Our body is home to a hundred trillion bacteria. There are ten of them for every one of our own cells. These residents, collectively known as the microbiome, are found throughout our bodies but the biggest populations live in our guts. They act like a hidden organ, which manufactures nutrients that we cannot produce, harvests energy from our food, and suppresses the growth of harmful bacteria that would make us ill. They are more than just passengers – they are our partners in life.
But they can be turned against us. Two new studies in mice have found that viruses can exploit gut bacteria to gain a foothold in our bodies and evade our immune systems. Our microscopic allies can turn into unwitting collaborators for dangerous infections.
When playing in an orchestra, timing is everything. Musicians take their cues from the conductor, and if any individual plays to her own rhythm, she could ruin the whole symphony. The same is true for our bodies.
We run on an internal daily cycle known as a body clock, or more formally a circadian rhythm. It affects everything from our body temperature to our hormone levels to how sleepy we feel. While we speak about a body clock as if it was a single thing, in fact, every one of our cells has its own clock. They are all set by the cyclical activity of certain ‘clock genes’. Trillions of these peripheral clocks tick away inside us. For example, those in blood vessels might control how our blood pressure or rate of blood flow rise and fall throughout the day.
These peripheral clocks get their timings from a master clock, which sits in a part of the brain called the suprachiasmatic nucleus, or SCN. It’s the conductor of the orchestra, synchronising the rhythms of the rest of the ensemble. If you get rid of the SCN, the rest of the clocks lose their rhythm. If you isolate the SCN, it will carry on ticking indefinitely; if you isolate other cells, their clocks eventually die away.
But Bo Cheng from Georges Health Science University has found that the peripheral clocks have more influence than we suspected. When he transplanted the arteries from a mouse with a deficient body clock into a normal animal, they developed arteriosclerosis, a disease where the blood vessels thicken and stiffen. Even though the conductor was giving the right rhythm, the musicians in the arterial section ignored his instructions and did their own thing, with disastrous results.
Two mice run headfirst into one another in a narrow plastic tube that isn’t wide enough for both of them. One of them must give way. In their earlier encounter, the first mouse exerted its dominance by forcing its rival to reverse down the tube. This time, things are different; the second mouse pulls rank and the first one backs down.
Mouse hierarchies don’t change this readily, but the second mouse has been given a boon by Fei Wang at the Chinese Academy of Science. By injecting a single gene into one part of its brain, Wang turned the subordinate animal into a dominant one.
Pop a “miracle berry” into your mouth, and you might wonder if it was named by an overreaching marketing department. The small red fruit tastes of very little – it has a “mildly sweet tang… [like] a less flavorful cranberry”. But it’s not the taste of the fruit itself that matters. To understand why the berry gets its name, you need to eat something acidic. The berries have the ability to make sour foods taste deliciously sweet. Munch one, and you can swig vinegar like it was a milkshake, or bite lemons as if they were candy.
The secret to the fruit’s taste-transforming powers is a protein called miraculin. Now, Ayako Koizumi from the University of Tokyo has discovered just how the protein acts upon our tongues.
When scientists struggle with a problem for over a decade, few of them think, “I know! I’ll ask computer gamers to help.” That, however, is exactly what Firas Khatib from the University of Washington did. The result: he and his legion of gaming co-authors have cracked a longstanding problem in AIDS research that scientists have puzzled over for years. It took them three weeks.
Khatib’s recruits played Foldit, a programme that reframes fiendish scientific challenges as a competitive multiplayer computer game. It taps into the collective problem-solving skills of tens of thousands of people, most of whom have little or no background in science. Here’s what I wrote about Foldit last year:
Imagine trying to photocopy a pile of papers, only for one of the copied sheets to magically jump back into the queue. It gets duplicated again. When the photocopier is finished, you’re left with two sets of papers and three copies of the mysteriously mobile sheet.
The same thing happens in the cells of a fly. Every time a cell divides, it duplicates its entire genome so the two daughter cells each have a copy. But some genes aren’t content to be duplicated just once. A selfish gene called a P-element has the ability to jump around its native genome. Like the paper jumping back into the photocopier queue, the P-element lands in parts of the fly genome that haven’t been copied yet. This ability allows it to spread throughout a genome, and even around the world.
It is easy enough to make software do what you want it to. You could tell your email client to recognise and immediately delete any unwanted messages – say, any from your mother-in-law that contain the word “visit”, but not the word “cake”. Now, Zhen Xie from Harvard University and MIT has found a way of filtering undesirable human cells – in this case, a specific type of cancer cell – with similar ease.
Xie has developed a genetic “logic circuit” that prompts cells to kill themselves if the levels of five molecules match those of a cancer cell. Yaakov Benenson, who led the study, says, “In the long term, the circuits’ role is to act like miniature surgeons that can identify and destroy cancer cells.” That is a very long way off, but the study is a promising step in the right direction.
Stem cells are bursting with potential. They can produce every type of cell in the human body. Small clumps of them can generate entire individuals. But this ability, known as pluripotency, is hard won. So stem cells must constantly repress genetic programmes that threaten to send them down specific routes, and rob them of their limitless potential. “Imagine you’re a stem cell,” says Mitchell Guttman from the Broad Institute of MIT and Harvard. “The worst thing that could happen is that you accidentally turn on, say, neural genes and become a brain cell.”
Now, Guttman has found that stem cells keep themselves ‘stemmy’ with a group of genes called lincRNAs. His discovery not only assigns an important role to these mysterious genes, it opens up a new potential way of precisely controlling what goes on inside a cell.
Many mental disorders can disrupt the sweet embrace of a long, continuous sleep, including alcoholism, depression, Alzheimer’s and parenthood. And that’s bad news. We know that a good night’s sleep helps to solidify our memories of the previous day’s experiences. And according to a new study, we need a certain amount of continuous sleep for those benefits to kick in.
From an evolutionary point of view, it seems strange that we sleep for hours on end. Rather than leaving ourselves unresponsive and vulnerable for large chunks of time, why not simply sleep over several shorter fragments?
This is not an easy question to answer. Until recently, it has been all but impossible to break up the continuity of sleep without also affecting its quality, or stressing out the animals in question. But Luis de Lecea from Stanford University has found a way. He has engineered mice with in-built silent alarm clocks. These animals can be woken up at will with a pulse of light delivered directly to their brains.
Erez Lieberman Aiden is a talkative witty fellow, who will bend your ear on any number of intellectual topics. Just don’t ask him what he does. “This is actually the most difficult question that I run into on a regular basis,” he says. “I really don’t have anything for that.”
It is easy to understand why. Aiden is a scientist, yes, but while most of his peers stay within a specific field – say, neuroscience or genetics – Aiden crosses them with almost casual abandon. His research has taken him across molecular biology, linguistics, physics, engineering and mathematics. He was the man behind last year’s “culturomics” study, where he looked at the evolution of human culture through the lens of four per cent of all the books ever published. Before that, he solved the three-dimensional structure of the human genome, studied the mathematics of verbs, and invented an insole called the iShoe that can diagnose balance problems in elderly people. “I guess I just view myself as a scientist,” he says.
His approach stands in stark contrast to the standard scientific career: find an area of interest and become increasingly knowledgeable about it. Instead of branching out from a central speciality, Aiden is interested in ‘interdisciplinary’ problems that cross the boundaries of different disciplines. His approach is nomadic. He moves about, searching for ideas that will pique his curiosity, extend his horizons, and hopefully make a big impact. “I don’t view myself as a practitioner of a particular skill or method,” he tells me. “I’m constantly looking at what’s the most interesting problem that I could possibly work on. I really try to figure out what sort of scientist I need to be in order to solve the problem I’m interested in solving.”
It’s a philosophy that has paid dividends. At just 31 years of age, Aiden has a joint lab at MIT and Harvard. In 2010, he won the prestigious $30,000 MIT-Lemenson prize, awarded to people who show “exceptional innovation and a portfolio of inventiveness”. He has seven publications to his name, six of which appeared the world’s top two journals – Nature and Science. His friend and colleague Jean-Baptiste Michel says, “He’s truly one of a kind. I just wonder about what discipline he will get a Nobel Prize in!”