Cell death has a central role in innate immune responses in both plants and animals. Besides sharing striking convergences and similarities in the overall evolutionary organization of their innate immune systems, both plants and animals can respond to infection and pathogen recognition with programmed cell death. The fact that plant and animal pathogens have evolved strategies to subvert specific cell death modalities emphasizes the essential role of cell death during immune responses. The hypersensitive response (HR) cell death in plants displays morphological features, molecular architectures and mechanisms reminiscent of different inflammatory cell death types in animals (pyroptosis and necroptosis). In this review, we describe the molecular pathways leading to cell death during innate immune responses. Additionally, we present recently discovered caspase and caspase-like networks regulating cell death that have revealed fascinating analogies between cell death control across both kingdoms.

The Yin and Yang of Plant Caspases: The function of plant metacaspases, identified by limited sequence homology to the animal caspases that control cell death, has remained elusive. Coll et al. (p. 1393 ) have now elucidated the actions of two metacaspases in the small plant Arabidopsis . One metacaspase, AtMC1, promoted cell death, and the other, AtMC2, acted antagonistically to stall cell death. The results help to elucidate the mechanisms by which plants control cell survival during development and defend against pathogen attack.

Programmed cell death (PCD) is a fundamental cellular process that has adopted a plethora of vital functions in multicellular organisms. In plants, PCD processes are elicited as an inherent part of regular development in specific cell types or tissues, but can also be triggered by biotic and abiotic stresses. Although over the last years we have seen progress in our understanding of the molecular regulation of different plant PCD processes, it is still unclear whether a common core machinery exists that controls cell death in development and disease. In this review, we discuss recent advances in the field, comparing some aspects of the molecular regulation controlling developmental and pathogen-triggered PCD in plants.

Xylem vascular wilt pathogens cause devastating diseases in plants. Proliferation of these pathogens in the xylem causes massive disruption of water and mineral transport, resulting in severe wilting and death of the infected plants. Upon reaching the xylem vascular tissue, these pathogens multiply profusely, spreading vertically within the xylem sap, and horizontally between vessels and to the surrounding tissues. Plant resistance to these pathogens is very complex. One of the most effective defense responses in resistant plants is the formation of physico-chemical barriers in the xylem tissue. Vertical spread within the vessel lumen is restricted by structural barriers, namely, tyloses and gels. Horizontal spread to the apoplast and surrounding healthy vessels and tissues is prevented by vascular coating of the colonized vessels with lignin and suberin. Both vertical and horizontal barriers compartmentalize the pathogen at the infection site and contribute to their elimination. Induction of these defenses are tightly coordinated, both temporally and spatially, to avoid detrimental consequences such as cavitation and embolism. We discuss current knowledge on mechanisms underlying plant-inducible structural barriers against major xylem-colonizing pathogens. This knowledge may be applied to engineer metabolic pathways of vascular coating compounds in specific cells, to produce plants resistant towards xylem colonizers.