Apoptosis

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g cell so that it does not release its contents and trigger a local inflammatory reaction. Cells undergoing apoptosis usually exhibit a characteristic morphology, including fragmentation of the cell into membrane-bound apoptotic bodies, nuclear and cytoplasmic condensation and endolytic cleavage of the DNA into small oligonucleosomal fragments (Steller, 1995). The cells or fragments are then phagocytosed by macrophages.
These signals can trigger apoptosis,
· lineage information
· damage due to ionizing radiation or viral infection
· extracellular signals

The execution of apoptosis minimizes the leakage of cellular constituents from dying cells. For example, proteases could damage adjacent cells or stimulate an inflammatory response. This cardinal feature of apoptosis distinguishes it from necrosis, which usually results from trauma that causes injured cells to swell and lyse, releasing the cytoplasmic material that stimulates an inflammatory response (Steller, 1995; Wyllie et al., 1980).
Extrinsic signals may either suppress or promote apoptosis, and the same signals may promote survival in one cell type and invoke the suicide program in others (Steller, 1995). For example, death receptors that are members of the tumour necrosis factor receptor (TNFR) family sit in cell membranes, but their intracellular domains have direct access to the cell death machinery that lies ready and waiting within the cell (Ashkenazi and Dixit, 1998). When members of the TNF ligand family bind to their receptors some of the pathways activated can include those that bring about cell death. Conversely, there are other factors, such as the neurotrophins, that bind to cell surface receptors and which act to prevent cell death!
Apoptosis research has been spurred by the observation that normal metazoan development and health require the precise regulation of cell death. Apoptosis plays a critical role in important biological processes such as morp...