Natural selection rapidly tunes lizard leg length

Evolution in animals is usually thought of as a process occurring over eons. Research in this realm has tended to focus on the descriptive tracking of the fossil records of long-dead creatures.

But scientists from Harvard and the University of California, Davis, who staged a survival-of-the-fittest scenario among lizards on small islands in the Bahamas, found they could study natural selection at work on a far more compressed time scale and in living animals. Their results show that not only can researchers observe evolution in action, but also that the effects of natural selection can change unexpectedly in a complex natural setting.

In the study appearing in today’s Science, Jonathan Losos of Harvard and colleagues first caught and tagged brown anoles on a dozen small islands around Great Abaco in 2003. They measured the hind leg length of all the reptiles. Then they imported an anole predator, the Northern curly tail lizard, to half of the islands.

Six months later, they found fewer anoles on the predator-inhabited islands than on the control islands. Predators presumably killed the missing ones. The anoles that survived on the predator-inhabited islands were the ones that started out with slightly longer legs. The results fit with the idea that longer legs helped the mainly ground-dwelling reptiles to outrun the terrestrial predator.

Surprisingly, in the next six months, selective pressure did a U-turn to favor decreased leg length as the anoles began to climb trees to escape. The shift from living on the ground to living in trees and bushes is a well-known behavioral response to predators, and lizards with shorter legs fare better at arboreal life.

Were the anoles to be left alone with the predator, the authors predict, they would evolve into a shorter-legged species. But nature had other plans—the experiment ended abruptly in 2004 when Hurricane Frances inundated the islands. Efforts are underway to set up another study over a longer observation period, Losos says.

Polymer coating keeps surfaces germfree

MIT researchers have developed a polymer coating that is deadly to influenza viruses and disease-causing bacteria. The polymer destroys the organisms on contact by poking long, spiky molecular “tentacles” through their protective outer coats. A simple one-step application of the polymer could render common surfaces like doorknobs, elevator buttons, and phones permanently self-sterilized and provide a way to slow the spread of flu and other illnesses.

The polymer, developed by researchers in the lab of Alexander Klibanov, is a water-insoluble hydrocarbon chain with long branches. The researchers painted the substance onto the surface of a glass microscope slide, anchoring the molecules at one end to the slide.

The polymer works quickly—it killed all of the flu viruses within five minutes of contact. With bacteria, the researchers found that the polymers do their damage by penetrating and physically disrupting the cell membrane. Flu viruses have a different kind of outer coat, but the polymers can also penetrate it.

The MIT team found that different polymers were also effective, providing that they were long enough to extend well out from the surface of the slide. In addition to the flu virus, the coated slides also killed disease-causing E. coli and Staphylococcus bacteria.

The article appeared online this week in the Proceedings of the National Academy of Science.

Regulatory role for antisense RNA discovered in yeast

The surprise of the past decade for biologists has been the emergence of RNA’s role as a key regulator of gene activity. The discovery that small, interfering RNA molecules control the fate of larger, protein-coding messenger RNAs landed University of Massachusetts researcher Craig Mello this year’s Nobel Prize.

However, the function of other types of noncoding RNAs has remained more of a mystery. Now, Whitehead Institute researchers have found that a different kind of RNA, antisense RNA, can also regulate gene expression.

Antisense RNA is one type of RNA that is made from DNA during the first step in protein synthesis. One strand of the DNA, the sense strand, is used to make messenger RNA (or sense RNA). The other, noncoding strand is used as a template for antisense RNA. Antisense RNAs are abundant in cells, but their function was unknown.

In a paper published in this week’s Cell, Gerald Fink and colleagues showed that antisense RNA produced from a gene, IME4, regulates that gene in yeast cells and ultimately determines the type of cells they become. This gene is needed for cells to undergo meiosis, a kind of cell division required for reproduction. The researchers found that when high levels of antisense RNA were produced from this gene, sense RNA production was diminished and the cells did not undergo meiosis.

These results should spur interest in antisense RNAs. It could be that these widespread but poorly understood molecules represent a new level of gene regulation.