WIND back the tape of life, Stephen Jay Gould once quipped, and the chance becomes vanishingly small that anything like human intelligence would grace the replay. Not everyone agrees. Matthew Herron and Michael Doebeli, from the University of British Columbia, challenge the late biologist's logic, at least when it comes to bacteria.

Drs Herron and Doebeli looked at E. coli, which reproduces rather more quickly than Homo sapiens does, making it possible to track its evolution in the lab. The bacteria were grown for six months, or 1,200 generations, in the presence of sugar (in the form of glucose) and vinegar (acetate). Each day, once the food supply was more or less exhausted, a sample of the population was transferred to a fresh batch of food, to maintain the ideal conditions for bacterial reproduction.

The researchers observed that their E. coli quickly began to specialise. The glucose specialists appeared to have an edge early on. Then, the acetate-eaters' population exploded, before the proportions reached roughly one to one at the end of the experiment (though there is no reason to rule out further fluctuations if the test was allowed to continue). The researchers then rewound the tape and repeated the procedure two more times. The ultimate proportions ended up roughly resembling each other—not that surprising given that organisms evolve to fill available niches. What was more interesting, the way the proportions varied over time turned out to be much the same in all three experiments. Crucially, the evolutionary paths looked alike at the molecular level, too.

Dr Herron and Dr Doebeli spotted this similarity when they sequenced, every 10 days or so, the bacterial DNA. This let them identify specific mutations as they happened. In all three experiments, the glucose-eaters' boom was preceded by changes to a number of genes involved in metabolism. One, called spoT, regulates metabolism in general. The others, belonging to a group known as rbs operon, deal with metabolising ribose, another sugar.

In particular, deletion of some rbs operon genes, which turns out to be rather common, switches off bacteria's ability to metabolise ribose. This ability, Dr Herron speculates, might be somehow competing with the capacity for digesting glucose. However, the mechanism remains mysterious.

Next, 400-500 generations later, other mutations, this time to a host of different genes, led some bacteria to develop a sour tooth. These then had oodles of food and no serious competition: the glucose-munchers which proliferated earlier shunned acetate, and the remaining unspecialised E. coli were no match for the acetate-eaters, which let the latter catch up with their sweet-toothed cousins. Natural selection took care of the rest.

It is unclear precisely what advantage many of the identified genes confer to the bacteria. And, while rbs operon is a known mutation "hot spot", as parts of the genome particularly susceptible to random genetic changes are known, is it not evident why the spoT gene should persistently be among the first in line to get tweaked. Evolutionary history might not, then, be quite predictable. But it does sometimes repeat itself.