scholarly journals Dissecting Contrasts in Cell Death, Hormone, and Defense Signaling in Response to Botrytis cinerea and Reactive Oxygen Species

2020 ◽  
pp. MPMI-07-20-0202
Author(s):  
Katariina Vuorinen ◽  
Olena Zamora ◽  
Lauri Vaahtera ◽  
Kirk Overmyer ◽  
Mikael Brosché

Plants require interaction between signaling pathways to differentiate and integrate stress responses and deploy appropriate defenses. The hormones ethylene, salicylic acid (SA), and jasmonic acid (JA) are important regulators of plant defenses. Numerous interactions between these signaling pathways are the cornerstone of robust plant immunity. Additionally, during the early response to pathogens, reactive oxygen species (ROS) act as signaling molecules. Here, we examined the extent of signal interaction in the early stages of Botrytis cinerea infection. To enable a comparison between B. cinerea infection with ROS signaling, we subjected plants to ozone treatment, which stimulates an apoplastic ROS burst. We used a collection of single, double, and triple signaling mutants defective in hormone signaling and biosynthesis and subjected them to B. cinerea infection and ozone treatment at different timepoints. We examined lesion size, cell death, and gene expression (both quantitatively and spatially). The two treatments shared many similarities, especially in JA-insensitive mutants, which were sensitive to both treatments. Unexpectedly, a B. cinerea–susceptible JA-insensitive mutant (coi1), became tolerant when both SA biosynthesis and signaling was impaired (coi1 npr1 sid2), demonstrating that JA responses may be under the control of SA. Extensive marker gene analysis indicated JA as the main regulator of both B. cinerea and ozone defenses. In addition, we identified the transcription factor SR1 as a crucial regulator of PLANT DEFENSIN expression and cell-death regulation, which contributes to resistance to B. cinerea. Overall, our work further defines the context of ROS in plant defense signaling. [Formula: see text] Copyright © 2020 The Author(s). This is an open access article distributed under the CC BY-NC-ND 4.0 International license .

2021 ◽  
Author(s):  
Daisuke Oikawa ◽  
Min Gi ◽  
Hidetaka Kosako ◽  
Kouhei Shimizu ◽  
Hirotaka Takahashi ◽  
...  

Deubiquitylating enzymes (DUBs) regulate numerous cellular functions by removing ubiquitin modifications. We examined the effects of 88 human DUBs on linear ubiquitin chain assembly complex (LUBAC)-induced NF-κB activation, and identified OTUD1 as a potent suppressor. OTUD1 regulates the canonical NF-κB pathway by hydrolysing K63-linked ubiquitin chains from NF-κB signalling factors, including LUBAC. OTUD1 negatively regulates the canonical NF-κB activation, apoptosis, and necroptosis, whereas OTUD1 upregulates the interferon (IFN) antiviral pathway. The N-terminal intrinsically disordered region of OTUD1, which contains an EGTE motif, is indispensable for KEAP1-binding and NF-κB suppression. OTUD1 is involved in the KEAP1-mediated antioxidant response and reactive oxygen species (ROS)-induced cell death, oxeiptosis. In Otud1-/--mice, inflammation, oxidative damage, and cell death were enhanced in inflammatory bowel disease, acute hepatitis, and sepsis models. Thus, OTUD1 is a crucial regulator for the inflammatory, innate immune, and oxidative stress responses and ROS-associated cell death pathways.


BioEssays ◽  
2006 ◽  
Vol 28 (11) ◽  
pp. 1091-1101 ◽  
Author(s):  
Tsanko S. Gechev ◽  
Frank Van Breusegem ◽  
Julie M. Stone ◽  
Iliya Denev ◽  
Christophe Laloi

2016 ◽  
Vol 397 (7) ◽  
pp. 657-660 ◽  
Author(s):  
Simone Fulda

Abstract Necroptosis has recently been identified as an alternative form of programmed cell death that is characterized by defined molecular mechanisms. Reactive oxygen species (ROS) are involved in the regulation of numerous signaling pathways, as they are highly reactive and can cause (ir)reversible posttranslational modifications. While the role of ROS in other modes of cell death has been extensively studied, its impact on necroptotic signaling and cell death is far less clear. The current minireview discusses the evidence for and against a role of ROS in necroptosis.


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