When the mitochondria receives cell death signals, these gateway proteins are believed to form pores within the mitochondrial membranes that let molecules pass into the cell, creating a cascade of chemical reactions that result in the death of the cell. Programmed cell death, or apoptosis, culls unneeded cells during development and growth.
Apoptosis also protects organisms by killing off defective cells.
Defects in apoptosis can cause harm, such as extended cell survival, which could allow cancer cells to expand. Also, faulty apoptosis can speed up the rate of cell death, contributing to neurodegenerative diseases, immunodeficiency disorders and infertility. Finding these gateway molecules could lead to new molecular targets that improve therapy for a vast array of disorders, according to the researchers. The details of the research are published in the April 27 issue of Science in which the researchers, led by Howard Hughes Medical Institute investigator Stanley J. Korsmeyer show for the first time two pro-apoptotic proteins, called BAX and BAK, which make up the critical initiating factors that trigger the apoptotic process in mitochondria. Korsmeyer and his colleagues at the Dana-Farber Cancer Institute at Harvard Medical School say that a control protein called tBID triggers BAX and BAK to form pores in the cell membrane, allowing cytochrome c to flow into the cell.