Features

Why is the sky blue? It's a simple question but one with a surprisingly complex answer if the sky belongs to a planet outside our solar system.

'If you are on Earth looking up the sky looks blue because other wavelengths of light are scattered by molecules like oxygen and nitrogen in the atmosphere,' explains Tom Evans of Oxford University's Department of Physics. 'If you look at the Earth from space it appears (mostly) blue both because of this effect and because water in oceans and lakes absorb other wavelengths, only reflecting blue light back into space.'

So viewed through an astronomer's eyes colour is much more than a pretty effect: it's an invaluable source of information.

Now, for the first time, scientists have determined the colour of a planet outside our solar system (an 'exoplanet'). Because they are so distant, and so much smaller than stars, seeing exoplanets directly with current telescopes is normally impossible (most of what we know about them comes from indirect observations, for instance of nearby stars).

An international team, led by researchers from Oxford University and Exeter University, took advantage of a secondary eclipse, when a planet disappears behind its star. They used the Hubble Space Telescope to study the moment the exoplanet 'HD 189733b' passed behind its parent star so that they saw both the star's light and light reflected off the planet (its 'albedo') and then, once HD 189733b has disappeared, just the star's light on its own.

From the difference in brightness between these two observations they were able to infer HD 189733b's brightness and by examining the wavelength of light reflected off it they were able to determine that it would appear a deep cobalt blue to our eyes.

But HD 189733b, which is 63 light-years away, isn't blue because it is like Earth.

'It's very different from the planets in our solar system,' Tom Evans, first author of a report of the research in Astrophysical Journal Letters, tells me. 'Unlike Jupiter or Saturn this gas giant orbits very close to its star, so it's bombarded with massive amounts of radiation and its atmosphere can reach a temperature of over 1000 degrees Celsius. The planet is also tidally locked so that one side is permanently facing its star whilst the other side is in eternal shadow.'

Suzanne Aigrain of Oxford University's Department of Physics, also an author of the report, comments: 'Despite these differences the laws of physics are the same, and as every planet with an atmosphere in our solar system has clouds we can infer that HD 189733b has clouds. We suspect that these clouds are made of silicate particles, but we don't know how and where they are formed, and the fact that they could be moving at very high speed (with winds of up to 7000 kilometres per hour) makes observations very difficult.'

The researchers believe that a large part of HD 189733b's blue appearance is down to sodium atoms in its atmosphere, as sodium atoms absorb more light at red wavelengths. 'If it wasn't for sodium absorbing the redder wavelengths, the planet would probably be more of a white colour,' Tom explains.

'This planet has been studied well in the past, both by ourselves and other teams,' says Frédéric Pont of the University of Exeter, leader of the Hubble observing programme and an author of this new paper. 'But measuring its colour is a real first — we can actually imagine what this planet would look like if we were able to look at it directly.'

HD 189733b's system is one of the best studied of all exoplanet systems because its star is bright and close to its planets, making interactions easier to spot. 'It's one of the most favourable systems, there aren't many where we can do the same thing,' comments Suzanne. But its parent star does pose some problems; it's an orange dwarf (or 'K-dwarf'), around four-fifths the size of our Sun, that's very magnetically active so it regularly shoots out flares and star spots that can interfere with observations.

'One of the next questions to answer is just how much of the parent star's light HD189733b is absorbing, because the wavelengths we've measured only account for about 20 per cent of the starlight that falls upon the planet,' Tom adds.

Determining exactly how much energy is being fed into its climate system overall has important implications for the circulation and weather on the planet. To do this, the astronomers will need to extend the measurement at longer wavelengths. This will allow them to confirm that none of the red or near-infrared light can escape from the atmosphere, as they currently suspect.

Other members of the Oxford team, along with collaborators at Bern University, will now begin to feed all the data from the recent observations into a model of the planet's atmosphere. 'A lot of what we do draws on models produced using data from gas giants in our own solar system. These enable us to make some basic predictions, although we know that if we push these models to extremes some of these assumptions break down,' Suzanne tells me.

'We would also like to do similar measurements for other planets, to understand how pervasive clouds are in these 'hot Jupiter' planets,' she adds. 'Currently Hubble is the only telescope we can do this with, and it's not clear how many planets we can do it for (HD189733b is one of the most favourable targets). But in the future we may develop clever techniques that enable us to do some of this from the ground, though it's harder because the Earth's atmosphere gets in the way.'

The hope is that with new, more powerful instruments like the James Webb telescope and especially the proposed European space mission EChO we might be able to get an even better glimpse of the atmospheres (and colours) of this and other exoplanets.

It's not an easy task to stand on top of a box on London's busy Southbank and try to entertain everyone and anyone in the passing crowds of tourists, school pupils, city workers and arts lovers. Even if you are a stand-up comedian, performance artist, or street entertainer, it would probably still be many people's idea of a tough gig.

Standing on that box and engaging people in the latest scientific research surely makes it even harder. Yet it doesn't appear to phase Dr Ravinder Kanda. Ravinder is a research associate in paleovirology and genomics in the Department of Zoology at Oxford University, and she is one of 12 scientists taking part in Soapbox Science on Friday July 5.

The event, supported by L'Oreal UNESCO For Women In Science Scheme, is now in its third year and gets some of the UK's leading female scientists to talk passionately about their subjects to the general public. Its aim is to help eliminate gender inequality in science by raising the profile, and challenging the public's view, of women and science.

OxSciBlog caught up with Ravinder to learn more about her research and what she'd be talking about to all comers from the top of her soapbox on the South Bank.

You also can read an interview with Ravinder about her research and her career in a blogpost on the Soapbox Science website.

OxSciBlog: What are endogenous retroviruses and why are they so interesting?
Ravinder Kanda: Only 2% of our DNA is used to build our bodies. The rest of it – noncoding DNA – is a mixture of old genes that have lost their function, repetitive strings of DNA whose function is not understood, and other elements. Endogenous retroviruses (ERVs) are a kind of noncoding DNA that make up 8% of our DNA. ERVs are all descended from viruses, very like those that cause disease, like HIV, which managed to insert themselves into our ancestors' DNA in the distant past.

OSB: When and how do we think ERVs got incorporated into our DNA?
RK: The way this particular group of viruses, called retroviruses, infect a cell involves inserting themselves into the DNA of the cell – they become part of our DNA. Once inside the DNA of a cell, new copies of the retrovirus can be produced using the cell's machinery. These new copies can then leave the cell and go on to infect other cells. Occasionally, a retrovirus will infect the germ-line cells – the cells that produce sperm and eggs. In this instance, the virus is now part of the DNA of that sperm or egg cell. When fertilisation occurs, this one cell divides to become two. Both cells now contain a copy of the virus. Two cells go on to make four – all have the viral DNA too. When that fertilised egg develops into an adult, every single cell in that individual's body contains the viral DNA. When this happens this virus is known as an endogenous retrovirus, meaning it is within our DNA. It is inherited by all the offspring of that individual.

There are around 100,000 copies of these ERVs in our genome. By comparing the DNA of other primates and mammals, we can estimate how long ago these ERVs inserted into the DNA of our ancestors. For example, it is estimated that the common ancestor of our closest relative, the chimpanzee, and modern day humans existed approximately 8 million years ago. If a particular ERV is present in the DNA of both humans and chimpanzees, we can say that it must have inserted into the DNA of our ancestor more than 8 million years ago. We can then look at the next closest relative, the gorilla, and see if the ERV is present in their DNA. If it is present in the the gorilla, the common ancestor of humans, chimpanzees and gorillas is thought to have existed around 15 million years ago and so we can say that the ERV inserted into the DNA of our ancestors 15 million years ago. Some of the ERV insertions are ancient, dating back 100 million years.

OSB: How might these 'DNA invaders' be good for us?
RK: In some instances, we have managed to 'borrow' some of the viral genes and use them for our benefit. The most famous example is a gene that is involved in pregnancy, specifically with the formation of the placenta. This gene comes from a virus and is essential for the formation of the placenta. Without it we would not be able to reproduce as we do. In other species, there are instances where having a particular ERV gives you some protection against infection from other related retroviruses. For example, sheep have a particular ERV that can block the receptors of a cell, preventing entry into the cell and therefore infection by other related viruses.

OSB: What can ERVs reveal about the evolution of infections in animals and humans?
RK: Many ERVs in our DNA are ancient, indicating that this invasion has been occurring for millions of years. By comparing those viruses that are present in DNA to viruses that currently infect and cause disease, we can see that some of these viruses are very good at making a leap and infecting different species to those in which they were originally found, something called cross-species transmission. For example, we know that HIV was a virus that originally infected primates. The subgroup of viruses to which HIV belongs – lentiviruses – has recently been discovered in the DNA of other species. These discoveries challenge our understanding of how these viruses might change and evolve.

OSB: What further research is needed to understand more about ERVs?
RK: Lots! We are only just beginning to understand what an influential role viruses may have played in many various aspects of the evolution of a species. One consideration is that some viruses can make the leap to infect other species, such as HIV. A better understanding of cross-species transmission, why or how this occurs, and why some viruses are better at doing this than others, may also help us identify potential 'hotspots' of infection. This could allow us to be better prepared against possible future threats.

For me personally, I am interested in the role that ERVs play with regards to offering immunity against infection from other viruses. The idea of using viruses against themselves is an interesting one. However, we need a better understanding of exactly how this occurs. We still have a long way to go.

A new tag-team approach to combating a type of skin cancer is showing early promise in the lab. The scientists in Oxford and Spain investigated a two-drug combination to better target cancer cells in melanoma.

The approach uses one drug to drive melanoma cancer cells that are invasive to become sensitive to a second drug. This second drug is a new compound that is activated very specifically in melanoma cells and not other cells in the body.

'Importantly, because the new drug is only activated in melanoma cells, there should be no side effects,' says Professor Colin Goding from the Ludwig Institute for Cancer Research at the University of Oxford.

The first drug, methotrexate, is an existing one that is currently used for diseases such as arthritis and psoriasis. The researchers found that methotrexate stops melanoma cells spreading to other parts or the body, and also sensitises the cells to the second drug, a new compound called TMECG, which kills the cancer cells.

When given alone, neither drug has any effect. But together, the researchers show that the two drugs kill melanoma cells very effectively in the laboratory and also in animal models – including cancer cells that are resistant to current therapies.

The research team – jointly led by Professor Goding and Professor José Neptuno Rodriguez-López from the University of Murcia in Spain – have shown the potential of the technique in human cells in the lab and in mice. They have published their findings in the journal Cancer Cell.

'The work is still at an early stage,' cautions Professor Goding. 'Although this combination treatment works very effectively in animals, we still need to improve the stability of the new drug in the blood to make it effective in patients. We also need to check that there is no toxicity associated with the new drug, though our preliminary results look very good.'

The researchers believe that it will be combinations of treatment approaches like this one that will help floor cancer, and deal with the great problem of tumours acquiring resistance to cancer therapies.

'The major problem with cancers is their capacity to become resistant to therapy and to spread to many parts of the body,' explains Professor Goding. 'Resistance is caused by there being different kinds of cancers cells within tumours, some of which may be resistant to therapy.'

Melanoma is a rare and serious type of cancer that begins in the skin and can spread to other organs in the body. The most common sign of melanoma is the appearance of a new mole or a change in an existing mole. Melanoma caught early can be treated very effectively by surgery. But unfortunately there is no long-term effective therapy once the disease has spread.

'There is a new drug called vemurafenib that gives a good response for the 50% of patients whose cancers have a mutation in the BRAF gene, but resistance occurs within some months,' says Professor Goding. 'Chemotherapy is largely ineffective, and though there is some success with a new form of immunotherapy, this is still at a very early stage.'

He outlines how cancers like melanoma may need to be treated in future: 'We envisage that treating cancer must be done using combinations of therapies that work by completely different mechanisms, such that cells resistant to one therapy would be sensitive to the other.

'We may need to give these combinations sequentially or in combination. So, if therapy A kills the vast majority of cancer cells there will be only few left that are resistant to therapy A, but should still be sensitive to therapy B. Since after therapy A there are few cells that survive, there is much less chance of resistance to therapy B occurring.

'In other words to treat cancer successfully we may need to think about the way we treat a bacterial infection, with combinations of antibiotics. Combinations of anti-cancer therapies may have much more success than giving one treatment alone.'

The researchers hope that the new strategy they have identified will form one treatment approach that, in combination with others, may contribute to a successful anti-melanoma therapy that is effective in the long-term.

Once upon a time all cells were solitary, going about the everyday business of life on their own.

Then, perhaps as many as 25 times in the history of life, some cells tried something different: banding together into groups. A few of these attempts gave rise to groups of cells that worked together rather like bees in a beehive, eventually resulting in the trillions-strong communities of cells that make up complex multicellular organisms like us.

So how did cells learn to stop 'being selfish' and embrace the multicellular lifestyle? In this week's Current Biology a team from Oxford University and Lund University report research using data from 168 species to examine the role genetic relatedness may have played in this transition, I asked team member Roberta Fisher of Oxford's Department of Zoology about this work…

OxSciBlog: How do we think cells made the leap to multicellular life?
Roberta Fisher: Multicellularity has evolved many times, and so it's likely that lots of different factors have favoured single cells becoming multicellular. It's thought that clumping together as a defence mechanism against predation may have favoured multicellularity in the green algae. There are also several species where multicellular behaviours help dispersal and reproduction, e.g. slime moulds.

OSB: Why is understanding genetic relatedness key to understanding this leap?
RF: We know that relatedness is important for social behaviours (you're more likely to help your relatives than a stranger), and multicellularity is essentially a social behaviour. Cells are joining together and interacting, much like bees in a hive or ants in a colony. So, we expect that genetic relatedness will be key in determining when multicellularity can evolve.

OSB: How did you investigate the role of relatedness in this process?
RF: The way multicellular groups form is key in determining whether cells will be highly related or not. If groups form by cell division, then the cells will be clonally related, whereas if groups form by aggregation then the cells will be less related. So, we don't directly measure relatedness, but look at how the multicellular groups form. And, luckily, multicellular organisms do tend to fall into the broad categories of ones that form via cell division (like us!) and ones that form by aggregation (like slime moulds).

OSB: What did you discover about how sterile/different 'castes' of cell might arise?
RF: Sterile cells are behaving altruistically, because they are giving up reproduction in order to help other cells. We found that sterile castes are much more likely to arise when cells are highly related. This is somewhat expected, because we know from theory and experimental work that altruistic behaviour is much more likely to evolve when you have high relatedness, but it has not been examined in this context before.

OSB: What does this tell us about the evolutionary costs/benefits of single cells teaming up?
RF: The benefits and costs of teaming up will vary from species to species. For some, there may only be a benefit of being multicellular for certain parts of the life-cycle and so the major transition to multicellularity is never made, because there are still big benefits to being unicellular. However, if the costs of being multicellular are low enough and benefits big enough, then cells can be selected to team up and help each other out.

OSB: How could your study guide further research in this area?
RF: Our study is the first of its kind looking at such a broad scale comparison of lots of different multicellular organisms. I think that other interesting evolutionary questions could be answered using this kind of comparative data.

A report of the research, entitled 'Group Formation, Relatedness, and the Evolution of Multicellularity', is published in Current Biology.

With batteries still struggling to pack the same power as petrol one of the great challenges for electric vehicles is extending their range.

A team led by researchers at Oxford University's Department of Engineering Science and The Oxford Martin School has been pushing the boundaries of what such machines can do with their prototype electric vehicle PEGGIE.

The PEGGIE crew had a successful debut at last year's Shell Eco-marathon Europe competition, a showcase for ultra energy-efficient vehicles built by student teams, and entered this year's event in Rotterdam on 19 May.

The Oxford team won the Technical Innovation Award ahead of nearly 200 other teams from across Europe for a series of innovations:

This year the car sported a photovoltaic array of 130 individual cells which continually reconfigure themselves for maximum efficiency, improving efficiency by over 5%: the team compare it to getting rid of your car's gearbox and instead having an engine that continually rebuilds itself so that its performance is optimised for the vehicle's speed and torque requirements at all times.

Not only does PEGGIE's design enable regenerative braking – recovering energy during braking – and free-wheeling but it also features a 'smart' clutch that electronically synchronises the speed and position of the clutch teeth and controls how they engage. Because this design minimises the forces at work inside the clutch the entire drivetrain can be built from smaller and lighter teeth, gears, and actuators.

To help the driver adopt the most efficient driving style possible she gets a handy Android app to refer to on a mobile handset attached to the controls. The app delivers a colourful map plotting torque along one axis and speed along another – rather like playing a computer game the aim is to drive keeping the crosshairs in the map's 'green zone' which indicates the most efficient style.

The Oxford team also improved PEGGIE's range by over 50% on last year, delivering a performance of 564 km/kWh (the equivalent of Oxford to Minsk on a pint of petrol) coming seventh in the solar electric class, an improvement on last year's twelfth place.

'The Shell Eco-Marathon was a fantastic, if at times traumatic, experience,' said Pete Armstrong, Team Technical Manager. 'It was an honour to be awarded the technical innovation prize, we were very impressed by other vehicles who had developed a range of exciting ideas and techniques in areas such as real-time throttle control and 3D printed components that could be swapped out quickly.

'We owe our result this year to the inspiration drawn from other teams when we debuted last year. Although there is a very competitive atmosphere, the overriding experience is one where hundreds of teams help each other out in the face of all the inevitable challenges that arise, exchange ideas and try to have fun in the process.'

If you are interested in getting involved in the PEGGIE team email [email protected] For sponsorship opportunities email [email protected]