK, likely via the perception of different DAMPs by as yet unknown pattern recognition receptors (PRRs). These kinases trigger the synthesis of jasmonic acid (JA) in the chloroplast. JA is conjugated to form JA-isoleucine (Ja-Ile), which interacts with its receptor, the F-box protein, COI1. JA-Ile specifically binds to COI1 protein and thereby promotes binding of COI1 to JASMONATE ZIM-DOMAIN (JAZ) proteins, which represent repressors of JA-induced responses in plants. This binding event facilitates the ubiquitination of JAZs by the SCFCOI1 ubiquitin ligase, which leads to the subsequent degradation of JAZs and the release of TF, such as MYC2, and the consecutive expression of JA-responsive genes. Alternatively, Ca2+-influxes which can, among others be triggered by the perception of eATP by the DORN1 receptor, initiate the formation of ROS by NADPH oxidase, downstream MAPK signaling cascades and consecutive activation of the same genes via as-yet unknown TF. After Wu and Baldwin (2010).
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Figure 5: Putative mechanisms for DAMP perception in plants. Wounding activates the MAPKs, WIPK, and SIPK, likely via the perception of different DAMPs by as yet unknown pattern recognition receptors (PRRs). These kinases trigger the synthesis of jasmonic acid (JA) in the chloroplast. JA is conjugated to form JA-isoleucine (Ja-Ile), which interacts with its receptor, the F-box protein, COI1. JA-Ile specifically binds to COI1 protein and thereby promotes binding of COI1 to JASMONATE ZIM-DOMAIN (JAZ) proteins, which represent repressors of JA-induced responses in plants. This binding event facilitates the ubiquitination of JAZs by the SCFCOI1 ubiquitin ligase, which leads to the subsequent degradation of JAZs and the release of TF, such as MYC2, and the consecutive expression of JA-responsive genes. Alternatively, Ca2+-influxes which can, among others be triggered by the perception of eATP by the DORN1 receptor, initiate the formation of ROS by NADPH oxidase, downstream MAPK signaling cascades and consecutive activation of the same genes via as-yet unknown TF. After Wu and Baldwin (2010).

Mentions: In order to respond specifically to current attack, plants employ PRRs, the two most common classes of which are surface-localized receptor kinases (RKs) or receptor-like proteins (RLPs) that are commonly characterized by leucine-rich repeats (LRR) motifs. These PRRs perceive both PAMPs and DAMPs and, thus, play a central role in the resistance to pathogens (Zipfel, 2014). However, many plant DAMPs trigger both JA- and SA-mediated responses and, thus, are also involved in the resistance to herbivores (Duran-Flores and Heil, 2014; Ross et al., 2014). Hallmark steps in the perception of herbivory in plants are membrane depolarization events and the formation of electric signals (Maffei et al., 2004, 2007; Fromm and Lautner, 2007), Ca2+ influxes into the cytosol, the formation of ROS via a membrane-bound NADPH oxidase, and MAPK signaling cascades that ultimately activate TF and, thereby, the expression of resistance-related genes (León et al., 2001; Wu and Baldwin, 2010). Among the known plant MAPKs, the MAPK3/MAPK6 pathway is most commonly reported from the wound response in plants (Smékalová et al., 2014). Two further highly important MAPKs in this context are SA-induced protein kinase (SIPK) and wound-induced protein kinase (WIPK), which trigger the synthesis of JA from membrane-bound linolenic acid in the chloroplast and, thus, the octadecanoid signaling cascade (see Figure 5). In principle, all these steps could be activated via the perception of DAMPs by as-yet unknown receptors. Unfortunately, as to the very best of our knowledge, only few receptors for plant DAMPs have been characterized so far.


Danger signals - damaged-self recognition across the tree of life.

Heil M, Land WG - Front Plant Sci (2014)

Putative mechanisms for DAMP perception in plants. Wounding activates the MAPKs, WIPK, and SIPK, likely via the perception of different DAMPs by as yet unknown pattern recognition receptors (PRRs). These kinases trigger the synthesis of jasmonic acid (JA) in the chloroplast. JA is conjugated to form JA-isoleucine (Ja-Ile), which interacts with its receptor, the F-box protein, COI1. JA-Ile specifically binds to COI1 protein and thereby promotes binding of COI1 to JASMONATE ZIM-DOMAIN (JAZ) proteins, which represent repressors of JA-induced responses in plants. This binding event facilitates the ubiquitination of JAZs by the SCFCOI1 ubiquitin ligase, which leads to the subsequent degradation of JAZs and the release of TF, such as MYC2, and the consecutive expression of JA-responsive genes. Alternatively, Ca2+-influxes which can, among others be triggered by the perception of eATP by the DORN1 receptor, initiate the formation of ROS by NADPH oxidase, downstream MAPK signaling cascades and consecutive activation of the same genes via as-yet unknown TF. After Wu and Baldwin (2010).
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Figure 5: Putative mechanisms for DAMP perception in plants. Wounding activates the MAPKs, WIPK, and SIPK, likely via the perception of different DAMPs by as yet unknown pattern recognition receptors (PRRs). These kinases trigger the synthesis of jasmonic acid (JA) in the chloroplast. JA is conjugated to form JA-isoleucine (Ja-Ile), which interacts with its receptor, the F-box protein, COI1. JA-Ile specifically binds to COI1 protein and thereby promotes binding of COI1 to JASMONATE ZIM-DOMAIN (JAZ) proteins, which represent repressors of JA-induced responses in plants. This binding event facilitates the ubiquitination of JAZs by the SCFCOI1 ubiquitin ligase, which leads to the subsequent degradation of JAZs and the release of TF, such as MYC2, and the consecutive expression of JA-responsive genes. Alternatively, Ca2+-influxes which can, among others be triggered by the perception of eATP by the DORN1 receptor, initiate the formation of ROS by NADPH oxidase, downstream MAPK signaling cascades and consecutive activation of the same genes via as-yet unknown TF. After Wu and Baldwin (2010).
Mentions: In order to respond specifically to current attack, plants employ PRRs, the two most common classes of which are surface-localized receptor kinases (RKs) or receptor-like proteins (RLPs) that are commonly characterized by leucine-rich repeats (LRR) motifs. These PRRs perceive both PAMPs and DAMPs and, thus, play a central role in the resistance to pathogens (Zipfel, 2014). However, many plant DAMPs trigger both JA- and SA-mediated responses and, thus, are also involved in the resistance to herbivores (Duran-Flores and Heil, 2014; Ross et al., 2014). Hallmark steps in the perception of herbivory in plants are membrane depolarization events and the formation of electric signals (Maffei et al., 2004, 2007; Fromm and Lautner, 2007), Ca2+ influxes into the cytosol, the formation of ROS via a membrane-bound NADPH oxidase, and MAPK signaling cascades that ultimately activate TF and, thereby, the expression of resistance-related genes (León et al., 2001; Wu and Baldwin, 2010). Among the known plant MAPKs, the MAPK3/MAPK6 pathway is most commonly reported from the wound response in plants (Smékalová et al., 2014). Two further highly important MAPKs in this context are SA-induced protein kinase (SIPK) and wound-induced protein kinase (WIPK), which trigger the synthesis of JA from membrane-bound linolenic acid in the chloroplast and, thus, the octadecanoid signaling cascade (see Figure 5). In principle, all these steps could be activated via the perception of DAMPs by as-yet unknown receptors. Unfortunately, as to the very best of our knowledge, only few receptors for plant DAMPs have been characterized so far.

Bottom Line: Danger signals are "damage-associated molecular patterns" (DAMPs) that are released from the disrupted host tissue or exposed on stressed cells.Ca(2+)-fluxes, membrane depolarization, the liberation of reactive oxygen species and mitogen-activated protein kinase (MAPK) signaling cascades are the ubiquitous molecular mechanisms that act downstream of the PRRs in organisms across the tree of life.Damaged-self recognition contains both homologous and analogous elements and is likely to have evolved in all eukaryotic kingdoms, because all organisms found the same solutions for the same problem: damage must be recognized without depending on enemy-derived molecules and responses to the non-self must be directed specifically against detrimental invaders.

View Article: PubMed Central - PubMed

Affiliation: Departamento de Ingeniería Genética, Centro de Investigación y de Estudios Avanzados del Instituto Politécnico Nacional-Irapuato Irapuato, México.

ABSTRACT
Multicellular organisms suffer injury and serve as hosts for microorganisms. Therefore, they require mechanisms to detect injury and to distinguish the self from the non-self and the harmless non-self (microbial mutualists and commensals) from the detrimental non-self (pathogens). Danger signals are "damage-associated molecular patterns" (DAMPs) that are released from the disrupted host tissue or exposed on stressed cells. Seemingly ubiquitous DAMPs are extracellular ATP or extracellular DNA, fragmented cell walls or extracellular matrices, and many other types of delocalized molecules and fragments of macromolecules that are released when pre-existing precursors come into contact with enzymes from which they are separated in the intact cell. Any kind of these DAMPs enable damaged-self recognition, inform the host on tissue disruption, initiate processes aimed at restoring homeostasis, such as sealing the wound, and prepare the adjacent tissues for the perception of invaders. In mammals, antigen-processing and -presenting cells such as dendritic cells mature to immunostimulatory cells after the perception of DAMPs, prime naïve T-cells and elicit a specific adaptive T-/B-cell immune response. We discuss molecules that serve as DAMPs in multiple organisms and their perception by pattern recognition receptors (PRRs). Ca(2+)-fluxes, membrane depolarization, the liberation of reactive oxygen species and mitogen-activated protein kinase (MAPK) signaling cascades are the ubiquitous molecular mechanisms that act downstream of the PRRs in organisms across the tree of life. Damaged-self recognition contains both homologous and analogous elements and is likely to have evolved in all eukaryotic kingdoms, because all organisms found the same solutions for the same problem: damage must be recognized without depending on enemy-derived molecules and responses to the non-self must be directed specifically against detrimental invaders.

No MeSH data available.


Related in: MedlinePlus