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How Solitons Explain the Puzzling Behavior of Phages
Bacterial viruses sometimes switch themselves off, a process that has always puzzled biologists. Now physicists think they know what’s going on.
Back in the 1970s, a Soviet physicist called Alexander Davydov came up with a remarkable theory to explain the way long molecular chains change shape.
Davydov began by deriving an equation called a Hamiltonian to describe the energy of a molecular chain. He then found that one solution to his equation was a certain kind of vibration called a soliton, a single self-sustaining wave.
He then reasoned that if a soliton became trapped at a site along the chain, the vibration would cause the chain to bend at that point, changing the shape of the molecule.
It took a while for this idea to catch on but so-called Davydov solitons are now thought to play an important role in the way protein chains fold.
Today, Andrei Krokhotin and Antti Niemi at Uppsala University in Sweden use this approach to explain a well known puzzle involving the behaviour of phages, viruses that infect bacteria.
A phage works by inserting itself into a bacteria’s DNA. It then takes over the cell’s molecular machinery to make numerous copies of itself, destroying the host cell in the process. This releases more phages which start the process again in other bacterial cells.
But sometimes, phages switch themselves off. They insert themselves into bacterial DNA and then just sit there doing nothing (except being copied during the normal processes of bacterial reproduction). The technical name for this switch is the lysogenic to lytic transition.
The question that puzzles biologists is how this switch works.
Now Krokhotin and Niemi think they know and say the key is the way that solitons get trapped in the phage’s molecular structure.
Like Davydov, these guys began by deriving an equation that describes the energy of a particular type of virus called a lambda phage that infects Escherichia coli bacteria. They then found that their equation could be solved by several solitons, some of which have opposite senses and so form soliton-antisoliton pairs.
Krokhotin and Niemi go on to work out where these solitons become trapped in the phage’s molecular structure and how this would affect its shape. (Incidentally, this method predicts that the lambda phage has a slightly different structure to the one every body imagined.)
Finally, they say that when energy is injected into the system, one soliton-antisoliton pair can annihilate each other, causing a dramatic and sudden change in the shape of the phage. This change in shape also switches the function of the phage and it is this that causes the lysogenic to lytic transition.
That’s an interesting piece of modelling but its most impressive feature is that makes a number of testable predictions about the lambda phage as it folds into shape. Krokhotin and Niemi say lambda phages must have a slightly different structure than previously thought. They also say their model predicts that the folds must occur in a specific order.
It’s only a matter of time before molecular biologists are able to tease apart these kinds of details. When they do, we’ll know one way or other whether Krokhotin and Niemi are right. Good science.
Ref: arxiv.org/abs/1104.2252: Solitons and Physics of the Lysogenic to Lytic Transition in Enterobacteria Lambda Phage
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