Hold your horses

People like fast things. Our amusement park rides zip on their tracks. We jump from planes for fun. Our video games have names like Need for Speed. We’re even willing to watch bad movies so long as they’re called Speed. But that doesn’t mean there isn’t value in taking things at a pace reminiscent of the olden days. Sometimes we like to slow things down. Sometimes we like to take the time to smell the roses. And sometimes bloggers will engage in hackneyed stock expressions, both in title and content, in order to slowly build up a contrast between quickness and slowness.

As I’ve explained in the past, Richard Lenski is running a 20+ year evolutionary experiment with E. coli. He has published some fantastic results (much to the chagrin of overwhelmed creationists), and now his lab has utilized his bacterial lineages to further probe how evolution works.

[Co-author Tim] Cooper and his colleagues looked at two Escherichia coli clone lineages, sampled after 500, 1,000 and 1,500 generations of evolution. They came from a long-term bacterial evolution experiment running in the lab.

By looking for the presence of five beneficial mutations, the researchers found that ‘hare’ bacteria had more advantageous genetic changes than ‘tortoises’ after 500 generations, suggesting they were more likely to go on to successfully survive and reproduce, and to eventually wipe out their competitors altogether.

The terms “hare” and “tortoise” refer to the speed with which each group experienced mutation. The more quickly mutating group would change so rapidly that it was unable to achieve the same beneficial mutations as the more slowly mutating group. Here’s how I like to think of it.

In the late 90’s, several children were treated with gene therapy for various diseases. This is when a virus is used as a vector for a gene that has the ability (hopefully) to correct whatever is wrong with the child. It’s how researchers cured color blindness in monkeys in 2009. Basically, a gene is missing, resulting in some malady. When the virus is inserted, so is the missing gene. This usually helps or fixes the given problem. However, in a number of the children from the 90’s, insertional mutagenesis occurred. This is where the inserted gene causes a mutation (for reasons we can skip). In these cases, it caused a downstream mutation. The result was leukemia years after the fact.

The reason I’m seemingly rambling is that it was a complex interaction of genes that caused the cancer. It happens often enough that one gene is mutated and it is the loss of function of that gene that causes cancer, but that wasn’t the case in the 90’s. Think of mosquito genocide. Ultimately it’s all such a complex question that the specific results cannot be known ahead of time.

The reason Lenski’s lab found that the slower mutating group of E. coli out-competed the faster group was because the faster group had too many changes. The high number of mutations prevented it from obtaining other certain mutations. A change in one location can have long-reaching implications for future change in another location, in a way superficially similar to that of children from the 90’s, it turns out; it isn’t the case that just any gene can jump into a genome or population and be beneficial, or even work.

This research is important because it is generally assumed that high mutational rate means high evolvability. And that is still going to remain the assumption. But this gives factual credence to the idea that genetic background matters in a very deep way. In fact, Lenski’s earlier work with the same E. coli demonstrated that mutations themselves can be very much contingent. What this all means is that life doesn’t proceed with a single ‘strategy’. High mutation rates have their advantages, but just the same so do lower rates. It’s like driving through the city versus walking through the city. Plenty can be seen and much ground can be covered by car, sure, but a stroll by foot reveals doors and windows and alleys and other things that otherwise could have gone unnoticed.