Mechanism that allows cells to self-destruct when stimulated by the appropriate trigger. It may be initiated when a cell is no longer needed, when a cell becomes a threat to the organism's health, or for other reasons. The aberrant inhibition or initiation of apoptosis contributes to many disease processes, including cancer. Though embryologists had long been familiar with the process of programmed cell death, not until 1972 was the mechanism's broader significance recognized. Apoptosis is distinguished from necrosis, a form of cell death that results from injury.
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Besides these two types of PCD, other pathways have been discovered. Called "non-apoptotic programmed cell-death" (or "caspase-independent programmed cell-death" or "necrosis-like programmed cell-death") these alternative routes to death are as efficient as apoptosis and can function as either backup mechanisms or the main type of PCD.
Other forms of programmed cell death include anoikis, almost identical to apoptosis except in its induction; cornification, a form of cell death exlusive to the eyes; excitotoxicity and Wallerian degeneration.
Plant cells undergo particular processes of PCD which are similar to autophagic cell death. However, some common features of PCD are highly conserved in both plants and metazoa.
PCD has been the subject of increasing attention and research efforts. This trend has been highlighted with the award of the 2002 Nobel Prize in Physiology or Medicine to Sydney Brenner (United Kingdom), H. Robert Horvitz (US) and John E. Sulston (UK).
Basic morphological and biochemical features of PCD have been conserved in both plant and animal kingdoms. It should be noted, however, that specific types of plant cells carry out unique cell-death programs. These have common features with animal apoptosis -- for instance, nuclear DNA degradation -- but they also have their own peculiarities, such as nuclear degradation being triggered by the collapse of the vacuole in tracheary elements of the xylem.
Janneke Balk and Christopher J. Leaver, of the Department of Plant Sciences, University of Oxford, carried out research on mutations in the mitochondrial genome of sun-flower cells. Results of this research suggest that mitochondria play the same key role in vascular plant PCD as in other eukaryotic cells.
The stalk is composed of dead cells which have undergone a type of PCD that shares many features of an autophagic cell-death: massive vacuoles forming inside cells, a degree of chromatin condensation, but no DNA-fragmentation. The structural role of the residues left by the dead cells is reminiscent of the products of PCD in plant tissue.
D. discoideum is a slime mold, part of a branch which may have emerged from eukaryotic ancestors about a billion years before the present. They apparently emerged after the ancestors of green-plants and the ancestors of fungi and animals had differentiated. But in addition to their place in the evolutionary tree, the fact that PCD has been observed in the humble, simple, six-chromosome D. discoideum has additional significance: it permits the study of a developmental PCD path which does not depend on the caspases which are characteristic of apoptosis.
This evolutionary step would have been more than risky for the primitive eukaryotic cells which began to engulf the energy-producing bacteria and conversely, a perilous step for the ancestors of mitochondria which began to invade their proto-eukaryotic hosts. This process is still evident today, between human white blood-cells and bacteria. Most of the time, invading bacteria are destroyed by the white blood-cells; however, it is not uncommon for the chemical warfare waged by prokaryotes to succeed, with the consequence known as infection by its resulting damage.
One of these rare evolutionary events, about two billion years before the present, made it possible for certain eukaryotes and energy-producing prokaryotes not only to coexist, but to mutually benefit from their symbiosis.
Mitochondriate eukaryotic cells live poised between life and death, because mitochondria still retain their repertoire of molecules which can trigger cell suicide. This process has now been evolved to happen only when programmed. Given certain signals to cells (such as feedback from neighbors, stress or DNA-damage), mitochondria release caspase activators which trigger the cell-death inducing biochemical cascade. As such, the cell-suicide mechanism is now crucial to all of our lives.
DPL-1 DP, LIN-35 Rb and EFL-1 E2F Act with the MCD-1 Zinc-Finger Protein to Promote Programmed Cell Death in Caenorhabditis Elegans
Apr 01, 2007; ABSTRACT The genes egl-1, ced-9, ced-4, and ced-3 play major roles in programmed cell death in Caenorhabditis elegans. To...