It’s well known that small changes in the initial conditions cause changes in the long term that are not predictable when it comes to complex systems. There is no complex system that I know of that’s more complex than evolution of organisms. It’s no wonder that small mutations cause evolutionary changes that are far reaching. It’s very fascinating all the same.
Small genetic mutations that add up over time could create an evolutionary express lane that leads to the rapid development of new traits, researchers from the University of Pittsburgh and the University of Wisconsin at Madison have found.
The team reports in the Proceedings of the National Academy of Sciences (PNAS) that slight changes in segments of DNA known as transcriptional enhancers—which determine the when, where, and how much in gene production—can activate dormant genetic imperfections. These alterations awaken specific genes to low-level activity, or "leakiness," in developing tissue different from the genes’ typical location. Just a few subsequent mutations build on that stirring to result in a new function for an old gene—and possibly a novel trait.
The Pitt-UW Madison work expands on research during the past 30 years demonstrating that new genes made from scratch are rare in animals, Rebeiz said. Instead, the diversity of living things is thought to stem from existing genes showing up in new locations. In a famous example of the lack of originality in animal genes, researchers at the University of Basel in Switzerland reported in Science in 1995 that a gene known as PAX6, a "master control" gene for the formation of eyes and other features in flies, mice, and humans, could cause the growth of additional eyes on the legs and antennae of fruit flies.
With their report in PNAS, Rebeiz and his coauthors offer the first explanation of what makes these genes go astray in the first place—and they identified the deviant DNA as the culprit.
The researchers found that the gene Neprilysin-1 present in the optical neurons of the fruit fly species Drosophilia santomea emerged in that location about 400,000 years ago—a blip in evolutionary terms—in the last common ancestor the fly shared with its relative D. yakuba. The mutation began with a transcriptional enhancer for the gene, which caused Neprilysin-1 to show up in different neurons than usual.
From there, Rebeiz said, the development of D. santomea’s distinguishing neurons plays out with the clarity of a film as four mutations in subsequent generations intensify the errant enhancer’s impact until Neprilysin-1’s presence in optical neurons become an exclusive feature of D. santomea. On the other hand, ensuing genetic alterations in D. yakuba actually extinguished this new expression and restored that fly’s Neprilysin-1 to its original location.