Molecular Mechanisms of the Apoptotic Process

Correct cell number is maintained by a balance of two physiological processes: cell division (mitosis) and cell death (apoptosis). Until 10 or so years ago the efforts of the scientific community were focused almost exclusively on analysis of the cell cycle, with cell death being overlooked. Commencing in 1965, John Kerr studied the process of shrinkage necrosis, which, with Andrew Wyllie and Alistair Currie, was renamed "apoptosis" in 1972 to distinguish this active process from necrosis. Since the late 1980s the importance of apoptosis has become fully appreciated, and the cell and molecular biology of apoptosis has been studied in great detail in a number of invertebrate and vertebrate model systems. This process is clearly highly conserved in metazoans and there is little doubt that the information garnered from the study of less complex species can often be translated to vertebrate model systems. An elegant case in point is the identification of the remarkable similarity between the C. elegans ced-9 gene and members of the mammalian Bcl-2 family. The enormous breadth and depth of the ongoing research (averaging 250 per week) makes it impossible to cover all aspects of this rapidly moving field.

The theme of the Fourth Conference on Cell Death will be the "Molecular Mechanisms of the Apoptotic Process". The meeting will include sessions on the molecular mechanisms involved in the induction of apoptosis, the control of the intracellular protease pathways responsible for this induction, the biochemical events that occur during apoptosis, particularly those events following caspase activation that mediate the death of the cell; and the role of these mechanisms in normal development and disease. This will provide an outstanding opportunity for the participants to obtain state-of-the-art information on the complex molecular mechanisms involved in apoptosis without losing sight of the physiological role of apoptosis in homeostasis and the pathological consequences of disruptions to the apoptotic program.