Mud time capsules show evolutionary arms race between host and parasite

Blogging on Peer-Reviewed ResearchEvolution can sometimes be seen as a futile contest. Throughout the natural world, pairs of species are locked in an evolutionary arms race where both competitors must continuously evolve new adaptations just to avoid ceding ground. Any advantage is temporary as every adaptive move from a predator or parasite is quickly neutralised by a counter-move from its prey or host. Coerced onward by the indifferent force of natural selection, neither side can withdraw from the stalemate.

Mud time capsules show evolutionary arms race between host and parasiteThese patterns of evolution are known as Red Queen dynamics, after the character in Lewis Carroll’s Through the Looking Glass who said to Alice, “It takes all the running you can do, to keep in the same place.”

These arms races are predicted by evolutionary theory, not least as an explanation for sex. By shuffling genes from a mother and father, sex acts as a crucible for genetic diversity, providing a species with the raw material for adapting to its parasites and keep up with the arms race.

Watching the race

We can see the results of Red Queen dynamics in the bodies, genes and behaviours of the species around us but actually watching them at work is another matter altogether. You’d need to study interacting species over several generations and most biologists have neither the patience nor lifespan to do so.

But sometimes, players from generations past leave behind records of the moves they made. Ellen Decaestecker and colleagues from Leuven University found just such an archive in the mud of a Belgian lake.

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MRSA gets piggyback from livestock to humans

Blogging on Peer-Reviewed ResearchMRSA gets piggyback from livestock to humansI’ve written an article for the Economist about a new strain of the antibiotic-resistant “superbug” MRSA (methicillin-resistant Staphylococcus aureus) that infects large numbers of farm pigs and can jump into humans.

The strain was first found in pig farms in the Netherlands and may be picking up new resistances from their porcine hosts because of the large amounts of antibiotics used to medicate livestock.

The piece is in the Science and Technology section of the November 29th issue of the Economist (out in the UK tomorrow) but you can already read it online. I’m pretty excited about this – it’s certainly the most prestigious magazine I’ve had the opportunity to write for.

Cooperating bacteria are vulnerable to slackers

Blogging on Peer-Reviewed ResearchAs a species, we hate cheaters. Just last month, I blogged about our innate desire to punish unfair play but it’s a sad fact that cheaters are universal. Any attempt to cooperate for a common good creates windows of opportunity for slackers. Even bacteria colonies have their own layabouts. Recently, two new studies have found that some bacteria reap the benefits of communal living while contributing nothing in return.

Cooperating bacteria are vulnerable to slackersBacteria may not strike you as expert co-operators but at high concentrations, they pull together to build microscopic ‘cities’ called biofilms, where millions of individuals live among a slimy framework that they themselves secrete. These communities provide protection from antibiotics, among other benefits, and they require cooperation to build.

This only happens once a colony reaches a certain size. One individual can’t build a biofilm on its own so it pays for a colony to be able to measure its own size. To do this, they use a method ‘quorum sensing’, where individuals send out signalling molecules in the presence of their own kind.

When another bacterium receives this signal, it sends out some of its own, so that once a population reaches a certain density, it sets off a chain reaction of communication that floods the area with chemical messages.

These messages provide orders that tell the bacteria to secrete a wide range of proteins and chemicals. Some are necessary for building biofilms, others allow them to infect hosts, others make their movements easier and yet others break down potential sources of food. They tell bacteria to start behaving cooperatively and also when it’s worth doing so.

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Space flight turns Salmonella into super-bug

Science fiction loves to play off the potential threat of threat of alien viruses. But a new study suggests that space travellers are much more likely to be threatened by germs from our own planet that become more virulent in space.

The Space Shuttle Atlantis carried some Salmonella as part of an experimentWarding off infections is a real priority for astronauts, especially if longer space missions to the Moon and Mars are to go ahead. People have a tendency to get sick in space and over half of the astronauts on the Apollo missions became ill during their trips or soon after their return to Earth.

Earlier research has shown that prolonged weightlessness weakens our immune systems by preventing key sets of genes from switching on. But that’s only part of the problem. A team of researchers from NASA, Arizona State University and 12 other institutions has shown that bacteria also react to zero-gravity conditions, by becoming more virulent, or able to cause disease.

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An entire bacterial genome discovered inside that of a fruit fly

Bacteria have the ability to transfer genes to one another. Now, scientists have found that one species, Wolbachia, has managed to transfer its entire genome into that of a fruit fly. These extreme gene transfers could be more common than we thought, and they have important consequences for genome-sequencing projects.

Wolbachia in yellow infecting insect cells in red.A humble species of fruit fly is the genetic equivalent of a Russian doll – peer inside its DNA and you will see the entire genome of a species of bacteria hidden within.

The bacteria in question is Wolbachia, the most successful parasite on earth and infects about 20% of the world’s species of insects. It’s a poster child for selfishness. To further its own dynasty, it has evolved a series of remarkable techniques for ensuring that it gets passed on from host to host. Sometimes it gives infected individuals the ability to reproduce asexually; at other times, it does away with an entire gender.

Now, Julie Dunning-Hotopp from the J. Craig Venter Institute and Michael Clark from the University of Rochester have found an even more drastic strategy used by Wolbachia to preserve its own immortality – inserting its entire genome wholesale into that of another living thing. Continue reading

The secret of drug-resistant bubonic plague

The bacterium that causes bubonic plague can pick up drug resistance from common bacteria responsible for food poisoning.

Yersinia pestis causes bubonic plague.The plague, or the Black Death, is caused by a microbe called Yersinia pestis (right). In the 14th century, this microscopic enemy killed off a third of Europe’s population.

While many people consign the plague to centuries past, this attitude is a complacent one. Outbreaks have happened in Asia and Africa over the last decade and the plague is now recognised as a re-emerging disease.

In 1996, two drug-resistant strains of plague were isolated from Madagascar. One of these, was completely resistant to all the drugs that are used to control outbreaks.

Any scientist currently studying tuberculosis can attest to the ability of bacteria to evolve resistance to drugs. In the case of drug-resistant plague, the secret to its powers is a plasmid – a small free-floating ring of DNA, that carries drug resistance genes.

Bacteria can trade plasmids across individuals, transferring genes between each other in ways that humans can only achieve with technology.

The worry is that common and less harmful bacteria could transfer drug-resistance plasmids over to Yersinia, resulting in new resistant strains.

Plague bacteria could pick up drug resistance from Salmonellla like this. Timothy Welch and colleagues from the United States Department of Agriculture showed that this concern is well-founded. They found that the plague plasmid is virtually identical in parts to plasmids from an increasingly common strain of Salmonella (left) that is also resistant to multiple drugs.

They even found related plasmids were in other drug-resistant bacteria isolated from meat samples across the USA during quality control checks.

A word of caution – this doesn’t mean that people risk contracting plague from eating meat. Even though the plasmids are strikingly similar, the bacteria involved are very different.

But it does mean that the plague bacterium could potentially gain drug resistance from other common resistant bacteria, if they should both find themselves in the same human or flea host.

Despite this scary scenario, Welch’s study also provides us with a silver lining. We are aware of the threat and we know how to monitor for it, by searching for the plasmid.

Monitoring is especially important because the plague has all the qualities you would look for in a potential biological weapon – a high fatality rate, no vaccine and possible air-borne transmission.

If the worst happens, we will want to be prepared.

 

Reference: Welch, Fricke, McDermott, White, Rosso, Rasko, Mammel, Eppinger, Rosovitz, Wagner, Rahalison, LeClerc, Hinshaw, Lindler, Cebula, Carniel& Ravel. 2007. Multiple antimicrobial resistance in plague: an emerging public health risk. PLOS ONE.

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Human gut bacteria linked to obesity

The obesity epidemic is a massive concern for the 21st century. New research shows that the bacteria that live inside our digestive systems could have a large impact on our risk of being obese.

There is a widespread belief, that being overweight or obese is a question of failing willpower, fuelled in no small part by food, fitness and beauty industries. But if we look at the issue of obesity through a scientific spyglass, a very different picture emerges.

Research is increasingly showing that a large part of the tendency to become obese is genetically controlled, often in very subtle ways. Genetic variation could mean that some people are more sensitive to the smell or sight of food, or are less able to sense when they are full. These small variations can play havoc in our modern environment, where calories are readily available and inactive lifestyles are common.

The microbiota, the bacteria that colonise our gutsBut it’s not just our own genes that we should be worried about. In terms of processing food, humans are hardly self-sufficient. Our guts are the home of trillions of bacteria that help to break down foodstuffs that our own cells cannot cope with. Together the genes expressed by these intestinal comrades outnumber our own by thousands of times, and yet we are still largely in the dark what they do.

Over 90% of these bacteria, collectively known as the microbiota, come from just two groups – the Bacteroidetes and the Firmicutes. Now, new research suggests that the proportion of these groups is an important factor in the obesity epidemic.

Mouse experiments are instrumental in understanding the causes of obesity. Ruth Ley, Peter Turnbaugh, Jeffrey Gordon and colleagues at Washington University first noticed the link between the microbiota and obesity by studying a special strain of fat mice.

These mice lack the hormone leptin, which controls the body’s ‘fat thermostat’. Without it, the mice cannot monitor the amount of fat in their body and quickly become obese through overeating. The team noticed that these mice had 50% fewer Bacteroidetes and 50% more Firmicutes in their bowels than their lean counterparts.

They saw the same thing in humans. The relative proportion of Bacteroidetes increased in obese people as they lost weight through low-fat or low-carbohydrate diets, while the Firmicutes became less abundant.

The link between the microbiota and obesity became even clearer when Gordon looked at a special strain of mice with no microbiota of their own. These intestinal tabula rasas proved to be strongly resistant to the fattening effects of unhealthy diets. After eight weeks on a 40% fat diet, these animals put on less than half as much weight as their normal peers, despite eating the same amount of food.

When the team transplanted the microbiota from fat and lean mice into the germ-free strains, those colonised by microbiota from fat donors packed on far more weight than those paired with lean donors.

To find out why the shifting bacterial balances were affecting body weight, Gordon and co. compared the microbiota of fat and lean mice at a genetic level. Samples from fat mice showed much stronger activation of genes that coded for carbohydrate-destroying enzymes, which break down otherwise indigestible starches and sugars. As a result, these mice were extracting more energy from their food than their lean cousins.

The bacteria were also manipulating the animals’ own genes, triggering biochemical pathways that store fats in the liver and muscles, rather than metabolising them. While these effects are relatively small, Gordon believes that they can lead to very large fluctuations in weight, over the course of months or years.

Obviously, the microbiota are not the whole story behind the obesity epidemic. We now need to understand how they interact with other things that affect our risk of becoming obese, not least of all, our own genes.

And there is much we still don’t know about our life-long passenger, such as how they sense and respond to their host’s condition, how they are passed on, or how they are affected by our diet. By answering these questions, scientists could then assess whether actively shifting our bacterial balances could help to stem the worldwide increase in obesity levels.

Backhed, Manchester, Semenkovich & Gordon. 2006. PNAS 104: 979-984.
Ley, Turnbaugh, Klein & Gordon. 2006. Nature 444: 1022-1023. Turnbaugh, Ley, Mahowald, Magrini, Mardis & Gordon. 2006. Nature 444: 1027-1031.

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