Table 1.
Abbreviation list.
Fig 1.
Domain architecture of NLR immune receptors and general activation mechanisms of resistosomes and inflammasomes in plants and animals, respectively.
NLRs are modular tripartite immune receptors comprised of an N-terminal signaling domain, a NOD and LRR domain. In plants, NLRs are broadly classified into sNLRs and hNLRs based on their function during the immune response. Sensors are divided into CC- or TIR-NLR, whereas helpers carry a CC domain at their N-terminus. Upon pathogen perception, CNLs oligomerize into a pentameric wheel-like structure, whereas TNLs oligomerize into a tetrameric structure collectively known as resistosomes. While CNLs can sense pathogen effectors and execute cell death by acting as permeable Ca2+ channels with no need of hNLRs, TIR domains from TNLs act as NAD+ hydrolases generating by-products or small molecules that bind to EDS1 complexes. Allosteric changes in EDS1 complexes allow interaction with hNLRs. Oligomerization of certain hNLRs into a pentameric resistosome with Ca2+channel activity at the PM drive ion flux imbalances that resultin HR-cell death [9,10]. CNL, coiled-coil-NLR; hNLR, helper NLR; HR, hypersensitive response; LRR, leucine-rich repeat; NLR, nucleotide-binding leucine-rich repeat; NOD, nucleotide oligomerization domain; PM, plasma membrane; sNLR, sensor NL; TNL, Toll Interleukin 1 receptor-NLR.
Fig 2.
Overview of cell death types and their general features in plants and animals.
During HR cell death in plants, ROS accumulation and calcium channel activity exerted by plant resistosomes drive Ca2+ entry into the cytoplasm. How intracellular Ca2+ spikes lead to downstream cell death features such as loss of chloroplast and mitochondrial and eventually cellular demise is currently unknown. DAMPs and phytocytokines are released from infected/damaged cells and activate defense responses in neighboring cells via perception by surface receptors. Although differentially regulated at the molecular level, pyroptosis and necroptosis are both pro-inflammatory forms of cell death that involve release of cellular content to the extracellular space (DAMP release and inflammatory cytokines). In both cell death modalities, rupture of the plasma allows for the influx and efflux of ions altering homeostasis in the cell. Ferroptosis is an iron-dependent mode of cell death in which peroxidation of lipids cause plasma membrane damage with partial rupture allowing entry of Ca2+ ions and release of DAMPs to the extracellular space. Apoptosis is a non-inflammatory and silent form of cell death in which membrane integrity is maintained during cellular dismantling. Cell shrinkage, chromatin condensation, and DNA fragmentation are typical hallmarks of apoptosis. Importantly, plasma membrane blebbing leads to apoptotic bodies that are eventually engulfed and eliminated by phagocytes. DAMP, danger-associated molecular pattern; HR, hypersensitive response; ROS, reactive oxygen species.