Conspiracy theories, TV thrillers and airport novels are full of the idea that the world is secretly run by a hidden society. We have come up with many names for this shadowy cabal of puppet-masters – the Illuminati, the Freemasons, and more. But a better name would be ‘parasites’.
Every animal and plant is afflicted by parasites. The vast majority are simple, degenerate creatures, small in size and limited in intelligence. They affect our health and development, and even our behaviour and culture. And by pulling the strings of key species, parasites can change the face of entire habitats.In a typical school textbook, an ecosystem consists of plants that feed plant-eaters, who in turn, line the bowels of predators. But parasites influence all of these levels, and as such, they can change the structures of entire communities.
The idea that nature is secretly manipulated by these tiny, brainless creatures is unsettling but manipulate us, they do. And by changing the behaviour of their hosts, parasites can change the face of entire habitats. Chelsea Wood and colleagues from Dartmouth College have found compelling evidence for this, by showing that a tiny flatworm can alter the structure of a tidal habitat by infecting small marine snails.
Alzheimer’s disease is the most common form of dementia in the world, affecting more than 26 million people. Creutzfeld-Jacob disease (CJD), another affliction is far less common, but both conditions share many of the same qualities. They are fatal within a few years of diagnosis, they are incurable and they involved the crippling degeneration of the brain’s neurons. Now, a group of Yale researchers have discovered that the two diseases are also linked by a pair of critical proteins.
Look into the brain of someone with Alzheimer’s disease and you will see large, insoluble “plaques” sitting between nerve cells. They consist of a protein fragment (or “peptide”) called amyloid-beta, accumulating in its thousands. These plaques are a hallmark of the disease, but even before they have formed, amyloid-beta peptides have already begun to cluster in small soluble groups. Even at this stage, they can impair memory, degrading the connections between separate neurons.
Juha Lauren wanted to work out how exactly clusters of amyloid-beta wreak havoc in neurons before they form plaques. In particular, he was after the identity of its molecular accomplices. Many proteins work their will in a cell by attaching to other proteins called receptors. To see if amyloid-beta does the same, Lauren’s team went fishing for receptors.
They created a synthetic version of the amyloid-beta peptide and connected it to a molecule called biotin – these were their hooks. Lauren lowered them into a massive pool of different proteins found in the brains of mice; if one of those was a receptor for amyloid-beta, it should take the bait and stick to it. As a rod, he used beads covered in a molecule called avidin, which sticks very strongly to biotin. The beads attracted biotin, which was stuck to amyloid-beta, which was in turn bound to its receptor.
From hundreds of thousands of proteins, their fishing trips pulled out just one that stuck to amyloid-beta, and it’s a familiar one – the prion protein. Incorrectly folded versions of this protein (PrPSC) are the culprits behind diseases like CJD, mad cow disease and scrapie. And now it seems that the normal, correctly folded version (PrPC) plays a role in Alzheimer’s disease too, by acting as the receptor for amyloid-beta. It’s the accomplice through which amyloid-beta clusters work their damaging effects on neurons.
Imagine that a massive hole appeared in a wall of your house, and you’d decided to fix it yourself. You head over to a DIY store and load up on plaster, tools and paint and look forward to many hard and tedious hours of work. If that seems like a chore, you might get some perspective by considering the plight of the gall aphid Nipponaphis monzeni. When holes appear in their homes, some unlucky individuals are tasked with repairing the damage using their own bodily fluids. They sacrifice themselves for the sake of some DIY.
Some species of aphids are heading towards the incredibly cooperative lifestyles of social insects like ants, bees and termites. They live in large hollow growths called galls, that sprout from the very plants whose sap they suck. The galls provide them with protection from predators, shelter from the elements and constant food. They are a precious resource indeed, and every colony of social aphids have a special caste of sterile individuals whose job it is to defend the gall and attack intruders. These are the soldiers.
But in a few species, such as N.monzeni, soldiers have a truly bizarre part-time job- they are suicide-plasterers. When their homes are breached, the soldiers leach their own bodily fluids onto the wounded area, mix it with their legs and plaster it over the hole. The liquids soon harden and within an hour, the gap has been plugged at the cost of the soldiers’ lives.
The aphids’ gall-repairing antics are remarkably similar to what happens when animals develop cuts and wounds. The fluid around the area clots and hardens to form a scab. This provides a temporary seal, that gives the surrounding cells enough time to grow, divide and restore the broken tissues. The exact same thing happens to the gall – the only difference is that its clots and scabs are provided not by the plant, but by the aphids it houses.
In the middle of the Pacific Ocean, Gonzalo Mucientes has discovered an invisible line in the sea that separates male mako sharks from females. The line runs from north to south with the Pitcairn Islands to its west and Easter Island to its east. On the western side, a fisherman that snags a mako will most probably have caught a male. Travel 10 degrees of longitude east and odds are they’d catch a female. This is a shark that takes segregation of the sexes to new heights.
Mucientes and colleagues from Spain, Portugal and the UK spent four months aboard a Spanish longline fishing vessel. Amid more typical catches, the boat often snagged shortfin makos and blue sharks. When they did, the researchers meticulously noted the boat’s position, and analysed the shark carcasses on board.
Their results showed a clear “line in the sea”. All in all, the fishermen captured 264 male makos, mostly towards the west of the line and 132 females predominantly in the east. Makos are found all over the world, but this study shows that at a more regional level, their populations are structured to an astonishing degree.
This segregation is even more surprising when you consider that makos are the world’s fastest sharks. They can clock speeds of up to 45 miles per hour, about eight times as fast as Michael Phelps at his peak. They really shouldn’t have any problems in covering vast tracts of water.
Following last week’s 400th anniversary post, I have another celebratory announcement. A year ago today*, I set foot in ScienceBlogs for the first time.
As previously noted, some things have changed while others are much the same. The posting rate has gone up, and traffic has almost quadrupled from about 4,000 views per week to something like 16,000 now. Nonetheless, I’ve kept to the basic rules – non-sensationalist, considered, writing based on primary sources, for a general audience.
Some thanks are in order. I’m very grateful to the following people:
Some trivia, for anyone who’s interested. In year, I’ve accumulated:
Right now, enough navel-gazing. More news (as in actual science news) this evening, and plenty more to round the week off. Segregated sharks, Alzheimer’s news, child-like voters, moral disgust, unenviable DIY and, if I can help it, some funky gibbons. See you later.
* Well, technically tomorrow, but today’s a slower news day.
In late 2007, seabirds off the coast of California began to die in record numbers. The waterproof nature of their feathers and been wrecked, and they were soaked to the skin. Without an insulating layer of air trapped within their plumage, the damp birds were suffering from extreme cold. These are exactly the type of problems that seabirds face when they blunder into oil spills, but in this case, not a drop of petroleum had entered the water. The problem was a biological one.
At the same time, Monterey Bay in California was plagued by a massive “red tide” – a bloom of microscopic algae called dinoflagellates. These blooms can include millions of cells in just a millilitre of water and some species churn out toxins that kill local wildlife. Sea lions, dolphins, sea otters, manatees, whales and even humans have all succumbed to these poisons, either directly or by eating contaminated food.
David Jessup from the Marine Wildlife Veterinary Care and Research Center found that these algae were the source of the birds’ misfortune, but not because they were secreting toxins. Instead, they produced a foam that was loaded with surfactants – wetting agents. These are the chemicals used in detergents; they lower the surface tension of a liquid and allow it to spread more easily over a surface. This foam was the agent behind the seabirds’ water-logged feathers.
The trauma of child abuse can last a lifetime, leading to a higher risk of anxiety, depression and suicide further down the line. This link seems obvious, but a group of Canadian scientists have found that it has a genetic basis.
By studying the brains of suicide victims, Patrick McGowan from the Douglas Mental Health University Institute, found that child abuse modifies a gene called NR3C1 that affects a person’s ability to deal with stress. The changes it wrought were “epigenetic”, meaning that the gene’s DNA sequence wasn’t altered but it’s structure was modified to make it less active. These types of changes are very long-lasting, which strongly suggests that the trauma of child abuse could be permanently inscribed onto a person’s genes.
Child abuse, from neglect to physical abuse, affects the workings of an important group of organs called the “hypothalamic-pituitary-adrenal axis” or HPA. This trinity consists of the hypothalamus, a funnel-shaped part of the brain; the pituitary gland, which sits beneath it; and the adrenal glands, which sit above the kidneys. All three organs secrete hormones. Through these chemicals, the HPA axis controls our reactions to stressful situations, triggering a number of physiological changes that prime our bodies for action.
The NR3C1 gene is part of this system. It produces a protein called the glucocorticoid receptor, which sticks to cortisol, the so-called “stress hormone”. Cortisol is produced by the adrenal glands in response to stress, and when it latches on to its receptor, it triggers a chain reaction that deactivates the HPA axis. In this way, our body automatically limits its own response to stressful situations.
Without enough glucocorticoid receptors, this self-control goes awry, which means that the HPA is active in normal situations, as well as stressful ones. No surprise then, that some scientists have found a link between low levels of this receptor and schizophrenia, mood disorders and suicide. So, childhood trauma alters the way the body reacts to stress, which affects a person’s risk of suicide or mental disorders later in life. Now, McGowan’s group have revealed part of the genetic (well, epigenetic) basis behind this link.
When people say that every cloud has a silver lining, they probably aren’t thinking about herpes at the time. Herpes may be unpleasant, but the viruses that cause it and related diseases could have a bright side. In mice at least, they provide resistance against bacteria, including the bubonic plague.
Herpes is one of a number of itchy, blistering diseases, caused by the group of viruses aptly-named herpesviruses. Eight members infect humans and cause a range of illnesses including glandular fever, chickenpox, shingles and, of course, herpes itself.
Almost everyone gets infected by one of these eight during their childhood. But herpesviruses are for life, not just for Christmas. After your body fights off the initial infection, the virus retreats into a dormant phase known as ‘latency’. It remains hidden and causes no symptoms, but has the potential to reactivate at a later date. In this way, herpesviruses can seem like life-long parasites, ensuring their own survival at the cost of their host’s future health. In extreme cases, latent viruses can lead to chronic inflammation, which in turn can cause autoimmune diseases, or some types of cancer.
But there is a bright side too. Erik Barton and colleagues from Washington University Medical School found that once infected mice entered the latent stage, they were surprisingly resistant to certain types of bacteria. Unlike their vulnerable uninfected peers, they even managed to ward off the deadly plague bug, Yersinia pestis.