Jan. 19, 1999 EAST LANSING, Mich. - Some of the world's most notorious disease-causing organisms are ones that evolve quickly to cope with their environment. Now, a team of MSU scientists has learned about what controls the speed of evolutionary adaptation.
The answers, as reported in the Jan. 15 edition of Science, may provide clues to controlling fast mutating disease-causing organisms such as E. coli and HIV, or pumping up beneficial bacteria, such as those that degrade toxic compounds, said Richard Lenski, an evolutionary biologist in the Michigan State University Center for Microbial Ecology.
"People find it intrinsically interesting to watch evolution in action," Lenski said. "And there is special interest in understanding the evolution of disease-causing organisms."
Lenski and his team of researchers working with colonies of E. coli bacteria discovered that it is possible to put organisms on an evolutionary fast track - but they also learned that that fast track has a speed limit.
For an organism to adapt, it needs two processes: mutation and natural selection. Mutation is a random change in the organism's genetic structure. Most mutants are harmful and don't survive. Occasionally, however, a mutation brings a useful change. Natural selection is the process that amplifies the useful mutations. If the mutations are useful, they survive and multiply.
The MSU team used E. coli bacteria as a model, in part because they reproduce rapidly. In about 100 days, 1,000 generations were watched. Lenski's team increased the supply of mutations in two ways: They increased the E. coli numbers and they used strains of bacteria that have elevated mutation rates.
Meanwhile, the first generations were put on ice for storage. Later, they were thawed and put into competition with their descendants to measure how well the new family lineage had evolved.
"In effect, we resurrect their ancestors from the dead," Lenski said. "We resurrect them, they eat glucose and reproduce, and we quantify how they compete with their descendants."
The result: Increasing the number of mutations speeds up evolution. Even though there are more detrimental mutations, natural selection still ensured the survival of the fittest beneficial mutations.
The new generations of bacteria ultimately were made stronger by their beneficial mutations and were able to out-compete their ancestors.
Yet the speed-up process had limits - bucking a widespread view among biologists. At a point, many mutations don't bring more rapid adaptability.
Lenski has a theory about why at some point the beneficial mutations exhaust their power. Because E. coli reproduces asexually, they are unable to combine the strength of mutations from different individuals. Eventually, it appears two beneficial mutants end up competing against each other and begin to cancel out the overall benefit to the generation.
These findings, Lenski said, also may help explain recent studies showing that disease-causing bacteria may have higher mutation rates than their non-pathogenic counterparts. One possible explanation may be that pathogens often experience bottlenecks.
A bottleneck is when a pathogen has to greatly reduce its population size to set up shop in a new host. Lenski uses a sneeze as an example: A droplet of sneeze contains millions of cold viruses. The immune system of the recipient of the sneeze would kill off virtually all of the germs. But a very few would get in through the bottleneck.
That means those few hardy viruses would have to reproduce rapidly and adapt quickly to become a full-blown cold and that it's likely those germs have higher mutation rates.
"In the case of disease-causing bacteria, it's sort of an arms race," Lenski said. "We would like to slow down our opponent. As a start, we would like to know what controls the rate at which our opponent adapts."
The creating of evolution in a test-tube continues work Lenski introduced in January 1995 with another Science publication using some 3,000 generations of E. coli to "replay life's tape" to recreate scenarios of evolution.
Lenski was joined in research by postdoctoral students Arjan de Visser and Clifford Zeyl, graduate student Philip Gerrish and Jeffrey Blanchard from the University of Oregon.
The research was funded in part by the National Science Foundation.
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