It looks like a win-win scenario. An Indian tree helps ants live in its branches in return for the protection the insects offer against grazing animals by patrolling the tree and . The trouble is, ants and worms that provide no protection also move in. But that might not be bad news for the tree after all.

and her team at the Indian Institute of Science in Bangalore fed an amino acid containing a heavy isotope of nitrogen to protective and to another, non-protective, species that lives in the tree. Later, they found traces of the isotope in the tree’s tissue, suggesting that both sets of ants benefit the tree by feeding it.

It is an excellent study, says at the French National Centre for Scientific Research in Montpellier. “Plant benefits from symbiosis with ants were thought to be mostly based on the protection against herbivores – but studies now suggest that plants also get nutrients from the activity of their symbionts,” he says.

Chanam’s team speculates that invertebrates were energy providers for the tree before the relationship developed to include the protection the ants offer.

“This helps us to resolve the classic conundrum of how co-operation can persist in the face of exploitation,” says at the University of Arizona in Tucson. “The apparent exploiters may be subtly benefiting their partners.”

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Imagine if we could turn back time. A team that has identified a new way in which cells age has also reversed the process in old mice whose bodies appear younger in several ways. The discovery has implications for understanding age-related diseases including cancers, neurodegenerative disorders and diabetes.

One way all mammalian cells produce energy is via aerobic respiration, in which large molecules are broken down into smaller ones, releasing energy in the process. This mainly occurs in the mitochondria – the “powerhouses” of cells. Mitochondria carry their own genomes, but some of the cellular components needed for respiration are produced partly by the nucleus, so the two must coordinate their activities.

As we age, mitochondrial function declines, which can lead to conditions such as Alzheimer’s disease and diabetes. To investigate why this decline occurs, at Harvard Medical School and her colleagues compared the levels of messenger RNA (mRNA) – molecules that convey genetic information around a cell – for the cellular components needed for respiration in the skeletal muscle of 6 and 22-month-old mice.

They found that the level of the mRNA in the nucleus did not change much between the young and old mice, whereas those from the mitochondria appeared to decline with age.

Similar changes were seen in mice that lacked a protein called SIRT1 – high levels of which are associated with calorie restriction and an increased lifespan. These mice also had higher levels of a protein produced by the nucleus called hypoxia inducible factor (HIF-1α).

What was going on? It appears that communication between the nucleus and the mitochondria depends on a cascade of events involving HIF-1α and SIRT1. As long as SIRT1 levels remain high and the two genomes communicate well, ageing is kept at bay. But another molecule called NAD+ keeps SIRT1 on the job; crucially, the amount of NAD+ present in the cell declines with age, though no one knows why, leading to a breakdown in communication.

Turning back time

The team wondered if this aspect of ageing could be reversed by increasing the amount of SIRT1 in the cells. To find out if that was possible, they injected 22-month-old mice twice daily for a week with nicotinamide mono nucleotide (NMN) – a molecule known to increase levels of NAD.

At the end of the week, markers of muscular atrophy and inflammation had dropped and the mice had even developed a different muscle type more common in younger mice. Together, these features were characteristic of 6-month-old mice.

“We found that modulating this pathway can improve mitochondrial function and age-associated pathologies in old mice, and therefore it gives a new pathway to target that can reverse some aspects of ageing,” says Gomes.

“This paper clearly demonstrates that NAD+ production is a sort of ‘Achilles’ heel’, [a lack of which] significantly contributes to ageing, and also that this problem can be ameliorated by boosting NAD+ production with key intermediates, such as NMN,” says , at Washington University School of Medicine in St Louis, Missouri.

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From cow burps to tree hiccups and melting permafrost, the potent greenhouse gas methane is produced in myriad ways. Now we can add another one to the list: electricity-generating microbes. The finding could one day allow us to control the generation of methane.

Methanosaeta microbes are one of the biggest natural producers of methane. They live in waste water and wetlands and were thought to break down acetate supplied by other nearby microbes, releasing methane and carbon dioxide in the process.

One of the neighbours of these Methanosaeta microbes, Geobacter bacteria, have a talent of their own. These bacteria shuttle electrons between one another using threadlike projections called pili.

Because species of these two genuses often colonise the same habitats, at the University of Massachusetts, Amherst, wondered whether the Geobacter species might also be providing electrons to the Methanosaeta.

To find out, her team cultured strains of both together. They found that methane production stopped when the Geobacter species was genetically engineered to prevent it from producing the conducting pili.

Carbon diet

This suggests that Methanosaeta microbes are taking electrons from the Geobacter species. To see what they do with them the team exposed the cultured strains to a source of carbon dioxide in which the carbon atoms were swapped with a different carbon isotope. This enabled the team to track the carbon atoms as they were shuttled from carbon dioxide to the newly formed methane.

Because the Methanosaeta microbes have genes that allow them to reduce carbon dioxide, together the results suggest that the microbes are using the electrons to reduce the carbon dioxide in the atmosphere to methane, via a process known as direct interspecies electron transfer (DIET).

This doesn’t rule out the acetate generation, but it suggests that DIET is the dominant process in waste water.

If the finding can be replicated in water from , it might mean that electron transfer could well be the largest mode of natural methane generation, says Rotaru.

She says the new finding could give us the power to control the generation of this source of methane at the flick of a switch. Interrupt the electrical connection between the microbes to turn off production in wetlands where it contributes to global warming; re-establish it whenever we wish to convert waste biomass to natural gas.

Once the process is better studied, she adds, climate models built assuming other modes of methane generation may have to be re-evaluated.

Journal reference: Energy and Environmental Science, DOI:

When you pay with cash, it’s likely you’re giving the cashier more than money. Bills and coins can spread bacteria – and the currency you use appears to play a major role.

Habip Gedik at the Okmeydani Training and Research Hospital in Istanbul, Turkey, and his colleagues in the Netherlands investigated how well bacteria survived on seven currencies: the euro, US dollar, Canadian dollar, Moroccan dirham, Croatian kuna, Romanian leu and Indian rupee.

The team sterilised banknotes of each currency before coating them with one of three types of bacteria: MRSA, VRE – another antibiotic-resistant bug that can cause hospital infections – or E.coli.

None of the bacteria survived for longer than 3 hours on the kuna. But the leu provided a happy home for all three species for at least 6 hours, and MRSA was detectable on it 24 hours later. No species survived for a day on any of the other currencies.

The team also studied to what extent the euro, leu and US dollar could spread E.coli or Staphylococcus aureus onto people’s skin. They made volunteers with clean hands rub contaminated bills for 30 seconds and then tested their fingers for bugs. People who handled euros coated in E.coli were bacteria-free, but those who handled the leu got both types of bacteria on their skin. People who handled US dollars laced with S. Aureus also got the bug on their fingers.

The leu is made of polymer fibres. Polymer banknotes last longer and are harder to counterfeit than traditional cotton-fibre ones, and the Bank of England announced this week that these wipe-clean notes could be introduced from 2016, following the example of countries such as New Zealand and Canada. The notes will be introduced only after a public consultation, although the Bank of England appears convinced of their benefits.

However, the study by Gedik and colleagues shows that plastic notes do appear to provide the best conditions for bacteria to survive and get passed on to others. The researchers think that these notes could help spread bacterial infections.

“I was amazed to see that some currencies act like breeding grounds for bacteria while others seem to be auto-sterilised,” says team member of Radboud University Nijmegen in the Netherlands.

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The usual way to treat brain infections is to give a high dose of antibiotics. That ensures enough of the drug gets across the blood-brain barrier, but it also raises the risk of side effects. What if a lower dose could be delivered directly to the brain?

A team led by of Chang Gung University in Taiwan tried lacing a polymer film with an antibiotic. They then implanted the film over the surface of healthy rats’ brains and monitored the uptake of the drug. All the antibiotic was absorbed after eight weeks, with no side effects.

The film dissolves in the process, so any recipient will not need additional surgery to remove it ().

This article appeared in print under the headline “Brain wrap wards off infection”