If you want to find an ocean animal that kills with speed, don’t look to sharks, swordfishes, or barracuda. Instead, try to find a mantis shrimp. These pugilistic relatives of crabs and lobsters attack other animals by rapidly unfurling a pair of arms held under their heads. One group of them—the smashers—have arms that end in heavily reinforced clubs, which can lash out with a top speed of 23 metres per second (50 miles per hour), and hit like a rifle bullet. These powerful hammers can shatter aquarium glass and crab shells alike.
Most research on mantis shrimps focuses on smashers, but these pugilists are in the minority. The majority are “spearers”, whose arms end in a row of fiendish spikes, rather than hard clubs. While the smashers actively search for prey to beat into submission, the spearers are ambush-hunters. They hide in burrows and wait to impale passing victims. They’re Loki to the smashers’ Thor.
Given their differing lifestyles, you might expect the spearers to be faster than the smashers. They rely on quick strikes to kill their prey, and they target fast victims like fish and shrimp rather than the tank-like, slow-moving crabs favoured by smashers. But surprisingly, Maya DeVries from the University of California, Berkeley, found that the fastest spearer strikes at just a quarter of the speed of the fastest smasher.
Sea snakes have some of the most potent venoms of any snake, but most of the 60 or so species are docile, rare, or sparing with their venom. The beaked sea snake (Enhydrina schistosa) is an exception. It lives throughout Asia and Australasia, has a reputation for being aggressive, and swims in estuaries and lagoons where it often gets entangled in fishing nets. Unwary fishermen get injected with venom that’s more potent than a cobra’s or a rattlesnake’s. It’s perhaps unsurprising that this one species accounts for the vast majority of injuries and deaths from sea snake bites.
But this deadliest of sea snakes has a secret: it’s actually two sea snakes.
By analysing the beaked sea snake’s genes, Kanishka Ukuwela from the University of Adelaide has shown that the Asian individuals belong to a completely different branch of the sea snake family tree than the Australian ones. They are two species, which have evolved to look so identical that until now, everyone thought they were the same. They’re a fantastic new example of convergent evolution, when different species turn up at life’s party wearing the same clothes.
Meet Laurax, a not-very-bold, not-that-exciting new fragrance. According to a panel of sniffers, it’s neither appealing nor revolting. It’s “intermediately pleasant”. People almost trip over themselves to describe it in non-descript terms—“fragrant”, “chemical” and “perfumery”.
Laurax isn’t going to set the perfume world ablaze in the near future, but its scientific implications are fascinating. This bizarre scent is actually a set of completely different fragrances that all smell roughly the same. It’s the odour version of “white”.
The colour that we call white is a blend of many different wavelengths of light. Add red and blue light together, and you get magenta. Add other colours and eventually, you converge on white. The same applies to sounds: if you combine tones of different frequencies, you eventually arrive at a perceptual hum called “white noise”. There’s no fixed formula for making white light or white noise. You don’t need to mix a specific set of colours or frequencies. As long as the individual ingredients are different enough, and roughly equal in intensity, whiteness emerges.
When the fruit bat Pteropus allenorum was finally described by scientists, it was already extinct. One specimen of the bat was shot in Samoa in 1856, skinned, stored in alcohol, and shipped to the United States. It spent the next 153 years, inconspicuous and ignored, on a shelf in the Academy of Natural Sciences in Drexel University. When bat specialist Kristofer Helgen visited the museum, he immediately recognised that it was a new species. Sadly, it was too late. There are no fruit bats in Samoa nowadays, so the jar on the shelf represents our only encounter with this now-extinct animal.
The fruit bat’s story isn’t an original one. The beetle Meligethes salvan was collected from the Italian Alps in 1912 and sat in Frankfurt’s Senckenberg Museum until it was described in 2003. In the intervening time, the valley from which it came had been almost entirely destroyed in the process of building a hydroelectric power plant. Biologists searched in the nearby valleys but couldn’t find it. The beetle may be extinct.
These examples show that the shelves and drawers of the world’s museums are among the planet’s most diverse habitats—ecosystems brimming with different species, many of which have never been seen before.
People often think that discoveries are made when biologists see new species in the field, and immediately recognise them as such. That’s largely not true. Field biologists often collect their specimens en masse, taking them back to their respective institutions, and keeping them in storage until they get a chance to peer at them properly. This means that many of the planet’s new species are sitting pretty in jars and drawers, gathering dust while they wait to be formally described.
How long is this shelf life? For the bat, it was 153 years, and for the beetle, 92. On average, it’s around 21 years, according to a new study from Benoît Fontaine from the Natural History of Museum in Paris.
This post contains material from an older one, updated based on new discoveries.
There are many things you don’t want gathering in large numbers, including locusts, rioters, and brain proteins. Our nerve cells contain many proteins that typically live in solitude, but occasionally gather in their thousands to form large insoluble clumps. These clumps can be disastrous. They can wreck neurons, preventing them from firing normally and eventually killing them.
Such clumps are the hallmarks of many brain diseases. The neurons of Alzheimer’s patients are riddled with tangles of a protein called tau. Those of Parkinson’s patients contain bundles, or fibrils, of another protein called alpha-synuclein. The fibrils gather into even larger clumps called Lewy bodies.
Now, Virginia Lee from the University of Pennsylvania School of Medicine has confirmed that the alpha-synuclein fibrils can spread through the brains of mice. As they spread, they corrupt local proteins and gather them into fresh Lewy bodies, behaving like gangs that travel from town to town, inciting locals into forming their own angry mobs. And as these mobs spread through the mouse brains, they reproduce two of the classic features of Parkinson’s disease: the death of neurons that produce dopamine, and movement problems.
This is the clearest evidence yet that alpha-synuclein can behave like prions, the proteins that cause mad cow disease, scrapie and Creutzfeld-Jacob disease (CJD). Prions are also misshapen proteins that convert the shape of normal peers. But there is a crucial distinction: prions are infectious. They don’t just spread from cell to cell, but from individual to individual. As far as we know, alpha-synuclein can’t do that.
Every time you put on some music or listen to a speaker’s words, you are party to a miracle of biology – the ability to hear. Sounds are just waves of pressure, cascading through sparse molecules of air. Your ears can not only detect these oscillations, but decode them to reveal a Bach sonata, a laughing friend, or a honking car.
This happens in three steps. First: capture. The sound waves pass through the bits of your ear you can actually see, and vibrate a membrane, stretched taut across your ear canal. This is the tympanum, or more evocatively, the eardrum. On the other side, the eardrum connects to three tiny well-named bones—the hammer, anvil and stirrup—which link the air-filled outer ear with the fluid-filled inner ear.
The bones perform the second-step: convert and amplify. They transmit all the pressure from the relatively wide eardrum into the much tinier tip of the stirrup, transforming large but faint air-borne vibrations into small but strong fluid-borne ones.
These vibrations enter the inner ear, which looks like a French whisk poking out of a snail shell. Ignore the whisk for now – the shell is the cochlea, a rolled-up tube that’s filled with fluid and lined with sensitive hair cells. These perform the third step: frequency analysis. Each cell responds to different frequencies, and are neatly aligned so that the low-frequency ones are at one end of the tube and the high-frequency ones at another. They’re like a reverse piano keyboard that senses rather than plays. The signals from these cells are passed to the auditory nerve and decoded in the brain. And voila – we hear something.
All mammal ears work in the same way: capture sound; convert and amplify; and analyse frequencies. But good adaptation are rarely wasted on just one part of the tree of life. Different branches often evolve similar solutions to life’s problems. And that’s why, in the rainforests of South America, a katydid—a relative of crickets—hears using the same three-step method that we use, but with ears that are found on its knees.
I had a delightful time at the SpotOn London 2012 conference this weekend, chatting to people about all things related to science, journalism and the internet. For reasons best known to them, the organisers decided to inflict me upon the attendees in three separate panels, videos of which are below.
This one’s on how to do smart journalism in the face of complex science. I lay out my thoughts on why people often criticise journalists for screwing up science reporting in boring ways, when there are more advanced forms of screw-up to consider and avoid.
This one’s about whether information from organisations like my former employers, Cancer Research UK, will replace traditional journalism. Spoiler: No.
And this one’s about safeguarding against fraud and dodgy practices in science. It touches on all the psychology-related material that I’ve been covering for the last year, and has a rather good discussion.
I’m taking a small break for a couple of days, but in the meantime, here are some links to news pieces I’ve written for The Scientist over the last month or so, which I’ve been a bit remiss in signposting to.
“Humans tend to embrace good news, while discounting bad news. We overestimate our odds of winning the lottery or living long lives, while underplaying our risk of cancer, divorce, or unemployment. Now, researchers from University College London (UCL) have found a way of removing these rose-tinted glasses, by aiming a magnetic field at a brain region called the left inferior frontal gyrus (IFG).”
The majority of the brain doesn’t produce new neurons—we’re born with the set that has to last us throughout our lives. That’s a problem for people with Parkinson’s and other diseases where neurons are destroyed. But one group of scientists has transformed another type of brain cell – pericytes – into neurons, using just two proteins, in laboratory cells and in mice. Other scientists have accomplished the same feat using skin cells, but the resulting neurons would then have to be transplanted. If you can do the same with brain cells, you could potentially create new neurons right there in the brain.
Mosses were some of the earliest land plants, which invaded terra firma half a billion years ago after evolving from green aquatic algae. Were they aided in their invasion by genes borrowed from fungi, bacteria and viruses? A new study certainly thinks so – it documented loads of borrowed genes in the genome of a living moss, which are involved in adaptations for life on land and are shared with other land plants. But many of the people I spoke to for this story were not convinced by the data.
“An international consortium of scientists known as the 1000 Genomes Project has published a long-awaited map of variation in the human genome, cataloging the subtle differences that shape our bodies and influence our risk of disease. The results… were derived from the genome sequences of 1,092 volunteers hailing from 14 populations in Europe, East Asia, Africa, and the Americas. They should help scientists more efficiently hunt for the genetic causes of disease, by comparing mutations in a patient’s genome against those seen in his own country or ethnic group.”
“Scientists at the Texas Biomedical Research Institute (TBRI) have created a fast and efficient way of identifying antibodies that recognize bacterial toxins or viral proteins in a few days, using simple equipment found in most facilities around the world.” It’s billed as a way of quickly and efficiently developing tests for potential bioterror agents, but could be a valuable tool for a lot of basic research.