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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. 

Summary Flooding represents a major threat to global agricultural productivity and food security, but plants are capable of deploying a suite of adaptive responses that can lead to short‐ or longer‐term survival to this stress. One cellular pathway thought to help coordinate these responses is via flooding‐triggered Ca²⁺signaling.We have mined publicly available transcriptomic data from Arabidopsis subjected to flooding or low oxygen stress to identify rapidly upregulated, Ca²⁺‐related transcripts. We then focused on transporters likely to modulate Ca²⁺signals. Candidates emerging from this analysis includedAUTOINHIBITED Ca²⁺ATPASE 1andCATION EXCHANGER 2. We therefore assayed mutants in these genes for flooding sensitivity at levels from growth to patterns of gene expression and the kinetics of flooding‐related Ca²⁺changes.Knockout mutants inCAX2especially showed enhanced survival to soil waterlogging coupled with suppressed induction of many marker genes for hypoxic response and constitutive activation of others.CAX2mutants also generated larger and more sustained Ca²⁺signals in response to both flooding and hypoxic challenges.CAX2 is a Ca²⁺transporter located on the tonoplast, and so these results are consistent with an important role for vacuolar Ca²⁺transport in the signaling systems that trigger flooding response. 

Land plants evolved to quickly sense and adapt to temperature changes, such as hot days and cold nights. Given that calcium (Ca 2+ ) signaling networks are implicated in most abiotic stress responses, heat-triggered changes in cytosolic Ca 2+ were investigated in Arabidopsis leaves and pollen. Plants were engineered with a reporter called CGf, a ratiometric, genetically encoded Ca 2+ reporter with an m C herry reference domain fused to an intensiometric Ca 2+ reporter G CaMP6 f . Relative changes in [Ca 2+ ] cyt were estimated based on CGf’s apparent K D around 220 nM. The ratiometric output provided an opportunity to compare Ca 2+ dynamics between different tissues, cell types, or subcellular locations. In leaves, CGf detected heat-triggered cytosolic Ca 2+ signals, comprised of three different signatures showing similarly rapid rates of Ca 2+ influx followed by differing rates of efflux (50% durations ranging from 5 to 19 min). These heat-triggered Ca 2+ signals were approximately 1.5-fold greater in magnitude than blue light-triggered signals in the same leaves. In contrast, growing pollen tubes showed two different heat-triggered responses. Exposure to heat caused tip-focused steady growth [Ca 2+ ] cyt oscillations to shift to a pattern characteristic of a growth arrest (22%), or an almost undetectable [Ca 2+ ] cyt (78%). Together, these contrasting examples of heat-triggered Ca 2+ responses in leaves and pollen highlight the diversity of Ca 2+ signals in plants, inviting speculations about their differing kinetic features and biological functions. 

In natural ecosystems, plants are constantly exposed to changes in their surroundings as they grow, caused by a lifestyle that requires them to live where their seeds fall. Thus, plants strive to adapt and respond to changes in their exposed environment that change every moment. Heat stress that naturally occurs when plants grow in the summer or a tropical area adversely affects plants’ growth and poses a risk to plant development. When plants are subjected to heat stress, they recognize heat stress and respond using highly complex intracellular signaling systems such as reactive oxygen species (ROS). ROS was previously considered a byproduct that impairs plant growth. However, in recent studies, ROS gained attention for its function as a signaling molecule when plants respond to environmental stresses such as heat stress. In particular, ROS, produced in response to heat stress in various plant cell compartments such as mitochondria and chloroplasts, plays a crucial role as a signaling molecule that promotes plant growth and triggers subsequent downstream reactions. Therefore, this review aims to address the latest research trends and understandings, focusing on the function and role of ROS in responding and adapting plants to heat stress.