October 10, 2012 § Leave a comment
Flowers might look all pretty and innocent to you and I, but deep down, they’re exploitative little bastards and masters of deceit.
Consider this: at the very least, most flowers will use their nectars and colors to bribe birds and insects into handling their pollinating needs, and more than a few don’t stop there. Serapias orchids and certain irises, for instance, often use their petals to offer deep tunnels and dark colors for their foot soldier bees to rest in overnight or during bad weather—shelter mimicking, it’s called. Craftier yet, Ophrys orchids famously imitate insect shapes (usually bees) and scents to lure lonely male bees onto their petals for a round of faux-sex for the bee and real pollination for the flower.
Now traditionally, three basic premises have shaped researchers’ concept of floral deception. First, only orchids engage in sexual deception. Second, sexual deception and shelter mimicking strategies are mutually exclusive among genera: an iris or a Serapias orchid might offer a bee a place to nap, but would never try to tempt it with its wiles, and vice versa in Ophrys orchids. Third, once a flower species has specialized itself to the point of sexual deceit — a strategy so refined it targets only one gender of a single species of a given pollinator — there’s no real going back. Evolution’s not a two-way street.
September 22, 2012 § Leave a comment
Picture yourself in the place of one of southern Australia’s many walking insects—say, a springtail or an ant. You’re making your way along the urbanized bushland of Adelaide, when out of nowhere, you’re thrown into the air, zipping up and over into a sticky nest of plant tentacles that promptly stir to life and begin to inexorably stuff you into a botanical pit of gastric juices.
Congratulations! You have met Drosera glanduligera, the tiny, carnivorous Australian Pimpernel Sundew and the world’s only known prey-catapulting plant. « Read the rest of this entry »
July 29, 2012 § Leave a comment
He must have had some really high insulin levels when he was growing up!
No, seriously. That’s what they say. They, in this case, being a quintet of biologists from the University of Montana (among other places), who’ve come out with a new study detailing the likely molecular underpinnings of the extravagantly long, wildly varied horn of the male Japanese rhinoceros beetle.
Yep, there it is: the giant branch coming off his face. It’s a terribly useful tool for a beetle, perfect for knocking male competitors out of the way during a fight for a lady beetles—which naturally makes bigger all the better. Unfortunately for the poorly endowed, the size of the horn is entirely determined by the growing conditions the beetle endured as a grub. Good food and low stress make for a huge, manly horn that can, in the best of times, grow up to nearly the length of the beetle. Poor nutrition, infection, or bad genes leads to a sad little stump that won’t be much use against a bigger male.
Now, the operating factor in all of this is insulin and the insulin-like growth factor (IGF) system. That’s also the molecular key that determines how big the beetle becomes as a whole. You’ve actually got the same thing; it’s what made you grow while you were on the up and up, and ditto me, my cat, fish, reptiles, crustaceans, and so on. More food leads to more insulin, which powers the engine that leads to more growth, and vice versa. It’s one of the oldest, most conserved systems in the evolutionary playbook. « Read the rest of this entry »
July 23, 2012 § Leave a comment
Stick a dog in a pasture full of sheep, you’re going to have yourself a full-on every-ovine-for-itself stampede to the center of the herd—because each and every sheep on that field wants to make sure his edible neighbor gets eaten first. There will be no heroics, and at long last, say researchers from the University of London, they’ve got the numbers to prove it.
The study, which appears online today in Current Biology, set out to quantify what’s known as the Selfish Herd hypothesis: animals that stick together do so to reduce their individual odds of being killed (Ha ha! Won’t eat me if it gets Bob first!). Sheep do it, in theory, as do crabs, seals, insects, fish, and just about every other animal that typically flocks. In this case, the researchers took 46 sheep, one Australian Kelpie working dog, and 47 GPS trackers—one per animal—then set the dog to work herding sheep through a gate in three trials over three different days. In each case, according to the second-by-second data collected from the devices, as soon as the dog came within roughly 70 meters of the group, the sheep clustered together, forming a tight herd in their haste to get not just next to their fellow sheep, but into the dead center of the group, which itself collectively and simultaneously shifted away from the threat.
Wait, what’s that you say? You’re not shocked? This was common knowledge? Correct, says Andrew King, lead author of the study. « Read the rest of this entry »
June 10, 2012 § Leave a comment
This is the sort of weather in which I can easily burn within the space of 30 to 45 minutes. That’s assuming I’m fool enough to stand outside in midday with neither sunscreen nor embarrassingly floppy hat. I do actually try to avoid that sort of behavior, but it can happen.
Within the first few hours of such exposure, my skin cells—keratinocytes—will begin churning out everything from inflammatory chemicals to immunosuppressants to nitric oxide, leaving me at once in pain, vulnerable to infection, and hot to the touch. White blood cells and prostaglandins will course through the area, adding to the mess. Worse yet, in some of my skin cells, the UV radiation will physically wrench apart and badly rebind key segments of my DNA, leaving misshapen bulges in its wake—like a long piece of string pinched in spots into tiny, doubled-up loops. My genetic copyediting team might be able to salvage some of these cells but others, past the point of no return, will push their self-destruct button and initiate suicide.
For the next few days, I will spend too much time taking cool showers and feeling sorry for myself.
But there’s one piece to this chain of events that’s missing: how did my skin know in the first place to do all this? What’s the molecular tripwire here?
Enter a new study from a crew of researchers out of San Diego, Miami, and New Jersey. With that question in mind, they performed an elegant series of experiments in both mice and skin cells in a dish. Their answer: it comes down to RNA. Specifically, sun-damaged RNA that tips off a molecular pattern-recognizer, which jumpstarts the inflammatory pathways, which snowballs into a miserable, sunburned chemical party on my skin. « Read the rest of this entry »