The Processes Senescence Aging Programmed Cell Death Apoptosis etcEvolving Concepts

These terms reflect concepts, and they need to be articulated as clearly as we can, albeit imperfectly, with our current knowledge in order to foster the development of this field. They refer to processes that may be similar overall, and different terms may even refer to identical processes. Not surprisingly, different professional groups sometimes use the same terms differently. Before getting into these conceptual problems further, it is important to recognize how these ideas developed, i.e., where they came from. First, it must be noted that senescence/aging studies on plants and animals developed almost totally independently with little or no interchange until relatively recently (Nooden and Thompson, 1985; Finch, 1990). Likewise, these terms are viewed very differently by groups studying organisms or organs with a pronounced and rapid degeneration as in leaves, flower petals or monocarpic plants as compared to those studying the gradual decline apparent in polycarpic plants and most animals.

What has particularly captured the interest of plant physiologists and plant biologists in general has been the dramatic degeneration of leaves and whole plants (Molisch, 1938; Leopold, 1961; Thomas and Stoddart, 1980) and the ability of hormones, particularly cytokinin (Van Staden et al., 1988) to retard that process, now widely termed senescence. Likewise, the highly visible senescence of flower parts is controlled by ethylene in many cases (Mattoo and Aharoni, 1988). These processes do progress with age, but they are not simply age-dependent. Senescence is not simply a passive accrual of "wear and tear". Senescence is often subject to correlative controls (i.e., it is controlled by other plant parts), and hormones often mediate these controls (Leopold and Nooden, 1984). Thus, these processes are clearly endogenous, not some gradual decline leading to increased vulnerability to acute life-terminating external forces such as drought, cold, herbivores or disease. These observations have led to formulation of the concept of senescence as an endogenous (i.e., developmental) process of degeneration leading to death (Leopold, 1961; Nooden and Leopold, 1978). In this sense, senescence is clearly also programmed cell death. Presently, it is easier (and maybe better) to define these terms as general concepts with a minimum of specifics until those are known with greater certainty.

By contrast, animal biologists and gerontologists focus mainly on the animals such as humans that show a gradual decline as opposed to those that die quickly after reproduction (Finch, 1990; Arking, 1991). Similarly, ecologists have tended to look at population dynamics with less emphasis on the sudden post reproductive death in monocarpic plants (see Watkinson, 1992; Chapter 23). While internal controls are recognized as possible factors in this gradual decline, external factors are clearly implicated in the final slippage toward death or the termination of life. Several scientific communities view this as senescence; however, the problem is complicated by the widespread use of aging to designate the same processes, especially in animals. Long ago, Medawar (1957) articulated the problems inherent in applying a standard dictionary term like aging, which represents the gamut of time-related changes, to biological processes occurring in living organisms. Finch (1990) also specifically avoids the use of aging to designate these processes in animals. The terminology differences between the animal and plant research communities are understandable, because endogenous controls of longevity are simply not very evident in the animals or organism populations studied. While it is true that longevity is a species characteristic and thereby can be presumed to be under genetic control, the process of decline toward death for most animals is a slow loss of vigor with time, and "wear and tear" (aging) has been the most evident explanation. Ecologists generally have been more concerned with understanding the results and less with the physiological mechanism underlying the process. In this view, senescence consists of decreasing fecundity and decreasing survival, i.e., an increase in mortality with age. Nonetheless, these declines may be attributed to internal factors (Watkinson, 1992). The extent to which the various declines with age are similar or different is unknown.

All these different approaches are valuable, but they have taken place in separate scientific communities and have produced different concepts of senescence. This book is aimed primarily at the experimental plant biology and agricultural communities and will use senescence primarily in the physiological sense. Chapter 23 will elaborate on a more demographic perspective and will bridge the understanding between the very different views in separate plant biology communities.

What is aging compared to senescence? The usage of aging is even more varied than senescence. No attempt will be made here to reconcile the different views of these concepts in the gerontology community. Indeed, they are evolving (Finch, 1990; Arking, 1991). There is a well-established, widespread, dictionary-based view of aging as passive, time-dependent changes in biological and non-biological entities. Consistent with this, in the experimental plant biology and the agricultural communities, aging is usually viewed as a passive accrual of lesions due mainly to external forces over time, e.g., "wear and tear" (Nooden and Leopold, 1978), although endogenous factors such as active oxygen species could also play a role in some tissues (Nooden and Guiamet, 1996). These endogenous factors may blur the line between aging and senescence. The clearest example of aging appears to be the loss of viability in seeds (Priestley, 1986; Roberts, 1988), but, no doubt, aging-type (passive) degeneration occurs in many places, and it must contribute to the decline of leaf function under some circumstances. For example, oxidative lesions generated during normal photosynthesis may accumulate over time in leaves (Munne-Bosch and Alegre, 2002). As the biochemical specifics of aging emerge, it should be possible to identify these in other tissues and assess their role in the life cycle and competitive ability of an organism. Aging is a very commonly used term to indicate simple changes with time, and it seems inappropriate to apply it to the complex developmental processes such as senescence and programmed cell death that are not simply determined by age/time.

The idea of programmed cell death and variations thereof have been around a long time in both the animal and plant literatures (Leopold, 1961; Kerr etal., 1972; Vaux, 2002). Cell death is important in development, and it is turning out to have diverse manifestations in a wide range of organisms. Much of the investigation of cell death has been done on animal cells by medical pathologists, but they tend to deal with cell death caused by traumas and disease. Because these ideas evolved in different professional groups, the terminology and conceptual problems described above for senescence and aging also apply there. While these considerations may at first glance seem out of place in a chapter on plant cell death, it must be remembered that these are likely to be universal eukaryotic cell processes, and therefore, much of this information will apply to plant cells.

Until recently, most accepted the idea that cell death could be accomplished by two general types of processes, one (necrosis, oncosis, necrotic cell death, toxicological cell death, accidental cell death, traumatic cell death) due primarily to acute exogenous factors such trauma, stress, toxins, disease, etc. and the other (apoptosis, programmed cell death, physiological cell death, cell suicide, necrobiosis, shrinkage necrosis, autoschizis) due primarily to endogenous factors. Now, however, it is becoming apparent that each of these groupings may include several different processes.

Overwhelming stress can cause a type of cell death often termed necrosis, whereas sublethal stress can induce programmed cell death. The pathologists and some others object to the term necrosis, mainly because it has a long history of a different use, at least in the pathology literature (Majno and Joris, 1996; Levin et al., 1999). Since necrosis was adapted primarily to designate cells that swell before death, it was proposed to call this "oncosis" after the Greek word "onko" for swelling, e.g., cell and organelle swelling, membrane rupture. The swelling is probably due to changes in ion concentrations and in osmotic equilibrium as the subcellular compartments break down (Levin, 1995; Trump and Berezesky, 1998). Necrosis then would refer to all types of cell death. Although concern has been expressed about confusing oncosis with malignancy; the term oncosis seems like a good idea. Certainly, the name oncosis describes the processes better. Oncosis differs from programmed cell death in other ways, e.g., ATP is required for PCD but not for oncosis (Nicotera et al., 1999) and the phosphatidyl serine does not move to the outer face of the plasma membrane during oncosis (O'Brien et al., 1997; Schlegel and Williamson, 2001).

Resolving the other set of terms, apoptosis, programmed cell death and variations thereof is a more complex matter, partly due to the enormous momentum these terms already have in the basic research literature (Lockshin, 1999). Ultimately, clarification will require knowing exactly what these active, endogenous cell destruction processes are. Nonetheless, a reasonable starting point has been outlined by Clarke (1990) who describes three cyto-logically different cell death processes: (1) apoptotic, (2) lysosomal/autophagic and (3) non-lysosomal vesiculate (Table 1-1, Fig. 1-1) with many examples of animal cells cited. These are outlined in Table 1-2 and Fig. 1-1. Probably, there are more endogenous pathways than the three listed in Table 1-1 and many variations of those. Although key features appear to distinguish these patterns, they seem more like syndromes defined by characteristics that may vary a bit. Even apoptosis and necrosis show some significant variations (Hunot and Flavell, 2001; Kumar and Vaux, 2002). For example, in apoptosis, the mitochondria may or may not play a central role or different caspases may be involved.

Table 1-1. Key Characteristics of Three Different Types of Developmental (Programmed) Cell Death Processes

I. Apoptosis

II. Autophagic degeneration

III. Non-lysosomal vesiculate degeneration

Condensation of the nucleus,

Numerous autophagic

Lysosomes not prominent,

chromatin and cytoplasm

vesicles form

but the cytoplasm may

become vacuolate

Cell membrane becomes convoluted

Tatuagem Capricornio

Figure 1-1. Schematic representations of the three commonest types of cell death (types 1, 2 and 3B). The drawings emphasize principally the most constant and best documented features of each type. Thus, some inconstant features, such as the swelling of mitochondria in types 2 and 3 have been omitted. However, the loss of nuclear DNA fragments to autolysosomes in type 2 cell death is shown despite the fact that this has so far been demonstrated in only one case. The different shades of gray indicate what is generally seen in ultramicrographs of lead-stained thin sections. This figure will be best understood if studied in relation to Table 1-2. From Clarke (1990).

The autophagic pathway may be fairly common in plants judging from the membrane whorls often observed within vesicles inside senescing plant cells (Nooden, 1988a); however, apoptosis is important in plants. Section IV will examine some of the key features of apoptosis found in plant cells, but these must be compared to the more complete picture available for animal cells. In any case, the pathway that is now commonly called apopto-sis is by far the best characterized in plants, and it seems to be very important in normal development.

Table 1-2. Summary of the Three Main Types of Cell Death0

Various designations

Nucleus

Cell membrane Cytoplasm

Heterophagic elimination

Type 1

Apoptosis; shrinkage

Nuclear

Convoluted,

Loss of ribosomes from

Prominent and

necrosis;

condensation,

forming

RER and from

important

precocious

clumping of

blebs

polysomes;

pycnosis; nuclear

chromatin leading

cytoplasm reduced in

type of cell death

to pronounced

volume becoming

pycnosis

electron-dense

Type 2

Autophagic cell

Pycnosis in some

Endocytosis at

Abundant autophagic

Occasional

death

cases. Parts of

least in

vacuoles; ER and

and late

nucleus may bleb

some cases;

mitochondria

or segregate

blebbing can

sometimes dilated;

occur

Golgi often enlarged

Type 3A

Non-lysosomal

Late vacuolization,

Breaks

General disintegration;

No

disintegration

then

dilation of organelles,

disintegration

forming "empty"

spaces that fuse with

each other and with

the extracellular

space

Type 3B

Cytoplasmic type

Late increase in

Rounding up

Dilation of ER, nuclear

Yes

granularity of

of cell

envelope, Golgi and

chromatin

sometimes

mitochondria

forming "empty"

spaces

aFrom Clarke (1990).

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