scholarly journals Breaking Bad News: Dynamic Molecular Mechanisms of Wound Response in Plants

2020 ◽  
Vol 11 ◽  
Author(s):  
Isaac Vega-Muñoz ◽  
Dalia Duran-Flores ◽  
Álvaro Daniel Fernández-Fernández ◽  
Jefri Heyman ◽  
Andrés Ritter ◽  
...  
Keyword(s):  
Molecular Mechanisms ◽  
Wound Response ◽  
Surrounding Tissue ◽  
Defense Gene Expression ◽  
Defense Gene ◽  
Breaking Bad ◽  
Damage Recognition ◽  
Pathogen Colonization ◽  
Recognition And Response ◽  
Molecular Patterns

Recognition and repair of damaged tissue are an integral part of life. The failure of cells and tissues to appropriately respond to damage can lead to severe dysfunction and disease. Therefore, it is essential that we understand the molecular pathways of wound recognition and response. In this review, we aim to provide a broad overview of the molecular mechanisms underlying the fate of damaged cells and damage recognition in plants. Damaged cells release the so-called damage associated molecular patterns to warn the surrounding tissue. Local signaling through calcium (Ca2+), reactive oxygen species (ROS), and hormones, such as jasmonic acid, activates defense gene expression and local reinforcement of cell walls to seal off the wound and prevent evaporation and pathogen colonization. Depending on the severity of damage, Ca2+, ROS, and electrical signals can also spread throughout the plant to elicit a systemic defense response. Special emphasis is placed on the spatiotemporal dimension in order to obtain a mechanistic understanding of wound signaling in plants.

scholarly journals The Immunity Regulator BAK1 Contributes to Resistance Against Diverse RNA Viruses

2013 ◽  
Vol 26 (11) ◽  
pp. 1271-1280 ◽  
Author(s):  
Camilla Julie Kørner ◽  
Dominik Klauser ◽  
Annette Niehl ◽  
Ana Domínguez-Ferreras ◽  
Delphine Chinchilla ◽  
...  
Keyword(s):  
Rna Viruses ◽  
Transcriptional Gene Silencing ◽  
Dependent Manner ◽  
Antiviral Defense ◽  
Defense Gene Expression ◽  
Defense Gene ◽  
Resistance Proteins ◽  
Post Transcriptional Gene Silencing ◽  
Effector Triggered Immunity ◽  
Molecular Patterns

The plant's innate immune system detects potential biotic threats through recognition of microbe-associated molecular patterns (MAMPs) or danger-associated molecular patterns (DAMPs) by pattern recognition receptors (PRR). A central regulator of pattern-triggered immunity (PTI) is the BRI1-associated kinase 1 (BAK1), which undergoes complex formation with PRR upon ligand binding. Although viral patterns inducing PTI are well known from animal systems, nothing similar has been reported for plants. Rather, antiviral defense in plants is thought to be mediated by post-transcriptional gene silencing of viral RNA or through effector-triggered immunity, i.e., recognition of virus-specific effectors by resistance proteins. Nevertheless, infection by compatible viruses can also lead to the induction of defense gene expression, indicating that plants may also recognize viruses through PTI. Here, we show that PTI, or at least the presence of the regulator BAK1, is important for antiviral defense of Arabidopsis plants. Arabidopsis bak1 mutants show increased susceptibility to three different RNA viruses during compatible interactions. Furthermore, crude viral extracts but not purified virions induce several PTI marker responses in a BAK1-dependent manner. Overall, we conclude that BAK1-dependent PTI contributes to antiviral resistance in plants.

scholarly journals Phosphatidylcholines from Pieris brassicae eggs activate an immune response in Arabidopsis

eLife ◽  
2020 ◽  
Vol 9 ◽  
Author(s):  
Elia Stahl ◽  
Théo Brillatz ◽  
Emerson Ferreira Queiroz ◽  
Laurence Marcourt ◽  
André Schmiesing ◽  
...  
Keyword(s):  
Pieris Brassicae ◽  
Fatty Acyl ◽  
Cell Surface Receptor ◽  
Ligand Specificity ◽  
Defense Gene Expression ◽  
Insect Eggs ◽  
Defense Gene ◽  
Surface Receptor ◽  
Acyl Chains ◽  
Molecular Patterns

Recognition of conserved microbial molecules activates immune responses in plants, a process termed pattern-triggered immunity (PTI). Similarly, insect eggs trigger defenses that impede egg development or attract predators, but information on the nature of egg-associated elicitors is scarce. We performed an unbiased bioactivity-guided fractionation of eggs of the butterfly Pieris brassicae. Nuclear magnetic resonance (NMR) spectroscopy and mass spectrometry of active fractions led to the identification of phosphatidylcholines (PCs). PCs are released from insect eggs, and they induce salicylic acid and H2O2 accumulation, defense gene expression and cell death in Arabidopsis, all of which constitute a hallmark of PTI. Active PCs contain primarily C16 to C18-fatty acyl chains with various levels of desaturation, suggesting a relatively broad ligand specificity of cell-surface receptor(s). The finding of PCs as egg-associated molecular patterns (EAMPs) illustrates the acute ability of plants to detect conserved immunogenic patterns from their enemies, even from seemingly passive structures such as eggs.

scholarly journals Molecular Crosstalk Between PAMP-Triggered Immunity and Photosynthesis

2012 ◽  
Vol 25 (8) ◽  
pp. 1083-1092 ◽  
Author(s):  
Vera Göhre ◽  
Alexandra M. E. Jones ◽  
Jan Sklenář ◽  
Silke Robatzek ◽  
Andreas P. M. Weber
Keyword(s):  
Defense Responses ◽  
Innate Immune ◽  
Energy Costs ◽  
Defense Gene Expression ◽  
Defense Gene ◽  
Fluorescence Measurements ◽  
Species Production ◽  
Molecular Patterns ◽  
Intrinsic Component ◽  
Molecular Crosstalk

The innate immune system allows plants to respond to potential pathogens in an appropriate manner while minimizing damage and energy costs. Photosynthesis provides a sustained energy supply and, therefore, has to be integrated into the defense against pathogens. Although changes in photosynthetic activity during infection have been described, a detailed and conclusive characterization is lacking. Here, we addressed whether activation of early defense responses by pathogen-associated molecular patterns (PAMPs) triggers changes in photosynthesis. Using proteomics and chlorophyll fluorescence measurements, we show that activation of defense by PAMPs leads to a rapid decrease in nonphotochemical quenching (NPQ). Conversely, NPQ also influences several responses of PAMP-triggered immunity. In a mutant impaired in NPQ, apoplastic reactive oxygen species production is enhanced and defense gene expression is differentially affected. Although induction of the early defense markers WRKY22 and WRKY29 is enhanced, induction of the late markers PR1 and PR5 is completely abolished. We propose that regulation of NPQ is an intrinsic component of the plant's defense program.

scholarly journals Expression of the Human NAD(P)-Metabolizing Ectoenzyme CD38 Compromises Systemic Acquired Resistance in Arabidopsis

2012 ◽  
Vol 25 (9) ◽  
pp. 1209-1218 ◽  
Author(s):  
Xudong Zhang ◽  
Zhonglin Mou
Keyword(s):  
Disease Resistance ◽  
Molecular Mechanisms ◽  
Systemic Acquired Resistance ◽  
Plant Immunity ◽  
Acquired Resistance ◽  
Defense Gene Expression ◽  
Signal Molecule ◽  
Defense Gene ◽  
P Concentration ◽  
Extracellular Compartment

Plant systemic acquired resistance (SAR) is a long-lasting, broad-spectrum immune response that is mounted after primary pathogen infection. Although SAR has been extensively researched, the molecular mechanisms underlying its activation have not been completely understood. We have previously shown that the electron carrier NAD(P) leaks into the plant extracellular compartment upon pathogen attack and that exogenous NAD(P) activates defense gene expression and disease resistance in local treated leaves, suggesting that extracellular NAD(P) [eNAD(P)] might function as a signal molecule activating plant immune responses. To further establish the function of eNAD(P) in plant immunity, we tested the effect of exogenous NAD(P) on resistance gene-mediated hypersensitive response (HR) and SAR. We found that exogenous NAD(P) completely suppresses HR-mediated cell death but does not affect HR-mediated disease resistance. Local application of exogenous NAD(P) is unable to induce SAR in distal tissues, indicating that eNAD(P) is not a sufficient signal for SAR activation. Using transgenic Arabidopsis plants expressing the human NAD(P)-metabolizing ectoenzyme CD38, we demonstrated that altering eNAD(P) concentration or signaling compromises biological induction of SAR. This result suggests that eNAD(P) may play a critical signaling role in activation of SAR.

Resolution-Associated Molecular Patterns (RAMPs) as Endogenous Regulators of Glia Functions in Neuroinflammatory Disease

2020 ◽  
Vol 19 (7) ◽  
pp. 483-494
Author(s):  
Tyler J. Wenzel ◽  
Evan Kwong ◽  
Ekta Bajwa ◽  
Andis Klegeris
Keyword(s):  
Molecular Mechanisms ◽  
Inflammatory Responses ◽  
Bioactive Lipids ◽  
Prothymosin Α ◽  
Neuroinflammatory Disease ◽  
Cellular Debris ◽  
Αb Crystallin ◽  
Endogenous Regulators ◽  
The Central Nervous System ◽  
Molecular Patterns

: Glial cells, including microglia and astrocytes, facilitate the survival and health of all cells within the Central Nervous System (CNS) by secreting a range of growth factors and contributing to tissue and synaptic remodeling. Microglia and astrocytes can also secrete cytotoxins in response to specific stimuli, such as exogenous Pathogen-Associated Molecular Patterns (PAMPs), or endogenous Damage-Associated Molecular Patterns (DAMPs). Excessive cytotoxic secretions can induce the death of neurons and contribute to the progression of neurodegenerative disorders, such as Alzheimer’s disease (AD). The transition between various activation states of glia, which include beneficial and detrimental modes, is regulated by endogenous molecules that include DAMPs, cytokines, neurotransmitters, and bioactive lipids, as well as a diverse group of mediators sometimes collectively referred to as Resolution-Associated Molecular Patterns (RAMPs). RAMPs are released by damaged or dying CNS cells into the extracellular space where they can induce signals in autocrine and paracrine fashions by interacting with glial cell receptors. While the complete range of their effects on glia has not been described yet, it is believed that their overall function is to inhibit adverse CNS inflammatory responses, facilitate tissue remodeling and cellular debris removal. This article summarizes the available evidence implicating the following RAMPs in CNS physiological processes and neurodegenerative diseases: cardiolipin (CL), prothymosin α (ProTα), binding immunoglobulin protein (BiP), heat shock protein (HSP) 10, HSP 27, and αB-crystallin. Studies on the molecular mechanisms engaged by RAMPs could identify novel glial targets for development of therapeutic agents that effectively slow down neuroinflammatory disorders including AD.

scholarly journals HOS15 is a transcriptional corepressor of NPR1-mediated gene activation of plant immunity

2020 ◽  
Vol 117 (48) ◽  
pp. 30805-30815
Author(s):  
Mingzhe Shen ◽  
Chae Jin Lim ◽  
Junghoon Park ◽  
Jeong Eun Kim ◽  
Dongwon Baek ◽  
...  
Keyword(s):  
Gene Expression ◽  
Ubiquitin Ligase ◽  
Transcriptional Activation ◽  
Plant Immunity ◽  
Gene Activation ◽  
Transcriptional Corepressor ◽  
Defense Gene Expression ◽  
Dynamic Regulation ◽  
Defense Gene ◽  
Transcriptional Corepressors

Transcriptional regulation is a complex and pivotal process in living cells. HOS15 is a transcriptional corepressor. Although transcriptional repressors generally have been associated with inactive genes, increasing evidence indicates that, through poorly understood mechanisms, transcriptional corepressors also associate with actively transcribed genes. Here, we show that HOS15 is the substrate receptor for an SCF/CUL1 E3 ubiquitin ligase complex (SCFHOS15) that negatively regulates plant immunity by destabilizing transcriptional activation complexes containing NPR1 and associated transcriptional activators. In unchallenged conditions, HOS15 continuously eliminates NPR1 to prevent inappropriate defense gene expression. Upon defense activation, HOS15 preferentially associates with phosphorylated NPR1 to stimulate rapid degradation of transcriptionally active NPR1 and thus limit the extent of defense gene expression. Our findings indicate that HOS15-mediated ubiquitination and elimination of NPR1 produce effects contrary to those of CUL3-containing ubiquitin ligase that coactivate defense gene expression. Thus, HOS15 plays a key role in the dynamic regulation of pre- and postactivation host defense.

scholarly journals A small cysteine-rich phytotoxic protein of Phytophthora capsici functions as both plant defense elicitor and virulence factor

2021 ◽  
Author(s):  
Zi-Hui Zhang ◽  
Jinghao Jin ◽  
Gui-Lin Sheng ◽  
Yu-Ping Xing ◽  
Wang Liu ◽  
...  
Keyword(s):  
Plant Defense ◽  
Virulence Factor ◽  
Phytophthora Capsici ◽  
Ectopic Expression ◽  
Defense Responses ◽  
Phytophthora Species ◽  
Plant Interactions ◽  
Defense Gene Expression ◽  
Callose Deposition ◽  
Defense Gene

Small cysteine-rich (SCR) proteins including fungal avirulence proteins play important roles in the pathogen-plant interactions. SCR protein-encoding genes have been discovered in the genomes of Phytophthora pathogens, but their functions during the pathogenesis remain obscure. Here, we report the characterization of one Phytophthora capsici SCR protein, namely SCR82 with similarity to Phytophthora cactorum phytotoxic protein PcF. The scr82 gene has 10 allelic sequences in the P. capsici population. Homologues of SCR82 were not identified in fungi or other organisms but in Phytophthora relative species. Initially scr82 was weakly expressed during the mycelium, sporangium and zoospore stages, but quickly upregulated when the infection initiated. Both ectopic expression of SCR82 and recombinant yeast-expressed protein (rSCR82) caused cell death on tomato leaves. Upon treatment, rSCR82 induced plant defense responses including the induction of defense gene expression, reactive oxygen species burst and callose deposition. Knockout of scr82 in P. capsici by CRISPR/Cas9 severely impaired its virulence on host plants and reduced significantly its resistance againstoxidative stress. Inversely, its overexpression increased the pathogen’s virulence and tolerance to oxidative stress. Our results collectively demonstrate that SCR82 functions as both an important virulence factor and plant defense elicitor, which is conserved across Phytophthora species.

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