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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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