<h5>Introduction</h5> In the multicellular organism, genetically regulated mechanisms determine not only which cells live, but also which cells die  . In the adult, steady-state condition, cell division must be counterbalanced by cell death. This physiologically important cell death is an active process, known as programmed cell death, or apoptosis. Apoptosis is characterized by profound morphological alterations of the cell and, specifically, the nucleus. Typically, apoptotic changes include cellular shrinkage, membrane blebbing and chromatin condensation  . The nuclear DNA of apoptotic cells is often fragmented into oligonucleosomal-sized units  . By contrast, ‘accidental’ cell death, or necrosis, is caused by an overwhelming injury resulting in cellular swelling and loss of membrane integrity  . Cell proliferation has been studied extensively, but genes regulating cell death have only recently attracted the attention of the biomedical research community. Perturbations of apoptosis contribute to the pathogenesis of several human diseases including cancer, acquired immunodeficiency syndrome and neurodegenerative disorders  . Thus, discovering ways to modulate apoptosis may have immense therapeutic potential. The fundamental importance of the cell-death pathway is further emphasized by its conservation throughout evolution  . In fact, genetic studies of two invertebrates, Caenorhabditis elegans and Drosophila melanogaster
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