Indeed another recent study found that the HR like

Indeed, another recent study found that the HR-like cell death triggered in rice epidermal cells by an avirulent or incompatible isolate of the fungal pathogen , which causes blast disease, is a ferroptotic cell death phenomenon (). Similar to the heat shock example given above, elevated levels of iron ions and ROS accompanied the -mediated cell death that could be inhibited by the iron chelators deferoxamine (DFO) and Ferrostatin 1 . In addition, Cytochalasin E (Cyt E), which inhibits 17-ODYA sale microfilament polymerisation, prevented ROS and Fe accumulation and ferroptotic cell death . In contrast, erastin, a small molecule that triggers iron-dependent ROS accumulation through glutathione depletion, promoted virulent -induced ferroptotic cell death . Interestingly, iron accumulation is not observed during the infection of rice by a virulent or compatible isolate. This suggested that virulent isolates have the ability to interfere with ferroptotic cell death during plant infection. Indeed, AVR-Pii, an effector from this pathogen, is known to suppress ROS accumulation during plant infection by inhibiting the rice NADP-malic enzyme , one of the sources of ROS involved in ferroptotic cell death. Therefore, this study is the first case showing that ferroptosis can actively play a beneficial role in the host. The work highlighted above shows that ferroptosis discovered earlier in animals also operates in plant cells. Although ferroptosis is a relatively new concept in plants, we suspect that the re-examination of many of the previously reported regulated cell death events might reveal evidence for ferroptosis because molecular events (e.g., iron- and ROS-dependent lipid peroxidation) leading to ferroptotic cell death have long been known to occur in plant cells . Additional work is also needed to determine commonalities (e.g., the involvement of ROS, caspases, and calcium signalling) and differences between ferroptosis and other known cell death pathways. It would also be interesting to test if the ferroptotic cell death observed during the interaction between rice and can be extended into other HR-like cell death events commonly observed in many other plant–pathogen and plant–pest interactions. How virulent plant pathogens suppress ferroptotic cell death and whether ferroptosis occurs in response to other abiotic stresses (e.g., UV light) Upstream induce cell death in above-ground plant parts are other areas of future research. Better understanding of ferroptosis would not only improve our knowledge on how plants adapt to their environment but would also pave the way for its exploitation for improved stress tolerance in crops. Acknowledgements S.K. is funded by a postdoctoral fellowship from CSIRO. We thank two anonymous reviewers for their useful comments on the manuscript.
Introduction Regulated cell death (RCD) is a critical and active process that not only maintains tissue homeostasis, but also causes tissue injury and inflammation-associated diseases [1]. Among the growing list of types of RCD [2] is ferroptosis, an iron-dependent form of non-apoptotic RCD, which can be induced by small molecular compounds such as erastin or RSL3 [3]. Although iron is one of the crucial elements required for cell proliferation and growth, excess free iron can lead to oxidative damage and subsequent cell death through the production of reactive oxygen radicals [4]. In particular, the iron-catalyzed formation of hydroxyl radicals can trigger lipid peroxidation and subsequent ferroptosis [3]. Recently, significant evidence suggested that lipid peroxidation during ferroptosis requires the activation of several key enzymes, such as acyl-coA synthetase long chain family member 4 (ACSL4) [[5], [6], [7]], lysophosphatidylcholine acyltransferase 3 (LPCAT3) [8], and arachidonate 15-lipoxygenase (ALOX15) [9]. In contrast, system xc− [3], glutathione peroxidase 4 (GPX4) [10], and nuclear factor, erythroid 2 like 2 (NFE2L2/NRF2) [10] antioxidant systems are the principal defense mechanisms for lipid peroxidation during ferroptosis.