Process of Apoptosis in the Soil Worm Caenorhabditis elegans

Campbell Biology

Three proteins, Ced-3, Ced-4, and Ced-9, are critical to apoptosis and its regulation in the nematode. Apoptosis is more complicated in mammals but involves proteins similar to those in C. elegans.
Source: Urry, Lisa A.. Campbell Biology (p. 230). Pearson Education. Kindle Edition.

The molecular mechanisms of apoptosis were worked out by researchers studying embryonic development of a small soil worm, a nematode called Caenorhabditis elegans. Because the adult worm has only about 1,000 cells, the researchers were able to work out the entire ancestry of each cell. The timely suicide of cells occurs exactly 131 times during normal development of C. elegans, at precisely the same points in the cell lineage of each worm. In worms and other species, apoptosis is triggered by signals that activate a cascade of “suicide” proteins in the cells destined to die.

Genetic research on C. elegans initially revealed two key apoptosis genes, called ced-3 and ced-4 (ced stands for “cell death”), which encode proteins essential for apoptosis. The proteins are called Ced-3 and Ced-4, respectively. These and most other proteins involved in apoptosis are continually present in cells, but in inactive form; thus, regulation in this case occurs at the level of protein activity rather than through gene activity and protein synthesis. In C. elegans, a protein in the outer mitochondrial membrane, called Ced-9 (the product of the ced-9 gene), serves as a master regulator of apoptosis, acting as a brake in the absence of a signal promoting apoptosis. When a death signal is received by the cell, signal transduction involves a change in Ced-9 that disables the brake, and the apoptotic pathway activates proteases and nucleases, enzymes that cut up the proteins and DNA of the cell. The main proteases of apoptosis are called caspases; in the nematode, the chief caspase is the Ced-3 protein.

Source:

Urry, Lisa A.. Campbell Biology (p. 230). Pearson Education. Kindle Edition.

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