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Chapter 20

Senescence and
Programmed Cell Death


Selective death of cells, tissues, and organs is an essential feature of plant development and survival. The term programmed cell death refers to any process by which protoplasm, with or without the cell wall that encloses it, is eliminated as part of a developmental or adaptive event in the life cycle of the plant. Plants dispose of unwanted cytoplasm or whole cells by several mechanisms, including self-ingestion (autophagy), lysis (lysigeny), or a kind of mummification (as seen in endosperm formation). PCD is essential for normal reproductive and vegetative development and for responses to environmental stresses. During senescence (a PCD-like process associated with the terminal stages of organ development), specific genes are expressed, some of which have been cloned and their promoters analyzed. Stay-green mutants are genetic variants in which expression of senescence-associated genes is impaired.
      Senescing cells are metabolically active. The chlorophyll degradation pathway is turned on, accompanied by the unmasking or accumulation of carotenoids and other pigments. Proteins are broken down, and the mobilized organic nitrogen and organic sulfur are exported from senescing leaves. Catabolism of nucleic acids releases inorganic phosphate. Photosynthesis declines, and peroxisomes are redifferentiated into glyoxysomes, which convert lipids to sugars. Metabolic regulation during senescence involves responses to cellular redox conditions, compartmentation, and differential susceptibility of enzymes to proteolysis. Senescence is sensitive to growth regulators, particularly to the senescence-promoter ethylene and to cytokinins, which act as senescence antagonists.
      Senescence is used both as part of adaptive strategies that ensure seasonal survival and as a tactic deployed when an unpredictable stress is experienced. Formation of TE and mobilization of cereal endosperm are examples of developmental PCD. Zinnia leaf mesophyll cells induced to form TE in culture are a valuable model of cell death. Several different pathways lead to death of starchy endosperm and aleurone cells in cereals. Ethylene can induce PCD in starchy endosperm cells, and GA and ABA regulate cell death in cereal aleurone. An example of PCD under an abiotic environmental stress is aerenchyma formation, which is a response to limited oxygen availability, such as when roots are flooded. Ethylene mediates aerenchyma formation, and signaling between ethylene production and hypoxia sensing is mediated by calcium.
      The hypersensitive response is an example of PCD related to biotic stress and has its own effect on the programmed nature of cell death. Lesion-mimic mutants are useful models for analyzing HR. Such mutations in Arabidopsis fall into two groups: those that trigger defense responses, and those that do not. Lesion-mimic mutants primarily affect cell death in the context of the defense response to pathogens but apparently have no effect on other events in developmental cell death. Reactive oxygen intermediates are a key trigger in PCD accompanying the HR. HR can be compared with apoptosis, a type of PCD in animals that has been intensively researched and has been an influential general model for PCD and its regulation. Future directions for PCD research include the relationship between programmed cellular processes and whole-organism aging.

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