Mark P.Mattson and Sic L. Chan
Apoptosis is a feature of many diseases and is critical for the sculpting and maintenance of tissues. New work demonstrates that calcium released from the endoplasmic reticulum synchronizes the mass exodus of cytochrome c from the mitochondria, a phenomenon that coordinates apoptosis.

One unresolved problem in cell biology has been to explain how a cell dies rapidly while maintaining its energy levels, preserving the structure of its mitochondria and endoplasmic reticulum, and not adversely affecting its neighbors. Research over the past decade has filled in some pieces of this puzzle by establishing the functions of several proteins including Bcl-2 family members, cytochrome c, and caspases in an evolutionarily conserved form of programmed cell death called apoptosis1. During development, apoptosis is necessary for tissues and organs to acquire their unique structures and functions. By eliminating ‘worn out’ cells, apoptosis also serves adaptive functions in self-renewing tissues of the adult, with bone marrow or blood and epithelia being well-studied examples2. Beyond its importance for understanding
development and tissue homeostasis, the molecular regulation of apoptosis has moved to the forefront of biomedical research: it is an important factor in prominent diseases, including cancers (in which tumor cells are resistant to apoptosis) and neurodegenerative disorders such as Alzheimer’s and Parkinson’s
diseases (where unwanted apoptosis of neurons occurs)3.

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