For almost a decade, Jillian Banfield has been travelling to a place that “pushes the limits of human endurance” – Richmond Mine in Northern California. Its abandoned caverns can reach 48 degrees Celsius and 100 per cent humidity. They are low in oxygen. They contain possibly the most acidic naturally occurring water on Earth, with a pH value of -3.6.
But even in these conditions, there is life. Bacteria grow within the cave, floating in thin films on top of its hot, acidic water. They are the lords of their extreme world, and they provide an unrivalled opportunity to study how wild microbes evolve.
Of all the super-senses that animals possess, the ability to sense the Earth’s magnetic field must be the most puzzling. We’ve known that birds can do it since the 1960s, but every new attempt to understand this ability – known as magnetoreception – just seems to complicate matters even further.
Take the latest discovery. Le-Qing Wu and David Dickman from the Baylor College of Medicine have found neurons in a pigeon’s brain that encode the properties of a magnetic field. They buzz in different ways depending on how strong the field is, and which direction it’s pointing in.
This is a big step. Scientists have identified parts of the brain that are important for magnetoreception, but no one has managed to nail down the actual neurons responsible for the sense. Miriam Liedvogel, who studies magnetic senses, calls it “a milestone in the field”. It’s a key puzzle piece that has been unavailable for a very long time.
But Wu and Dickman’s discovery doesn’t solve the magnetoreception puzzle. If anything, it makes it more complex. Until recently, scientists thought that birds had two separate magnetic detectors – one in the eye and one in the beak. And it looks like the new magnetic neurons don’t hook up to either of these. “We can’t say where the signals come from,” says Dickman.
If these neurons are responding to magnetic fields, which part of the bird is feeding them their information? Is there a third sensor?
Here’s the sixth piece from my new BBC column
Every year, millions of people are born with debilitating genetic disorders, a result of inheriting just one faulty gene from their parents. They may have been dealt a dud genetic hand, but they do not have to stick with it. With the power of modern genetics, scientists are developing ways of editing these genetic errors and reversing the course of many hard-to-treat diseases.
These gene therapies exploit the abilities of viruses – biological machines that are already superb at penetrating cells and importing genes. By removing their ability to reproduce, and loading them with the genes of our choice, we can transform viruses from causes of disease into vectors for cures.
After a few shaky starts, some of these approaches are beginning to hit their stride. Thirteen children with SCID, an immune disorder that leaves people fatally vulnerable to infections, now have working immune systems. Several British patients with haemophilia, which prevents their blood from clotting properly, can now produce a clotting protein called factor IX, which they once had to inject. A British man and three Americans with inherited forms of progressive blindness can see again.
It is still early days as far as trumpeting gene therapy cures are concerned, but even if they do succeed there is still one significant limitation that cannot be overlooked. Treating adults and children in this way will do for some disorders, but genetic disorders cause irreparable organ damage, or even death, very early. “With some of the diseases that we look at, five years old is too late. Sometimes, you don’t get to the age of five,” says Simon Waddington from University College London. “Every single one is a little bit niche but when you list them all out, there’s quite a lot of them.”
Around 8 to 10 per cent of your DNA comes from viral ancestors. These sequences are the remains of prehistoric viruses that inserted their DNA into the genes of our ancestors, hundreds of millions of years ago. Some of them became permanent residents, and were passed down from parent to child. These endogenous retroviruses, or ERVs, are a legacy of epidemics past.
We understand how ERVs got into our DNA in the first place. But why have they been such successful invaders, to the point where they fill around a tenth of our genome? Gkikas Magiorkinis from the University of Oxford has an answer. By comparing the ERVs of 38 mammals, from humans to dolphins, he has found that the critical step in these invasions was the moment when the viruses hung up their coats.
Many insects eventually evolve to resist insecticides. This process typically takes many generations and involves tweaks to the insect’s genes. But there is a quicker route. Japanese scientists have found that a bean bug can become instantly resistant to a common insecticide by swallowing the right bacteria.
The bug forms an alliance with Burkholderia bacteria, and can harbour up to 100 million of these microbes in a special organ in its gut (see arrow above). Some strains of Burkholderia can break down the insecticide fenitrothion, detoxifying it into forms that are harmless to insects. In fields where the chemical is sprayed, these pesticide-breaking bacteria rise in number. And if bugs swallow them, they become immune to the otherwise deadly chemical.
I’ve written about this story for The Scientist, so head over there to read the details of the study.
On an uneventful day, five passers-by in busy Oxford shopping street suddenly stop and look upwards. They have spotted a camera mounted on a nearby roof, pointed straight at them. But these aren’t strangers who have suddenly realised that Big Brother is watching them. They are actors, who are taking part in a natural experiment that looks at how information spreads through crowds of people.
Andrew Gallup from Princeton University is behind the camera. Using its lens, and technology based on the video-gaming graphics cards, he can track the movement of each pedestrian, and calculate where they’re looking. With this set-up confirmed that people have a natural tendency to look where others are looking. But this contagion of glancing is much weaker than popular psychology books would have us believe.
The sexual success of the male spotted bowerbird depends on his gardening skills. In his patch of forest, where he displays to mates, he cultivates a small fruiting shrub called the ‘bush tomato’, with purple flowers and green fruit.
It’s not clear if his actions are deliberate or inadvertent, but it is clear that he doesn’t eat the fruit. The plant is there to provide him with decorations, to make his boudoir that much more enticing to a female. Aside from humans, the spotted bowerbird is the only other animal that grows a plant for purposes other than food.
It looked like we had the polar bear’s origin story nailed down. Genetic studies suggested that between 111 and 166 thousand years ago, a group of brown bears, possibly from Ireland, split off from their kin. In a blink of geological time, they adapted to the cold of the Arctic, and became the polar bears we know and worry about. Fossils supported this story: the oldest polar bear bone is between 110 and 130 thousand years old.
But according to Frank Hailer at the Biodiversity and Climate Research Centre in Frankfurt, this story is wrong in two important ways. First, the polar bear aren’t just a branch of the brown bear family tree. They’re a separate lineage in their own right. Second, they around four times older than anyone had thought, arising around 600 thousand years ago.
If this new vision is right, the bear’s journey to polar dominance wasn’t a speedy sprint, but a more leisurely stroll. As a species, polar bears have seen many ice ages. Rather than being a symbol of extraordinarily fast evolution, they’ve actually had plenty of time to adapt to life in the freezer.