Programmed cell death and innate immunity
Plants and animals have a genetically
programmed “suicide” mechanism,
termed programmed cell death. By this mechanism, unwanted cells (such as
cancer cells, infected cells and cells that have already completed their
roles during development) are safely terminated in a strictly controlled
manner. Upon infection by viruses or other pathogens, infected cells
undergo cell death so that proliferation of pathogens and transmission
to other cells can be limited.
In plants, programmed cell death is called the Hypersensitive Response (HR). The HR is part of a strong defense mechanism designed to protect the host plant against pathogens, many of which are bacteria, such as Pseudomonas syringae, viruses, such as Tobacco mosaic virus, and fungi, such as Cladosporium fulvum.
In animals, one of the main types of programmed cell death is apoptosis. Apoptosis is characterized by the activation of proteinases termed Caspases and by morphological changes (shrinkage/fragmentation of cells, membrane blebbing, chromatin condensation/fragmentation). Virus-infected animal cells can undergo cell death on their own or with the help of other cell types (such as NK cells in mammals). To prevent the death of host cells, many viruses carry anti-apoptotic genes that suppress the cell death machinery (e.g. caspase inhibitors) or mimic “survival” genes of the host (e.g. viral homologues of the Bcl-2 family proteins).
As part of a defense response to pathogen insult, plants undergo a localized, programmed cell death at the site of infection, known as the Hypersensitive Response (HR). Seen here is a tobacco leaf (Nicotiana tabacum cv. Xanthi) that has been infiltrated by the bacterial plant pathogen Pseudomonas syringae pv. tomato DC3000. The arrows indicate the white lesions (HR) resulting from cell death. These macroscopic lesions are visible when plants are infiltrated by a high concentration of pathogen. In nature, this programmed cell death occurs at a microscopic, cell-to-cell, level.
