Evolution in a test tube

Evolution test tube

Biologists have observed the evolution of a virus into two incipient species — a process known as speciation that Charles Darwin proposed to explain the branching in the tree of life, where one species splits into two distinct species during evolution.

"Speciation has been notoriously difficult to thoroughly investigate because it happens too slowly to directly observe. Without direct evidence for speciation, some people have doubted the importance of evolution and Darwin's theory of natural selection," said Justin Meyer, an assistant professor of biology at University of California San Diego.

"Many theories have been proposed to explain speciation, and they have been tested through analyzing the characteristics of fossils, genomes, and natural populations of plants and animals. With our experiments on top of that, no one can doubt whether speciation occurs," Meyer added.

For their experiment, conducted over six years at the University of California San Diego and at Michigan State University, Meyer and his colleagues cultured a bacteria-infecting virus, known as 'Bacteriophage Lambda', capable of infecting E. Coli bacteria. The virus uses two receptors —molecules on the outside of the cell wall— to attach themselves and then infect cells. When the biologists supplied the bacteriophage with two types of bacteria that varied in their receptors, the virus evolved into two new species, one specialized on each receptor type.

"The virus we started the experiment with, the one with the nondiscriminatory appetite, went extinct. During the process of speciation, it was replaced by its more evolved descendants with a more refined palette." explained Meyer.

"A jack of all trades is a master of none. The specialized viruses were much better at infecting through their preferred receptor and blocked their 'jack of all trades' ancestor from infecting cells and reproducing. The survival of the fittest led to the emergence of two new specialized viruses."

According to another study published last week, viruses within Salmonella rapidly spread genes throughout the bacterial population during a gut infection. The entestinal inflammation caused by Salmonella infection activates the bacteriophages within the bacteria to spread genes throughout the colony. The findings reveal how genetic traits encoded in the viruses, such as increased virulence, can rapidly emerge in pathogenic bacteria during infection.

Some bacteriophages kill their hosts immediately. Others take up residence long-term. These temperate phages ensure their retention within a bacterial host by providing the bug with one or more genetic benefits, such as antibiotic resistance or increased virulence. But when the host bacterium is in trouble, it’s a different matter: the phage rapidly replicates, kills the host cell, and heads off to infect nearby healthy bacteria. By transferring their beneficial genes to new hosts in this way, the viruses play a key role in bacterial evolution.

Read: New evidence that viruses are alive after all

Last year, in a creative stroke inspired by Hollywood wizardry, scientists from Harvard Medical School in Boston, USA have designed a simple way to observe how E. Coli bacteria move as they become impervious to drugs. To do so, the team constructed a dining table sized petri dish and filled it with 14 liters of agar, a seaweed-derived jellylike substance commonly used in labs to nourish organisms as they grow.

To observe how the Escherichia Coli bacteria adapts to increasingly higher doses of antibiotics, the researchers divided the dish into sections and saturated them with various doses of medication. The outermost rims of the dish were free of any drug. The next section contained a small amount of antibiotic—just above the minimum needed to kill the bacteria—and each subsequent section represented a 10-fold increase in dose, with the center of the dish containing 1,000 times as much antibiotic as the area with the lowest dose.

Over two weeks, a camera mounted on the ceiling above the dish took periodic snapshots that the researchers spliced into a time-lapsed montage. The result? A powerful, unvarnished visualization of bacterial movement, death and survival; evolution at work, visible to the naked eye (see video above).

“We know quite a bit about the internal defense mechanisms bacteria use to evade antibiotics but we don’t really know much about their physical movements across space as they adapt to survive in different environments,” said study first author Michael Baym, a research fellow in systems biology at Harvard Medical School.

Beyond providing a telegenic way to show evolution, the experiment yielded some key insights about the behavior of bacteria exposed to increasing doses of a drug. Some of them are:

-Bacteria spread until they reached a concentration (antibiotic dose) in which they could no longer grow. At each concentration level, a small group of bacteria adapted and survived. As drug-resistant mutants arose, their descendants migrated to areas of higher antibiotic concentration.

-Multiple lineages of mutants competed for the same space. The winning strains progressed to the area with the higher drug dose, until they reached a drug concentration at which they could not survive. Progressing sequentially through increasingly higher doses of antibiotic, low-resistance mutants gave rise to moderately resistant mutants, eventually spawning highly resistant strains able to fend off the highest doses of antibiotic.

-Ultimately, in a dramatic demonstration of acquired drug resistance, bacteria spread to the highest drug concentration. In the span of 10 days, bacteria produced mutant strains capable of surviving a dose of the antibiotic trimethoprim 1,000 times higher than the one that killed their progenitors. When researchers used another antibiotic—ciprofloxacin—bacteria developed 100,000-fold resistance to the initial dose.

-Initial mutations led to slower growth—a finding that suggests bacteria adapting to the antibiotic aren’t able to grow at optimal speed while developing mutations. Once fully resistant, such bacteria regained normal growth rates. The fittest, most resistant mutants were not always the fastest. They sometimes stayed behind weaker strains that braved the frontlines of higher antibiotic doses.

“What we saw suggests that evolution is not always led by the most resistant mutants,” Baym said. “Sometimes it favors the first to get there. The strongest mutants are, in fact, often moving behind more vulnerable strains. Who gets there first may be predicated on proximity rather than mutation strength.”

Source: ScienceDaily; Harvard

Image: Amitchell125 at English Wikipedia

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