"The concept of programmed cell death (PCD) came from plants" (Jones, 2001). This rather surprising assertion is based on early studies on plant reactions to fungal invasion (Allen, 1923) and a long standing interest in senescence by plant scientists (Molisch, 1938; Leopold, 1961). Nevertheless interest in the phenomenon was promoted greatly by animal studies focused on specific changes in cellular structure (Lockshin and Williams, 1965; Kerr et al., 1972). Later Barlow (1982) reasoned regarding plants that if cells die at a predictable time and location, if the death has some beneficial effect on tissue differentiation and is encoded in the hereditary material of the species, it represents a specific process of ontogenesis. This definition excluded necrotic cell death due to accidental or random injury such as exposure to some toxins or a lethal temperature. As history has revealed, cell death in many plant processes is programmed and meets many or all of Barlow's criteria. The study of PCD has become an important area of plant biology, and this chapter will develop that theme. Owing to space limitations and the desire to consider recent findings, we have relied on reviews often and have not cited individually the papers in Barlow (1982).

There is insufficient information at present to conclude that animal and plant cells regulate PCD through a common, basic mechanism (Chapter 1). Nevertheless, some of the biochemical steps that regulate and execute PCD in animal cells have recently been identified in plant cells in culture. Early in the apoptosis of mammalian cells, phosphatidyl serine is exposed at the outer face of the plasma membrane and is detectable by the binding of annexin V (Martin et al., 1995). Similarly, in protoplasts from tobacco cells, an early stage in PCD induced by camptothecin or salicylic acid was the binding of annexin V (O'Brien et al., 1997, 1998).

Plant Cell Death Processes 19

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Other indicators of PCD in animal cells are chromatin condensation and nDNA fragmentation, detected either by the occurrence of internucleosomal lengths of DNA ("DNA ladders") on agarose gels, or in situ by the terminal deoxynucleotidyl transferase-mediated dUTPnick end labeling (TUNEL) of exposed DNA 3' hydroxyl groups (Gavrielli et al., 1992). Cultured plant cells undergo chromatin condensation and test positive for TUNEL when exposed to agents that induce PCD (Wang et al, 1996a; O'Brien et al, 1997, 1998), although at high concentration some agents (e.g. H2O2) caused isolated cells or protoplasts to show symptoms of necrosis (oncosis) rather than PCD. Caspases, cysteine proteases that cleave polypeptides after Asp residues, are almost always required for apoptosis in mammalian cells (Salvesen and Dixit, 1997; Thornberry and Lazebnik, 1998), but a role for caspases in plant PCD is unclear (Lam and del Pozo, 2000; Beers et al., 2000). Much of the evidence for participation of caspase-like proteases in PCD in plant cells relies on the activity of peptidase-specific inhibitors. Induction of PCD in cultured soybean cells by oxidative stress quickly activated cysteine proteases (Solomon et al., 1999), and both cysteine protease activity and PCD were blocked by ectopic expression of the gene for the cysteine protease inhibitor, cystatin. Other examples of circumstantial evidence for the participation of caspase-like proteases in plant PCD are cited by Lam and del Pozo (2000).

Apoptosis in animal cells often involves fragmentation into membrane-bound apoptotic bodies that are quickly engulfed by surrounding macrophages or phagocytes, but no such mechanism for dealing with dead cells is available to plants. Mature plant cells, unlike animal cells, usually have a vacuole that constitutes 80-95% of the cell volume; additionally, the protoplast normally is enclosed by a cell wall that would prevent expulsion of apoptotic bodies were they to occur. It is to be expected, therefore, that some of the anatomical and biochemical steps in PCD will be unique to plant cells.

It is implicit in the concept of PCD that in most cases, at a given time, certain cells die and others do not. Why do only certain cells die? This question immediately prompts the thought that there is some selectivity in differentiation between the surviving and the suicidal cells. This chapter examines examples of PCD which seem to depend on cell differentiation as one means of targeting. The most direct possible relationship of PCD with cell differentiation would be that a cell differentiates and during that process dies. An obvious example is differentiation of xylem tracheary elements as a vital part of vascular development. A second relationship between cell death and differentiation would be that cells differentiate, perform an intermediate function for a time, and later they die. There are a number of examples of this pattern of development associated with reproduction including embryo and pollen development and aleurone cells. A third case involves cells that appear identical; yet, at a specific time and place or condition, a subset of them dies. An example would be the thin-walled parenchyma cells (Esau, 1965), including those in the root cortex, which can undergo PCD to form aerenchyma and similar internal spaces. Cell death occurs in a distinctive pattern and some of the cortical cells survive. Thus, in addition to discernable differentiation, there may be changes associated with cell lineage, position or packing within a tissue which mark or potentiate specific cells to die. Regardless, this third example is common enough to be important to plant development and will be included in this chapter.

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