Size Matters: How C. elegans Asymmetric Divisions Regulate Apoptosis

Apoptosis is a form of programmed cell death used by metazoans to eliminate abnormal cells, control cell number, and shape the development of organs. The use of the nematode Caenorhabditis elegans as a model for the study of apoptosis has led to important insights into how cells die and how their corpses are removed. Eighty percent of these apoptotic cell deaths occur during nervous system development and in daughters of neuroblasts that divide asymmetrically. Pioneering work defined a conserved apoptosis pathway that is initiated in C. elegans by the BH3-only protein EGL-1 and that leads to the activation of the caspase CED-3. While the execution of the apoptotic fate is well understood, much less is known about the mechanisms that specify the apoptotic fate of particular cells. In some cells fated to die, this regulation occurs at the level of the egl-1 gene transcription, and investigators have identified several lineage-specific transcription factors that both positively and negatively regulate egl-1. In this review, we focus on a second set of molecules that appear to influence apoptosis by controlling the position of the cleavage plane in divisions that produce apoptotic cells.