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To Stop Evolution: New Way Of Fighting Antibiotic Resistance Demonstrated By Scripps Scientists

ading mechanisms that would make even the most six-sigma-compliant NASA engineer jealous.

Nevertheless, all organisms are prone to some level of damage because no replication machinery is perfect, and with large genomes of billions of bases of DNA to be copied many billions of times over the lifetime of an organism, a certain level of spontaneous mutations will occur -- mistakes that escape repair and become part of the DNA of the cell in which they occur. Scientists have generally thought that slowly over time, these mutations accumulate and species diverge.

However, Romesberg and his colleagues believe that cells are not just the passive victims of random mutations, but have ways of initiating mutations in their own DNA. Evidence for this includes the fact that the rates of mutation in some cells does not seem consistent with the mutation rates associated with DNA replication.

Some cells, like bacteria subjected to antibiotics, seem to acquire mutations at a much higher rate. Romesberg reasons that these rapid mutations may sometimes be part of a mechanism organisms have to rapidly evolve when they need to.

Stress and Mutations

A few years ago, when he was first starting to think about this, Romesberg encountered a paper in a scientific journal that discussed certain genes that "make mutations," as he put it. When these genes are deleted from cells, the cells lose their ability to mutate, even when subjected to massive amounts of ultraviolet light.

This brought Romesberg to the conclusion that mutation is a programmed stress response -- a survival mechanism. If the cell senses damage, and if the damage persists beyond its ability to repair it, the cell will turn on its mutation machinery and open the floodgates for evolution.

Take the bacterium Escherichia coli for instance. When E. coli cells are subjected to damage, they upregulate repair enzymes, which then go to work trying to fix the problem. If the dama
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Source:Scripps Research Institute


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