skip to main content
US FlagAn official website of the United States government
dot gov icon
Official websites use .gov
A .gov website belongs to an official government organization in the United States.
https lock icon
Secure .gov websites use HTTPS
A lock ( lock ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

Explore Research Products in the PAR
It may take a few hours for recently added research products to appear in PAR search results.


Title: Cytoplasmic Ca2+ influx mediates iron- and reactive oxygen species-dependent ferroptotic cell death in rice immunity
Iron- and reactive oxygen species (ROS)-dependent ferroptosis occurs in plant cells. Ca2+acts as a conserved key mediator to control plant immune responses. Here, we report a novel role of cytoplasmic Ca2+influx regulating ferroptotic cell death in rice immunity using pharmacological approaches. High Ca2+influx triggered iron-dependent ROS accumulation, lipid peroxidation, and subsequent hypersensitive response (HR) cell death in rice (Oryza sativa). DuringMagnaporthe oryzaeinfection, 14 different Ca2+influx regulators altered Ca2+, ROS and Fe2+accumulation,glutathione reductase(GR) expression, glutathione (GSH) depletion and lipid peroxidation, leading to ferroptotic cell death in rice. High Ca2+levels inhibited the reduction of glutathione isulphide (GSSG) to GSHin vitro. Ca2+chelation by ethylene glycol-bis (2-aminoethylether)-N, N, N’, N’-tetra-acetic acid (EGTA) suppressed apoplastic Ca2+influx in rice leaf sheaths during infection. Blocking apoplastic Ca2+influx into the cytoplasm by Ca2+chelation effectively suppressed Ca2+-mediated iron-dependent ROS accumulation and ferroptotic cell death. By contrast, acibenzolar-S-methyl (ASM), a plant defense activator, significantly enhanced Ca2+influx, as well as ROS and iron accumulation to trigger ferroptotic cell death in rice. The cytoplasmic Ca2+influx through calcium-permeable cation channels, including the putative resistosomes, could mediate iron- and ROS-dependent ferroptotic cell death under reducedGRexpression levels in rice immune responses.  more » « less
Award ID(s):
2016143
PAR ID:
10555945
Author(s) / Creator(s):
; ; ; ; ; ; ;
Publisher / Repository:
Frontiers in Plant Science
Date Published:
Journal Name:
Frontiers in Plant Science
Volume:
15
ISSN:
1664-462X
Format(s):
Medium: X
Sponsoring Org:
National Science Foundation
More Like this
  1. ; ; ; ; ; ; ; ; ; ; et al (, Science)
    Plant nucleotide-binding leucine-rich repeat receptors (NLRs) regulate immunity and cell death. In Arabidopsis , a subfamily of “helper” NLRs is required by many “sensor” NLRs. Active NRG1.1 oligomerized, was enriched in plasma membrane puncta, and conferred cytoplasmic calcium ion (Ca 2+ ) influx in plant and human cells. NRG1.1-dependent Ca 2+ influx and cell death were sensitive to Ca 2+ channel blockers and were suppressed by mutations affecting oligomerization or plasma membrane enrichment. Ca 2+ influx and cell death mediated by NRG1.1 and ACTIVATED DISEASE RESISTANCE 1 (ADR1), another helper NLR, required conserved negatively charged N-terminal residues. Whole-cell voltage-clamp recordings demonstrated that Arabidopsis helper NLRs form Ca 2+ -permeable cation channels to directly regulate cytoplasmic Ca 2+ levels and consequent cell death. Thus, helper NLRs transduce cell death signals directly. 
    more » « less
  2. ; ; ; ; ; ; ; ; ; ; et al (, Proceedings of the National Academy of Sciences)
    TIR domains are NAD-degrading enzymes that function during immune signaling in prokaryotes, plants, and animals. In plants, most TIR domains are incorporated into intracellular immune receptors termed TNLs. In Arabidopsis, TIR-derived small molecules bind and activate EDS1 heterodimers, which in turn activate RNLs, a class of cation channel–forming immune receptors. RNL activation drives cytoplasmic Ca 2+ influx, transcriptional reprogramming, pathogen resistance, and host cell death. We screened for mutants that suppress an RNL activation mimic allele and identified a TNL, SADR1. Despite being required for the function of an autoactivated RNL, SADR1 is not required for defense signaling triggered by other tested TNLs. SADR1 is required for defense signaling initiated by some transmembrane pattern recognition receptors and contributes to the unbridled spread of cell death in lesion simulating disease 1 . Together with RNLs, SADR1 regulates defense gene expression at infection site borders, likely in a non-cell autonomous manner. RNL mutants that cannot sustain this pattern of gene expression are unable to prevent disease spread beyond localized infection sites, suggesting that this pattern corresponds to a pathogen containment mechanism. SADR1 potentiates RNL-driven immune signaling not only through the activation of EDS1 but also partially independently of EDS1. We studied EDS1-independent TIR function using nicotinamide, an NADase inhibitor. Nicotinamide decreased defense induction from transmembrane pattern recognition receptors and decreased calcium influx, pathogen growth restriction, and host cell death following intracellular immune receptor activation. We demonstrate that TIR domains can potentiate calcium influx and defense and are thus broadly required for Arabidopsis immunity. 
    more » « less
  3. ; ; ; (, New Phytologist)
    Summary Root hair tip‐growth involves coordinated Ca2+and ROS signaling to promote growth while maintaining tip integrity. MILDEW RESISTANCE LOCUS‐O (MLO) proteins act downstream of FERONIA (FER) receptor‐like kinases in pollen tubes and synergids to regulate calcium dynamics. This study uses a constitutively active MLO (faNTA) to identify a new role for the FER/MLO signaling module in regulating [Ca2+]cytoscillations in growing root hairs.faNTA was used as a tool to manipulate Ca2+influx infermutants. Light sheet fluorescence imaging was used to image the reporter R‐GECO1 to observe [Ca2+]cytdynamics during root hair elongation in various genotypes.We show that faNTA is sufficient to restore normal root hair development, [Ca2+]cytoscillations, and ROS levels tofer‐4. MLO15 was identified as a regulator of root hair tip growth based on disrupted root hair growth and [Ca2+]cytsignatures inmlo15‐4. We also link the FER/MLO module to ROS accumulation by showing that faNTA is sufficient to restore ROS levels infer‐4root hairs, but is unable to complement the burst root hairs ofrbohc.We propose that MLOs act downstream of FER to mediate Ca2+influx and promote ROS production to regulate root hair tip growth. 
    more » « less
  4. ; ; ; (, International Journal of Molecular Sciences)
    In terrestrial plants a basal innate immune system, pattern-triggered immunity (PTI), has evolved to limit infection by diverse microbes. The remodeling of actin cytoskeletal arrays is now recognized as a key hallmark event during the rapid host cellular responses to pathogen attack. Several actin binding proteins have been demonstrated to fine tune the dynamics of actin filaments during this process. However, the upstream signals that stimulate actin remodeling during PTI signaling remain poorly characterized. Two second messengers, reactive oxygen species (ROS) and phosphatidic acid (PA), are elevated following pathogen perception or microbe-associated molecular pattern (MAMP) treatment, and the timing of signaling fluxes roughly correlates with actin cytoskeletal rearrangements. Here, we combined genetic analysis, chemical complementation experiments, and quantitative live-cell imaging experiments to test the role of these second messengers in actin remodeling and to order the signaling events during plant immunity. We demonstrated that PHOSPHOLIPASE Dβ (PLDβ) isoforms are necessary to elicit actin accumulation in response to flg22-associated PTI. Further, bacterial growth experiments and MAMP-induced apoplastic ROS production measurements revealed that PLDβ-generated PA acts upstream of ROS signaling to trigger actin remodeling through inhibition of CAPPING PROTEIN (CP) activity. Collectively, our results provide compelling evidence that PLDβ/PA functions upstream of RBOHD-mediated ROS production to elicit actin rearrangements during the innate immune response in Arabidopsis. 
    more » « less
  5. ; ; ; ; ; ; ; ; ; ; et al (, Advanced Science)
    ABSTRACT Environmental stress demands precise coordination among organelles to maintain cellular homeostasis. InArabidopsis, high light (HL) exposure triggers chloroplast‐dependent remodeling of mitochondrial and endoplasmic reticulum (ER) morphology specifically in adaxial and abaxial epidermal cells, but not in mesophyll cells. Live‐cell imaging reveals that HL rapidly suppresses mitochondrial motility, followed by fusion‐driven elongation and ER cisternal expansion. Inhibition of photosynthetic, but not mitochondrial, electron transport abolishes these changes, confirming chloroplast activity as the upstream trigger. Pharmacological analyses show that exogenous H2O2induces mitochondrial elongation, whereas calcium chelation blocks both H2O2‐ and HL‐induced responses, demonstrating that chloroplast‐derived H2O2activates a Ca2+flux essential for remodeling. Proteomic and functional studies identify the Ca2+‐binding GTPase MIRO1 as a central integrator of this pathway. MIRO1 overexpression mimics HL‐induced morphodynamics, while mutations disrupting its Ca2+‐binding or acetylation motifs abolish the response, establishing Ca2+‐dependent MIRO1 activity as a prerequisite for remodeling. Together, these findings reveal an epidermis‐specific, light‐responsive network in which chloroplast‐derived H2O2initiates Ca2+signaling through MIRO1 to coordinate mitochondrial and ER remodeling—a spatially restricted mechanism of organellar communication and stress adaptation at the plant–environment interface. 
    more » « less
  • Citation Formats
  • MLA
  • APA
  • Chicago
  • BibTeX
  • Text Encoded Conversion
  • XML
  • Save / Share this Record
  • Send to Email