Error Catastrophe Theory

Running a cell is a complex affair. RNA and proteins have to be synthesized on a regular basis to maintain and run the cell's machinery (see chapter 8 for a cell primer). Production of proteins, either for enzymes or structural materials, occurs in a two-step process: transcription of the gene to produce mRNA, followed by translation of the message to produce the protein. For cells that are actively dividing, a third step, replication of the DNA, precedes the other two. Errors can occur all along the way; when they do, defective genes, mRNA, and proteins are produced. The error catastrophe theory, first proposed in the 1960s, suggests that over time, the number of errors build up to a catastrophic level leading to the death of the cell and, possibly, the entire organism.

Soon after this theory was proposed, many scientists conducted experiments that attempted to force a buildup of errors to see how the cells would cope with it. Bacteria were grown on a medium containing defective amino acids to maximize the error frequency of protein synthesis. Similar experiments were conducted on fruit flies (Drosophila) and mice, both of which were given food containing defective amino acids. To everyone's surprise, these experiments had no effect on the bacteria's or animal's health, vigor, or life span. Somehow the cells were able to avoid an error catastrophe. Today we understand why those experiments failed: Cells have elaborate repair systems and strategies that detect and destroy defective molecules. If a defective protein is synthesized, it is quickly broken down and replaced with a normal copy. Only in cases where the repair systems have been damaged would an error catastrophe occur (see Werner's syndrome in chapter 5).

In its original formulation, the error catastrophe theory focused on protein synthesis, which apparently can tolerate a high error frequency. Consequently, many scientists began to wonder if errors in the genome, or possibly a defective regulation of the genes, might be responsible for the aging process. After all, cells avoid an error catastrophe at the trans-lational level because they can always try again with a fresh mRNA from a good gene. But if the genes themselves are damaged, or programmed for senescence, the outcome would be a gradual decline in cell vigor and the eventual death of the organism.

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