A Blog by

Yes, Rats Can Swim Up Your Toilet. And It Gets Worse Than That.

They eat our food. They furnish their nests with our detritus. They chew through our sheet metal, our lead pipes and our concrete. They outsmart us at every turn. They are our shadow, our enemy, our next door neighbor.    —”Rat City!Spy magazine, 1988

“You have to think like the rat,” my new friend Gregg told me. At the time, we were pushing Gregg’s homemade rat detector through a small hole in my basement ceiling. He had bought an endoscope camera online—the kind a doctor uses to hunt for polyps in one’s nether regions—and attached it to a bent wire coat hanger. The camera’s images would be displayed on his laptop.

Gregg became obsessed with rats when they took over his girlfriend Anne’s house, across the street from mine. Having tracked and conquered her rats, he was eager to bring his rat-buster skills and tools to my infestation. Gregg showed up on a Sunday afternoon with the endoscope and a two-gallon bleach sprayer and explained my role: Simply turn the endoscope’s light up or down on his command as he threaded the coat hanger through ceilings and walls.

In the ceiling space above the basement bathroom, we hit the mother lode: towering piles of little black rat turds appeared on the laptop screen. “Here’s your nest,” Gregg proclaimed, our first small victory in what had been a long, losing battle. As I wrote in May, I had already suffered an invasion of live rats, followed by stinking dead rats and a Flymageddon of bottle flies and flesh flies that hatched out of their carcasses.

I had learned a few things about rats by this point: They are creatures of habit. They establish trackways through a house, following the same paths each day: in, out, to food, to nest. And they can, in fact, rise up from the sewers.

VIDEO: WATCH OUT! A rat’s super swimming ability and flexibility enable it to make its way easily from the city streets to your toilet. See how they do it.

This last point became central to my investigation. When my husband, Jay, cut out a section of the bathroom ceiling where Gregg’s endoscope had led us, we found that our rat nest was centered around an old sewer drain pipe that, unbeknownst to us, had been cut but never capped during the removal of an upstairs toilet. Dark oily smudges marked the rim where rats had climbed up from the sewers and dropped into my basement ceiling space.

Upon further research, I found that not only is it pretty easy for a rat to climb up a three-inch toilet drain pipe (most of the time there’s not even water in it), but I live in a part of D.C. with a combined sewer system, so the storm drains on the street and the pipes from the toilets run to the same place. A combined sewer is one big, happy, Rat Central Station. 

Having figured out how our rats were getting in, and assuming that any remaining rats would have been scared away by our noisy labors and hole-poking, Jay capped the pipe, and we congratulated ourselves on a mystery solved.

Maybe you read my last post, and you can see where this is going.

One With the Rats

Rats’ superpowers are near-mythical: They can swim for three days. They can fit through holes the size of a quarter. They’ve even been said to have no solid bones, just cartilage (definitely false, and I can’t confirm whether they can collapse their ribcages). I looked to science for the truth. But I was surprised by the dearth of studies on the Norway rat—the common city rat, Rattus norvegicus—in the wild (the wild in this case being any city on Earth). Despite our long human history with lab rats, we know very little about the lives of the rats in our homes.

In fact, as veterinary scientist Chelsea Himsworth told me, “We probably know more about the ecology of polar bears than we do about rats.” Himsworth is studying how rats spread disease in cities as part of the Vancouver Rat Project.

“The interesting thing about Norway rats is they don’t exist in the wild,” Himsworth said. Their migrations—through Asia, over continents and across oceans—are our migrations. They’ve been in contact with humans for so long that they not only live with us, they depend on us almost entirely for food.  

They don’t stray far from our homes. One of the most important findings of the Vancouver Rat Project has been that rats form highly stable family groups or colonies, block by block in a city. And when people break up rat families, say by indiscriminate trapping or poisoning, the remaining rats are forced to move—and that’s when they tend to spread disease.

Sewer Rats

I was, of course, trying not to be indiscriminate at all. I wanted to kill them all—the whole rat family.

I told this to Robert Corrigan, who was described to me as the “rat king of New York City.” He seems okay with the title. Corrigan has spent his career fighting rats up and down the Eastern Seaboard, which—with its dense population, waterways, and old pipes—is pretty much rat heaven.

Corrigan said he agreed with Gregg in part: To wipe out an infestation you have to think like a rat. “But I also think it’s not difficult to out-think a rat,” he said. Unlike many animals, a rat must have both food and water every single day to survive. No skipping meals.


“If it doesn’t have food and water, it goes into this kind of ‘crazy mode,'” Corrigan said. Rats have a very low tolerance for hunger—so to get rid of them simply ask where they’re getting food and eliminate the source.

But what about my rats?, I asked him. How were they getting food? Clearly they were coming up an old toilet pipe from the sewer, and there wasn’t any food in my basement ceiling.

That’s where it got a little ugly. I was right about the combined sewer system, Corrigan said; it does make it easier for rats to get into toilets. As if to make the point, the day after we capped our toilet pipe, a rat popped up in my next-door neighbor’s toilet.

Plus, toilet drainage turns out to be a boon for sewer rats. “Lots of food gets flushed,” Corrigan pointed out. (This remains hard for me to fathom, but I do recall a landlord once complaining about a tenant who always flushed chicken bones down the toilet.)

“Also, if push comes to shove, human feces and dog feces contain undigested food,” Corrigan said.

“They don’t turn up their nose at anything that floats by.”

Let’s pause on that for a moment. What Corrigan is saying is that the rats in my basement ceiling were climbing up and down a toilet pipe into the sewer every day, whereupon they ate and quite possibly dragged back up caches of food that may or may not have included human excrement.

“That’s repulsive to humans, but it’s called coprophagy, and it’s part of the reason rats are so successful,” he said. “They don’t turn up their nose at anything that floats by.” 

Not Again

So it was smart of us to cap the sewer pipe. But little did I know when we cut off the entrance and exit to the basement ceiling, that at least two more rats remained in the ceiling—or that only one would survive. Survivor Rat chewed its way out of the house, leaving in its wake a gnawed-off condensation tube spewing water into the basement ceiling. Loser Rat didn’t hold out long enough and died in unknown quarters, spawning a new flock of flesh flies.

When the big striped monsters began to emerge and cruise the basement skies, I pretty much lost it. I Can’t. Do. This. Again.

Caving to the chemical solution, I bought a bug-fogging bomb and waited until I thought most of the flies would be emerging from their pupal cases—when I’d have the best chance of killing them. (Check out this video of  house flies emerging.)

I approached a hole we’d cut in the ceiling where I’d observed flies emerging. Using salad tongs, I pinched the plastic cover and pulled it back an inch. A rain of black flies drip-dropped from the hole onto the floor, buzzing. They had emerged from their cases but couldn’t quite fly yet. Perfect. I yanked the cover the rest of the way off, jumped back as a mass of flies hit the ground, some taking wing, and hit the button on the fogger.

Then I dropped my tongs and ran.

Those are dead flies. Multiply by entire basement.  Photo by Erika Engelhaupt
Those are dead flies. Multiply by entire basement. Photo by Erika Engelhaupt

Here is what I came home to.

It wasn’t as bad as Flymageddon.

A Blog by

This Is What Happens When You Use Rat Poison: Flymageddon

I killed the rats in my basement ceiling. At the time, they were my biggest problem.

Then I found myself in my car one night with the headlights aimed at my back door, hoping to lure a swarm of carrion flies out of the house. Carrion flies, if you’re not familiar, are the kind that lay their eggs on dead things. So then that was my biggest problem.

It all started with a gnawing sound in my basement, in the ceiling above the family room. The steady crunch-crunch of rat teeth on rafters didn’t bother me much at first; I just turned up the volume on the TV. But then the entire basement began to smell of rat urine, which turns out to smell a lot like people urine. Eventually, it didn’t matter how much Febreze I sprayed; we had hit, as I called it, RATCON 5.

My next step was to push little green blocks of rat poison into the ceiling space behind the recessed lights. This turned out to be a mistake. Not only is rat poison bad for the environment and wildlife, but this tactic also left the sated rats free to scurry into some far corner of the ceiling space to die. An exterminator poked around up there, and shrugged. “Can’t find ’em.” Soon, my basement took on a new odor: eau de dead rat.

For the next week, I slept with my windows wide open for fresh air, and the flimsy lock on my bedroom door set against possible intruders.

But the gnawing stopped. And I celebrated my hard-won victory. I had toughed out the stink, and the worst was past. I thought.

Two weeks later,  I came home from a trip and opened the door to Flymageddon.

The house was filled with giant flies.  I realized instantly that the dead rats had become a breeding ground for blowflies. Blowflies are described by Wikipedia as medium to large flies, but I would describe them more as flying bookends.

Dozens buzzed around the kitchen, thunking into me as I made my way in. I needed a weapon, and I needed one fast. Years ago, Uncle Rocky and Aunt Martha, who live in Abilene, gave me a gag gift in the form of a giant three-foot, turquoise Texas-Size Fly Swatter. Turns out, it was the best gift ever.

So there I was. I gripped the Texas Fly Swatter like a baseball bat and slowly opened the basement door.  I could hear the hum. My pulse was pounding.

Bluebottle fly. Ripanvc
Kinda pretty, actually. The bluebottle fly.

I flipped on the light and saw thousands of big dark flies, each the size of a dime, peppering the walls and window shades. Flies filled the air, and bumped against the ceiling with little buzzing thuds. Suddenly a squadron broke ranks and rushed straight up the basement stairs at me.

Or at least it seemed like they were flying toward me. I was watching a black wave of flies boil out of a light fixture in the ceiling, so I was a little distracted. But I’m pretty sure I made a noise like a creaky hinge, and slammed the door shut.

Now what? No way was I opening that door again without chemical weapons.

So armed with a can of Raid, I cracked open the basement door, stuck my arm in and sprayed a long satisfying ssssssssssssss. Yessssssssssss, I thought as I sprayed.

Now normally, I’m the live-and-let-live, shoo-em-out the door kind of person. So I also tried opening the kitchen door and stirred up a cluster of flies to usher them out. In return, they promptly flew straight for my head. All bets were off.

I needed a plan—and a partner. I was home alone, but that didn’t stop me from dragging my husband Jay into the scene from 500 miles away. I called him on speakerphone blubbering about flies.

The great thing about being married is that you can take turns being brave, and when one of you is freaking out and ready to burn your house down, the other one can spring into action. And even from 500 miles away, Jay sprung. “Go downstairs and open all the windows to let them out,” he instructed. I politely declined. As in, “What?! NO NO NO NO! Not until some of them are dead. Or most of them.”

Jay thought.

“OK,” he said, “Turn off all the lights in the house, and go turn on the car’s headlights. In fact, put the brights on. Then, open the basement door.” Flies, of course, are drawn to light. It’s not entirely clear why some insects fly toward light, but it’s probably why you’ll find flies clustered on windows. (At least at my house you will.)

Erika Engelhaupt
One of the fallen in my battle with the flies. Erika Engelhaupt
One of the fallen in my battle with the flies.

It sounded like a plan that might work. So I carefully unlocked the basement door from outside; a couple dozen flies hovered between the glass and the window shade. I pushed the door open and ran for the safety of the car.

“Don’t fall and hurt yourself running from flies!” Jay yelled, still on speakerphone. “They can’t hurt you.” At this point, he’s picturing me laid up with a broken leg, a victim of my own horror of animals that don’t even have mouths that can bite.

“I know that, logically,” I said. But when it comes to a swarm, it’s not about logic. Since I write a blog called Gory Details, you might think it should be hard to turn my stomach, but it’s not. There’s a psychology test for how easily disgusted a person is, and I turn out to be entirely average.

So this is how I found myself in my car at 10:30 p.m., watching flies meander out the door and trying to decide how long I could run the brights before the battery died.

On cue, my mother called. Hoping to help, she looked up flies in the encyclopedia and reported that the pupal stage lasts two weeks. (My mother does not use the Internet much.) Her book didn’t say how long the adults live. “Hm, well, anyway, they’ll die eventually,” she said, “if you wait long enough.”

And I waited. The flies have kept coming. Every morning now, I vacuum up the night’s casualties, and every evening I come home to more. The other day, I arrived at work and dropped my purse on my desk, and a fly flew out. To cope, the Texas Fly Swatter and I have created a no-fly zone in my bedroom.

In the meantime, I have learned a few things about my opponents. I have three kinds; one is big with a shiny blue backside and another small and the prettiest green up close. The big blue ones might be the bluebottle fly Calliphora vomitoriaappropriately named—or  Calliphora vicina, the urban bluebottle fly. The little green guys are probably a species of Lucilia, the nice entomologists at bugguide.net told me after I posted photos.

As those petered out, the biggest flies emerged—flesh flies of the genus Sarcophaga. Like sarcophagus. They’re enormous, and they buzz when they fly, and they are still in my house.

My little Lucilia.  Erika Engelhaupt
My little Lucilia.
Erika Engelhaupt

All three have their charms. Lucilia maggots have an amazing ability to eat dead flesh and ignore the living, so they’re used in maggot therapy to eat away dead, infected tissue. This works fantastically, but of course assumes that you can talk someone with, say, an oozing foot ulcer into letting a mass of maggots eat away at their foot—I suppose you say to the person that they’re only going to eat your dead foot.

I thought talking to a forensic entomologist might help me appreciate my new housemates. Sibyl Bucheli studies insects at Sam Houston State University (home to a great criminal justice program) in Huntsville, Texas (home to the busiest execution chamber in the United States). I knew I’d like her when her email arrived with a photo of her wearing a Wonder Woman tiara. (You should also check out her entomology lab’s Harlem Shake video.)

Bucheli told me about the first recorded case of forensic entomology in the 1300s. It involved carrion flies—maybe one of the species zipping around my head as I talked to her. The Chinese lawyer Sung Tzu was investigating a stabbing in a rice field and had all the workers lay out their sickles. Blowflies immediately landed on just one, even though it had been wiped clean, and Sung Tzu knew that the sickle bore traces of blood.

One of Bucheli’s students tested this method, she tells me—and found that blowflies can indeed find a bloodied and wiped-clean surface within minutes, or even seconds.

As for my flies, Bucheli says I’m probably on the second generation by now, at least. The flies have been multiplying, babies growing up and having babies of their own. I suppose it would be sweet, if the family home being handed down wasn’t a dead rat.

What’s more, she gives me bad news about the yellow-orange spots all over my windows. “That’s fly poop,” she says. “Sorry. They’re pooping on your curtains.”

Still, she made me feel a little better about them. For one thing, she’s totally brave about flies, and it made me want to be just like her. Bucheli has been at actual crime scenes, with dead bodies covered in flies. Even then, they don’t bother her. “I feel calm if I’m in a place with a million flies,” she said. “But if I’m in a city with a million people around me, that freaks me out… I understand the flies.”

They’re just being flies—eating, mating, pooping, laying eggs. They aren’t out to get me, or anyone else. “The whole six-legs, four-wings thing is beauty to me,” Bucheli said.

I’m trying to get there. In fact, I only used the Texas Fly Swatter once this morning.

But last night, after I cleared the sofa of dead flies and settled in for an episode of Bones, I heard it. The crunch-crunch of rat teeth on rafters.

This time, it’s war.

[to be continued]


(Note: I have updated the link to a test for how easily disgusted a person is. It now takes you to the appendix of Valerie Curtis‘ excellent book “Don’t Look, Don’t Touch: The Science Behind Revulsion.”)

A Blog by

Why Naked Mole Rats Don’t Get Cancer

The problem with writing about the naked mole rat is the long list of bizarre traits that you don’t have space to talk about. For this post, let’s  forget that they look like a wrinkled finger with teeth. Put aside their inability to feel pain in their skin, their tolerance for chokingly low oxygen levels, their bizarrely rubbish sperm or their poor temperature control. Don’t even think about how they live in ant-like colonies, complete with queens and workers. Ignore their ability to live for more than 30 years—an exceptional lifespan for a rodent of their size.

Instead, let’s talk about the cancer angle.

They don’t get it.

No one has ever seen a naked mole rat with a tumour. Scientists have raised large colonies of these rodents and watched them for many years. They’ve never seen an individual spontaneously develop cancer.

Now, Xiao Tian, Jorge Azpurua and Christopher Hine from University of Rochester have discovered one of the secrets behind this exceptional resistance. The team were trying to grow skin cells from naked mole rats in laboratory flasks, when they noticed something weird. The liquid that the cells were growing in would get viscous and syrupy within a few days.

This was because the cells secreted a sugar called hyaluronan, which was thickening the liquid. Hyaluronan is common in the skin, cartilage and other connective tissues of mammals. Like mortar in a wall, it’s one of many molecules that fill the spaces between cells and provide them with support. The naked mole rat makes an exceptionally large version of the sugar that’s over five times bigger than ours. And it has a lot of it.

There are two innovations behind the naked mole rat’s hyaluronan-fest—ineffective versions of the enzymes that digest hyaluronan, and altered versions of the protein that makes it. This hyaluronan-maker, known as HAS2, is made of 552 amino acids. The naked mole rat has altered just two of these, which are always the same in other mammals. These tiny changes were enough to allow it to make a monster hyaluronan.

Andrei Seluanov, who led the study, suspects that the larger hyaluronan physically cages potential cancer cells, preventing them from breaking free and growing into tumours. But it also allows cells to stop each other from growing if they become too crowded. This is called ‘contact inhibition’—it’s why healthy cells form a flat layer if they’re grown in a dish but cancerous ones pile on top of each other.

Based on an earlier study, Seluanov’s team suspected that naked mole rat cells are protected against cancer because they’re especially sensitive to contact inhibition. Now, they’ve shown that large hyaluronan is responsible. The rodents’ cells are very receptive to the sugar; as they get close, hyaluronan sticks to their surface and triggers a genetic programme that stops them from growing.

As a final test of their ideas, the team switched on a couple of cancer genes in naked mole rat cells and transplanted them into mice. Normally, nothing would happen—the cells are that resistant to cancer. But when the team also interfered with hyaluronan, either by stopping its production or boosting its destruction, the naked mole rat cells finally did the unthinkable—they formed tumours.

Seluanov thinks that hyaluronan is probably the naked mole rat’s “primary anti-cancer mechanism”. After all, disrupting it makes the rodent’s cells as cancer-prone as those of a mouse. Not so fast, cautions Rochelle Buffenstein from the University of Texas Health Science Center, who discovered the naked mole rats’ cancer resistance. “This is now the third study to provide a potential mechanism,” she says. “Clearly there are multiple anti-cancer defenses employed in the naked mole rat.” Others might include mass suicide of overgrowing cells, and a tolerance for DNA-damaging oxygen molecules.

So why did this animal evolve its super-sized hyaluronan? The answer might have nothing to do with cancer.  Seluanov says that the large sugars are slightly elastic and surround themselves with water molecules—two properties that make the naked mole rat’s skin very loose and stretchy. This allows it to move through tight underground tunnels without ripping its flanks as it rubs against dirt, rocks or tubers. Perhaps the large hyaluronans evolved as an adaptation for underground life, and a cancer-free existence was just a neat bonus!

Does this discovery mean anything for humans? It’s tempting to think that hyaluronan holds the secret to stopping cancer, but we have to tread carefully. In the early days of hyaluronan research, scientists were confused by the fact that the molecule seemed to both prevent and cause cancer (the Daily Mail would have loved it).

Since then, we’ve discovered that the sugar’s size is responsible for its dual nature. Bryan Toole from the Medical University of South Carolina, who studies hyaluronan, says that high concentrations of the large versions can stop cells from turning cancerous, while smaller versions can actually promote cancer. In a similar way, the large forms tamp down inflammation while the small ones exacerbate it, which may relevant to cancer since inflammation is tied to several tumours. “It’s not clear how the cell distinguishes between the two,” adds Seluanov. That’s something the team still needs to find out.

Reference: Tian, Azpurua, Hine, Vaidya, Myakishev-Rempel, Ablaeva, Mao, Nevo, Gorbunova & Seluanov. 2013. High-molecular-mass hyaluronan mediates the cancer resistance of the naked mole rat. Nature http://dx.doi.org/10.1038/nature12234

For more on the naked mole rat, check out Dan Engber’s award-winning piece at Slate.

Correction: An earlier version of this piece suggested that hyaluronan is a protein, which it isn’t. Your friendly neighbourhood science writer regrets the error.

A Blog by

Spiny mice defend themselves with self-flaying skin and fast healing factors

When Marvel Comics created a short superhero who could heal horrific injuries, perhaps instead of “Wolverine”, they should have named him “African spiny mouse”. These tiny rodents can jettison strips of skin from their own hides when captured by predators, and heal those same wounds with extraordinary speed.

Healing powers are common in the animal world. Salamanders and starfish can regrow lost limbs, while some flatworms can regenerate their bodies from a single cell. But mammals lag behind – while some species can grow back a lost tail, when most of us lose our body parts, we do so permanently. The spiny mice are an exception.

Biologists have noted that these rodents have very weak skin, which seems to slough off easily when they are handled. Led by these anecdotal reports, Ashley Seifert from the University of Florida has studied the skin-shedding ability in greater depth, focusing on two species: Kemp’s spiny mouse (Acomys kempi); and Percival’s spiny mouse (Acomys percivali).


A Blog by

Newly discovered rat that can’t gnaw or chew

If you only looked at mammals, you could reasonably believe that the chisellers have inherited the earth. Of all the various species of mammals, forty percent are rodents. Rats, mice, squirrels, guinea pigs… all of them have the same modus operandi. They gnaw their way into their food with self-sharpening chisel-like teeth.

Whether tiny gerbil or huge capybara, rodents eat with the same special teeth. The upper and lower jaws each have a single pair of incisors that grow continuously through their lives. The front of each tooth is made from hard enamel, while the back is made of soft dentine. As the rodent gnaws, the incisors scrape at each other, and the dentine wears away faster than the enamel. This creates a permanently sharp edge, useful for cracking into wood, nuts and flesh alike. Once gnawed, the rodent passes its food to the back of their mouths to be chewed by grinding molars.

But on the Indonesian island of Sulawesi, Jacob Esselstyn has discovered a new species of rodent that radically departs from this universal body plan: a “shrew-rat” that he calls Paucidentomys vermidax.Its name –a mash-up of Latin and Greek—gives a clue to its lifestyle. It means “worm-devouring, few-toothed mouse”.


A Blog by

Empathic rats spring each other from jail

You enter a room with two cages. One contains a friend, who is clearly distressed. The other contains a bar of chocolate, which clearly isn’t. What do you do? While a few people would probably go for the chocolate first (and you know who you are), most would choose to free the friend. And so, it seems, would a rat.

Inbal Ben-Ami Bartal from the University of Chicago found that rats will quickly learn to free a trapped cage-mate, even when they get nothing in return, or when there’s a tasty chocolate distraction around. Bartal thinks that the rats conduct their prison breaks because they empathise with one another. This ability to understand and share the feelings of another individual is found in humans, apes, elephants, dolphins and other intelligent animals. It seems that rats belong in this club too.


A Blog by

The rubbish sperm of the naked mole rat

The naked mole rat must be one of the strangest mammals in existence. They live in underground colonies like those of ants and bees, with a fertile queen lording over sterile workers. They feel no pain in their skin, they live unusually long lives, they can cope with chokingly low levels of oxygen, and they seem to be immune to cancer. Their sight is poor, they can’t control their body temperature very well, and their teeth jut out beyond their lips. And they look like wrinkled sausages.

Now, just when you thought they couldn’t get any weirder, we can add another bizarre trait to the naked mole rat’s extensive list: they have really rubbish sperm.


A Blog by

Mole rat continuously grows new teeth in shark-like conveyor

A shark continually grows new teeth. Those at the front of its mouth fall away, only to be replaced by fresh rows that move forward like conveyor belts. By contrast, we humans only have two sets of teeth. The first falls away during childhood leaving a second set to last us for the rest of our lives. Most mammals are like us, but there are some notable exceptions.

The silvery mole rat of Kenya and Tanzania continually replaces its molars in an unsettlingly shark-like way. New ones sprout from the back of its jaw and slowly make their way forwards. The front ones, having been ground away, are absorbed.


A Blog by

Crested rat slobbers poison on its fur, dares predators to bite

The African crested rat is a thief, but its loot only becomes obvious if you take a bite out of it. Doing so would give you a mouthful of ouabain, a poison so strong that it can kill an elephant. The rat doesn’t make the poison itself. Instead, it pilfers it from the local Acokanthera schimperi tree. It gnaws on the roots and bark, chews them up, and slavers a coarse toxic gel onto the special hairs on its flanks. Local people use the same poison to coat their arrowheads. The rat uses it as a chemical shield.

The crested rat is found throughout eastern Africa. It is normally sluggish but when threatened, it puts on a vivid display. It pulls its head back, turns sideways onto its attacker and parts the grey fur on its flanks using special muscles. These actions draw attention to a leaf-shaped crest of brown hairs on its side, which are encircled by a “target” of black and white. It’s almost as if the rat is daring a predator to bite it.

Any animal that takes up the invitation is in for trouble. Domestic dogs do so from time to time, and they end up stumbling about and frothing at the mouth. They often die of rapid heart failure. In two cases where the animals survived, they took weeks to recover. For these reasons, people have long thought that the rat is poisonous; now Jonathan Kingdon from the University of Oxford has proved them right.


A Blog by

House mice picked up poison resistance gene by having sex with related species

Since 1948, people have been poisoning unwanted rats and mice with warfarin, a chemical that causes lethal internal bleeding. It’s still used, but to a lesser extent, for rodents have become increasingly resistant to warfarin ever since the 1960s. This is a common theme – humans create a fatal chemical – a pesticide or an antibiotic – and our targets evolve resistance. But this story has a twist. Ying Song from Rice University, Houston, has found that some house mice picked up the gene for warfarin resistance from a different species.

Warfarin works by acting against vitamin K. This vitamin activates a number of genes that create clots in blood, but it itself has to be activated by a protein called VKORC1. Warfarin stops VKORC1 from doing its job, thereby suppressing vitamin K. The clotting process fails, and bleeds continue to bleed.

Rodents can evolve to shrug off warfarin by tweaking their vkorc1 gene, which encodes the protein of the same name. In European house mice, scientists have found at least 10 different genetic changes (mutations) in vkorc1 that change how susceptible they are to warfarin. But only six of these changes were the house mouse’s own innovations. The other four came from a close relative – the Algerian mouse, which is found throughout northern Africa, Spain, Portugal, and southern France.

The two species separated from each other between 1.5 and 3 million years ago. They rarely meet, but when they do, they can breed with one another. The two species have identifiably different versions of vkorc1. But Song found that virtually all Spanish house mice carry a copy of vkorc1 that partially or totally matches the Algerian mouse version. Even in Germany, where the two species don’t mingle, a third of house mice carried copies of vkorc1 that descended from Algerian peers.


A Blog by

Pocket Science: plague-running mice, and how to watch mutations in real time

Not Exactly Pocket Science is a set of shorter write-ups on new stories with links to more detailed takes, where available. It is meant to complement the usual fare of detailed pieces that are typical for this blog.


Plague-running mice create epidemics

The bacterium behind bubonic plague – Yersinia pestis has a notorious track record for massacring humans, creating at least three major pandemics including the Black Death of the 14th century. But it’s mainly a disease of rodents and it regularly infects the black-tailed prairie dogs of North America. It’s an enigmatic killer. It will remain relatively silent for years before suddenly exploding into an epidemic that kills nearly all the prairie dogs in infected colonies within a few weeks. Now Daniel Sakeld from Stanford University has found the culprit behind these lurk-and-kill cycles – the tiny grasshopper mouse.

Prairie dog colonies, and their diseases, are generally isolated from one another. Even though Yersinia is very persistent, it eventually fades away unless it finds a new group of hosts. The grasshopper mouse provides it with just such an opportunity by acting as an alternative and highly mobile host for Yersinia. It’s a plague-runner. By scampering across the grasslands, it inadvertently creates a network between otherwise unconnected colonies, opening up corridors for Yersinia to spread.

By creating a mathematical model, and observing both rodents in the wild, Sakeld found that when the mouse is absent, only a small proportion of prairie dogs are plagued by plague. In these conditions, infections spread very slowly during fights and hostile takeovers between neighbours. When mouse numbers pass a threshold, fatal plague epidemics are virtually guaranteed.

The numbers of grasshopper mice in the grasslands rises and falls over time, a cycle that could spell life or death for the prairie dog. These patterns of lengthy lurking and sudden death are also shared by many other deadly diseases like anthrax and hantaviruses. In these cases, alternate hosts like the grasshopper mouse might also be involved in the sudden rise of deadly epidemics.

Reference: PNAS http://dx.doi.org/10.1073/pnas.1002826107


Events occur in real time – watching the birth of mutations

Life is a massive game of Chinese whispers – information is constantly being passed on and as this happens, errors build up. Every time a cell divides in two, its genetic information is copied and there’s a small chance that mistakes (or ‘mutations’) will creep in. Some of these mutations will be beneficial, others will be fatal. Either way, they provide fuel for evolution, producing the variation that natural selection acts upon.

Now, Marina Elez from University Paris Descartes Medical School has found a way to spot mutations in real time. She can look at dividing cells and literally watch the moment when mutations show up across the entire genome. The technique works in bacteria, and it could be expanded to study the birth of mutations in more complex cells or even cancers.

Studying mutations isn’t easy. They’re very rare and most don’t produce any noticeable effects that would give away their presence. More often not, they’re repaired by proofreading proteins, which watch for errors in copied DNA and edit them back into shape. Elez realised that these proofreaders could lead her to the location of mutations – all she needed to do was follow. She focused on one bacterial proofreader called MutL, which forms large clusters around mutations that it can’t repair. Elez tagged MutL with a molecule that glows in the dark. The result: bacteria that give off tiny pinpricks of light at every point of their genome with an irreparable mutation.

By counting these bright dots, Elez could estimate the mutation rate in her bacteria. And fortunately, her estimate was a good match for the predictions of earlier studies. Elez also thinks that the approach should work in other living things because proofreading proteins like MutL are very similar from species to species. The technical challenges might be greater in more complicated cells, but the principle of watching mutations in real time is sound. And that opens up all sorts of possibilities. You could, for example, look at tumours, to see when and where the genetic changes that create a cancer will emerge.

Reference: Current Biology http://dx.doi.org/10.1016/j.cub.2010.06.071


A Blog by

“Weedy” mice dominate a warming world while other small mammals suffer

Deer_mouseToday’s mammals are facing the twin threats of a rapidly warming planet and increasingly intrusive human activity. As usual, the big species hog the limelight. The world waits on bated breath to hear about the fates of polar bears, whales and elephants, while smaller and more unobtrusive species are ignored. But smaller mammals are still vital parts of their ecosystems and it’s important to know how they will fare in a warmer world. Now, thanks to Jessica Blois from Stanford University and a hoard of new fossils, we have an idea. As they say, all this has happened before


A Blog by

Rapamycin – the Easter Island drug that extends lifespan of old mice

Blogging on Peer-Reviewed ResearchIt’s 1964, and a group of Canadian scientists had sailed across the Pacific to Easter Island in order to study the health of the isolated local population. Working below the gaze of the island’s famous statues, they collected a variety of soil samples and other biological material, unaware that one of these would yield an unexpected treasure. It contained a bacterium that secreted a new antibiotic, one that proved to be a potent anti-fungal chemical. The compound was named rapamycin after the traditional name of its island source – Rapa Nui.

Skip forward 35 years and rapamycin has made a stunning journey from the soil of a Pacific island to the besides of the world’s hospitals. Its ability to suppress the immune system means that it’s given to transplant patients to stop them from rejecting their organs and its ability to stop cells from dividing has formed the basis of potential anti-cancer drugs. But the chemical has an even more interesting ability and one that has only just been discovered – it can extend lifespan, at least in mice.

David Harrison, Randy Strong and Richard Miller, leading a team of 13 American scientists, have found that capsules of rapamycin can extend the lifespans of mice that eat them by 9-14%. That’s especially amazing given that the mice were already 20-months-old at the time of feeding, the equivalent in mouse years of a 60-year-old human.

There will undoubtedly be headlines that proclaim the discovery of the fountain of youth or some such, but it is absolutely critical to say up front that this is not a drug that people should be taking to extend their lives. Rapamycin has a host of side effects including, as previously mentioned, the ability to suppress the immune system. Harrison says, “It may do more harm than good, as we know neither optimal doses nor schedules of when to start for anti-ageing effects.” So the new discovery doesn’t put an anti-ageing pill within our grasp. It’s far better to see it as a gateway for understanding more about the basic biology of ageing, and for designing other chemicals that can provide the same benefits without the unwanted risky side effects.

Nonetheless, it’s still very exciting, especially since the nutrition market is already awash with supplements that claim to slow the ageing process but which have little evidence to back their claims. Likewise, scientists have tested a number of different chemicals but the few positive effects have typically been small or restricted to a specific strain of mouse. Rapamycin is different – as Harrison himself explains, “no other intervention has been this effective when starting so late in life on such a diverse population.”


A Blog by

Different neuron networks control fear of different threats

Blogging on Peer-Reviewed ResearchIf you wanted to turn a rat into a fearless critter, unfazed by cats or bigger rats, the best way would be to neutralise a small pair of tiny structures in its brain called the dorsal premammillary nuclei, orPMD. According to new research by Simone Motta at the University of Sao Paolo, these small regions, nestled within a rat’s hypothalamus, control its defensive instincts to both predators and other rats.

But not all neurons in the PMD are equal. It turns out that the structures are partitioned so that different bits respond to different threats. The front and side parts (the ventrolateral area) are concerned with threats from dominant and aggressive members of the same species. On the other hand, the rear and middle parts (the dorsomedial area) process the threats of cats and other predators. And both areas are distinct from other networks that deal with the fear of painful experiences, such as electric shocks.

This complexity is surprising. Until now, scientists have mostly studied the brain’s fear system by focusing on an area called the amydgala, which plays a role in processing memories of emotional reactions.  And they have generally assumed that fearful responses are driven by the same networks of neurons, regardless of the threat’s nature.

There’s good reason to think that. Hesitating in the face of danger is a sure-fire way to lose one’s life, so animals respond in a limited number of instinctive ways when danger threatens. They freeze to avoid detection, flee to outrun the threat, or fight to confront it. These automatic “freeze, fight or flight” responses are used regardless of the nature of the threat. Rats, for example, behave in much the same way when they are menaced by cats or electrified floors alike, and actually find it very difficult to do anything else.

This limited repertoire of action convinced scientists that animals process different fears in the same way, relying on the same network of neurons to save their hides from any and all threats. Motta’s research shows that this idea is wrong, certainly for rats and probably for other mammals too. The brain’s fear system isn’t a one-size-fits-all toolkit; it has different compartments that respond specifically to different classes of threats.


A Blog by

Drugs and stimulating environments reverse memory loss in brain-damaged mice


You swallow the pill. As it works its way through your digestive system, it slowly releases its chemical payload, which travels through your bloodstream to your brain. A biochemical chain reaction begins. Old disused nerve cells spring into action and form new connections with each other. And amazingly, lost memories start to flood back.

Dementia results in massive neuron loss, but that doesn't mean memories are destroyed.The idea of a pill for memory loss sounds like pure science-fiction. But scientists from the Massachussetts Institute for Technology have taken a first important step to making it a reality, at least for mice.

Andre Fischer and colleagues managed to restore lost memories of brain-damaged mice by using a group of drugs called HDAC inhibitors, or by simply putting them in interesting surroundings.

They used a special breed of mouse, engineered to duplicate the symptoms of brain diseases that afflict humans, such as Alzheimer’s. The mice go about their lives normally, but if they are given the drug doxycycline, their brains begin to atrophy. The drug switches on a gene called p25 implicated in various neurodegenerative diseases, which triggers a massive loss of nerve cells. The affected become unable to learn simple tasks and lose long-term memories of tasks they had been trained in some weeks earlier.

Fischer moved some of the brain-damaged mice from their usual Spartan cages, to more interesting accommodation. Their new cages were small adventure playgrounds, replete with climbing frames, tunnels and running wheels, together with plentiful food and water. In their new stimulating environments, the mice returned to their normal selves. Their ability to learn improved considerably, and amazingly, seemingly lost memories were resurrected.