Abstract
Programmed cell death (PCD) in animals mainly refers to lytic and non-lytic forms. Disruption and integrity of the plasma membrane are considered as hallmarks of lytic and apoptotic cell death, respectively. These lytic cell death programs can prevent the hosts from microbial pathogens. The key to our understanding of these cases is pattern recognition receptors, such as TLRs in animals and LRR-RLKs in plants, and nod-like receptors (NLRs). Herein, we emphatically discuss the biochemical and structural studies that have clarified the anti-apoptotic and pro-apoptotic functions of Bcl-2 family proteins during intrinsic apoptosis and how caspase-8 among apoptosis, necroptosis, and pyroptosis sets the switchable threshold and integrates innate immune signaling, and that have compared the similarity and distinctness of the apoptosome, necroptosome, and inflammasome. We recapitulate that the necroptotic MLKL pore, pyroptotic gasdermin pore, HR-inducing resistosome, and mitochondrial Bcl-2 family all can form ion channels, which all directly boost membrane disruption. Comparing the conservation and unique aspects of PCD including ferrroptosis among bacteria, animals, and plants, the commonly shared immune domains including TIR-like, gasdermin-like, caspase-like, and MLKL/CC-like domains act as arsenal modules to restructure the diverse architecture to commit PCD suicide upon stresses/stimuli for host community.