ABSTRACT
How do otherwise healthy cells become committed to die? How do cells execute this destructive decision once the apoptotic fate determination has been made? Experiments on model systems such as the nematode and the fruit fly have begun to answer these questions at the molecular level. By applying classical genetic tools in combination with modern molecular techniques, studies of PCD in these organisms have provided remarkable insights into the nature of cellular suicide and offered the first molecular clues regarding genetic components required for apoptosis. The apparent conservation of at least some apoptosis genes (see below) suggests that this information could eventually permit us to develop treatments for human diseases that are caused, or exacerbated by, the misregulation of apoptosis.
