Spiders make the front page

Spiders don’t usually get much good press. Whenever I told people I was writing a story for the Pittsburgh Post-Gazette on spider personalities, most people made a face like “ewww!!”

But spiders are some of the most interesting creatures you could imagine and — if you take the time to look at them — also beautiful.

Anyway, I tried to spread some of my enthusiasm by introducing Pittsburgh newspaper readers to behavioral ecologist and social spider personality expert extraordinaire  Jonathan Pruitt, who I wrote about here a couple of years ago. Now the story has ended up on the front page, complete with staged photo of Jonathan with his hands full of social spider webs, a la Spiderman. FYI, coating himself in spider webs is not something Jonathan does most days.

I also spent a fun day shadowing one of his visits to local schools, where students participate in spider research.

Sadly, one of my sidebars is missing from the online story, which included a description of how researchers use modified vibrators to simulate a prey item struggling in a web, to test communal foraging responses. Apparently it’s the most practical tool for the job :)

A Cocktail of Biology

DNA is not just found at crime scenes. It’s in every living thing – you, your cat, the bacteria on your hands and the grass under your feet. It’s in every meal you’ve ever eaten and, under the right circumstances, it’s even in your cocktail.

Strawberry picture

Supermarket strawberry. Hell yes I took this hazy photo with a $30 phone and a droplet of water.

The DNAquiri is a cocktail recipe that won Best in Show at the 2011 Science Hack Day San Francisco because it is also a protocol for extracting DNA from strawberries. The recipe calls for only three ingredients – frozen strawberries, pineapple juice and high-proof rum – but the final product is a complex cocktail of curiosities.

This post is another of my recycled school assignments, in which I was given the slightly daunting task of writing a story in the form of a list. I decided the best kind of list is a recipe, and the best kind of recipe is one that involves both science and cocktails. A deep bow and a tip of the hat to Margot at Hypatian Axis for drawing my attention to the quirky back story of the modern strawberry.

1) Strawberries

Strawberries are a convenient source of DNA because they are delicious and they are octoploid. Octoploid means that each cell in a strawberry contains eight copies of every gene. In contrast, human cells are diploid, with only two copies of each gene, one from mom and one from dad. In the same way, strawberry cells have four copies from mom and four copies from dad, and yes, strawberry plants do have parents. In fact, according to G.M. Darrow in The Strawberry: History, Breeding and Physiology,the mother and father of the cultivated strawberry were the stars of an unlikely transcontinental plant romance.

It all started in 1712, when some unusually plump strawberries caught the eye of a French spy in Chile. The spy was Amédée François Frézier, an engineer in the French Army Intelligence Corps who was spying on Spanish defenses in South America. He noticed that the strawberries cultivated by the locals were much larger than European strawberries and selected several specimens with excellent fruit to take back to France.

Although these plants survived an arduous 6-month voyage to Europe, they did not immediately live up to Frézier’s enthusiastic description. The king’s gardener could not get them to reliably produce oversized fruit “as big as a Walnut, and sometimes as a Hen’s Egg”. By choosing only fruiting plants, Frézier had inadvertently selected only females. At that time, nobody realized that strawberry species often have separate sexes, which is relatively unusual for plants. Male plants carry pollen, while female plants bear fruit, so those female strawberry immigrants were effectively infertile. This is where we meet dad.

Dad was the Virginia strawberry, a wild species still common in the Eastern US that was introduced into Europe in the 1600s. While botanical gardens initially struggled to produce Chilean strawberries, enterprising farmers succeeded by alternating rows with other strawberry varieties. These included some male plants with pollen that could fertilize the Chilean females. The Virginia strawberry gave the best results and the descendents of this pairing became the modern strawberry, which is strongly flavored like its Virginian ancestors, but large like the Chileans. Part of the reason the match worked genetically is that while the European strawberry varieties were mostly diploid (with two copies of each gene per cell), both the Virginia and Chilean strawberries were octoploid2.

This octoploid romance means that every cell of a supermarket strawberry is jam-packed with DNA, making it easier for us to extract enough DNA to see with the naked eye. But first, you need to get the DNA out of the cell.

When strawberries freeze, the water in the cells forms ice crystals that puncture the cell membranes. So if you put frozen strawberries in a Ziploc bag and then squash them, warm them to 50°C then chill them again, some of the DNA will spill out of the leaky cells. Force the pinkish mush through a strainer to get rid of the lumps and you’ll have a strawberry cell extract, otherwise known as juice.

2) Pineapples

The strawberry juice contains DNA, but it also contains all kinds of other stuff from inside the cells, including proteins. Proteins translate the genetic information in DNA into action; DNA sequences carry the instructions for making lots of different kinds of proteins, which in turn do many different jobs. But when all those strawberry proteins are released from the cell into the juice, some of those jobs interfere with the process of DNA extraction.

For example, some of the proteins wrap around the DNA strands, winding them into bundles that don’t extract well. Other proteins chop up the DNA. To counter the effects of all these proteins, you can add “protein-chopping” proteins called proteases. Proteases chop other proteins into bits and although they can be found in all cells, they are found in conveniently large quantities in pineapples. In fact, pineapples have such high concentrations they are used in industrial applications. They are even available in the supermarket, sold as a meat tenderizer that works by digesting the collagen protein that gives meat its structure.

Pineapple - up-close (macro)

Pineapple close-up. By Uri_Breitman (Flickr) [CC BY-NC 2.0]

This is also why pineapple has a bit of a bite to it — that burning sensation when you eat too much pineapple is from proteases damaging proteins on the surface of your tongue.

To digest away the protein in your strawberry mush, simply add some cold, unpasteurized pineapple juice and let the proteases do their work. Now your Ziploc bag contains strawberry DNA and strawberry proteins being chopped up by pineapple proteins. But the DNA is still invisible.

3) Rum

Your next step is to force the DNA to stick together into a clump that you can see. To do this you pour a layer of ice-cold, high-proof rum over the strawberry cell extract. “High proof” just means a high concentration of alcohol (ethanol), in this case 70%, which is about twice as high as normal rum.

In watery liquids, such as strawberry guts and pineapple juice, DNA is coated in a loosely bound layer of water molecules (called a “hydration shell”). This coating prevents the DNA, which is negatively charged, from binding the positively charged ions (like the sodium from table salt2) that are also floating around in solution. But ethanol disrupts the hydration shell and makes the DNA more attractive to positively charged ions. Under these conditions, the DNA will tightly bind positively charged ions that neutralize the overall charge of the DNA. Because the DNA molecules are now neutral, instead of repelling each other, they tend to stick to each other, forming much larger, visible blobs (see note 3 below for my original, quite wrong explanation).

Understandably, ethanol at a high enough concentration to cause DNA to stick together is highly toxic to cells (you could use high-proof rum as effective but expensive disinfectant). But the ethanol in your bottle of rum was originally made by cells — yeast cells.

Yeast are fungi, like mushrooms, but they are microscopic, consisting of only a single cell. They excrete ethanol during the process of extracting energy from fruit sugars. Grapes and other fruit are the natural habitat of yeast, at least during the summer. According to scientists at the University of Florence, yeast’s winter home is in the guts of wasps that feed on grapes. These wasps provide a warm and moist refuge from the elements while fruit is out of season and once the fruit ripens they provide transportation to the site of the annual sugar feast.

Yeast on grapes

Grapes. By Scharks [CC-BY-SA-2.0], via Wikimedia Commons

Preventing other microbes from joining in on the feast is part of the reason why yeast cells excrete ethanol. Yeast get their energy from sugar by converting it to ethanol and carbon dioxide, a process called fermentation. Fermentation generates much less energy than respiration, the method that humans use to metabolize sugar, but fermentation is much faster and has the added benefit of producing a toxic by-product, ethanol. When a wasp inoculates a grape with yeast cells, the yeast rapidly convert their surroundings into an acidic, alcoholic soup that is inhospitable to most other microbes.

Humans have taken advantage of yeast’s curious lifestyle to produce alcoholic drinks, but we have also used it to advance scientific knowledge. For example, studies of yeast fermentation overturned Louis Pasteur’s hypothesis that cells were powered by a mysterious vital force that fundamentally distinguished living from non-living things.

The basic unit of life is the cell, which can grow and divide to make more cells. Pasteur had found that some chemical reactions — like fermentation of sugar to alcohol — could only be catalyzed by live yeast. Vitalists like Pasteur argued that live cells possessed a “vital spark” that allowed them to become more than the sum of the biochemical reactions occurring inside their cell membranes.

As recounted by Christian Reinhardt in Nobel Laureates in Chemistry, 1901-1992, Pasteur’s strain of vitalism was dealt a death blow by Eduard Buchner, a German chemist who was trying to extract proteins from yeast cells without damaging the proteins in the process. He managed this in 1896 by grinding yeast with sand and then filtering out the slurry of broken cells to produce a non-living “yeast juice.” There were no yeast cells remaining in the juice, but it did contain many of the biochemicals, like proteins, that had once been inside the cells. To stop this mix from spoiling before it could be used in other experiments, Eduard, who had once worked in a cannery, tried the method that preserves fruit in jams — ­adding a high concentration of sugar. To his surprise, within 15 minutes of adding sugar to the yeast juice, it started to froth like a fermenting beer.

Rising bubbles from yeast fermentation

Bubbling yeast fermentation. By Jim Champion (Flickr: Rising bubbles) [CC-BY-SA-2.0], via Wikimedia Commons

Buchner was able to show that the proteins in the yeast juice could produce carbon dioxide and ethanol from sugar in a way that was identical to fermentation by live cells. Pasteur was wrong, and no vital force was necessary to explain the metabolic activities of the cell. Cells were really just the sum of their parts.

Buchner’s experiments were a key moment in the dawn of biochemistry, the field that uses non-living extracts of living things (like your strawberry juice) to understand the chemical reactions that allow cells to function. One of the most important discoveries of biochemistry has been that many of these chemical reactions are similar in all organisms, and that all living things share the same genetic code. So, once you see a white film form in a layer between the pink strawberry juice and the amber rum, take a cocktail stick, twirl it around in the film and remove a blob of DNA. This unassuming clump of slime is the hidden genetic material that helped make those delicious strawberries. Be sure to give your drink a good stir before you toast the shared heritage between yeast, pineapples, strawberries and yourself.

DNAquiri blob extraction

Blob of unknown identity. By me.

Sad taster’s note and party poopery: I’ve tried the DNAquiri recipe twice and each time have achieved a very respectable yield of white slime and an almost drinkable cocktail (it’s a bit strong for me). However, I’m going to guess that the slime is not actually DNA, but instead is pectin, a cell wall carbohydrate that gives fruit jams and jellies their gel-like consistency. I base this guess on a suggestion from the UK’s National Centre for Biotechnology Education and the fact that the slime isn’t as stringy as I’m used to for DNA. Please weigh in, all you fruit DNA experts! I want to know!

1More party poopery: Darrow’s story about the origin of the three strawberry flowers on the Fraser coat of arms is probably false. Darrow recounts an old myth that Frézier and the Scottish Fraser clan were descended from one Julius de Berry, who was knighted in 916 by the Emperor of France, King Charles the V. According to the legend, de Berry was knighted in reward for his miraculous ability to provide unseasonably ripe strawberries for a feast. He was given a new coat of arms and a new name, Fraise, which is French for strawberry.

2At this point, anyone who has ever done a DNA precipitation before will be all like “where’s the salt???!”  Typically, it is necessary to add salt to the mixture to provide enough positive ions to neutralize the DNA. The creators of the DNAquiri left the salt out so that the final cocktail was not profoundly disgusting, but I suspect that this favors the precipitation of polysaccharides (like pectin) more than nucleic acids. (note added May 25, 2013).

3 This is not the original version of the explanation I had. Embarrassingly, it originally read:

The interior of a cell is watery and DNA is a ”water-loving” or hydrophilic substance that dissolves readily. But just as oil and water don’t mix, hydrophilic substances don’t mix well with “water-hating” or hydrophobic substances, like ethanol. When immersed in ethanol, DNA molecules stick together into much larger, visible blobs.

Then @EricGumpricht called me out on my decision to call ethanol “water hating,” which was convenient for my word limit, but of course, not remotely true — cocktails wouldn’t be much fun if spirits weren’t miscible with water! I was trying to describe ethanol precipitation without turning this into a chemistry lesson and talking about dielectric constants and whatnot, but I failed miserably (as usual, I blame sleep deprivation and my unwillingness to proofread blog posts). I’ve experimented with an explanation that doesn’t mention polarity because otherwise I ended up with a pretty dull essay. If you have taken high school chemistry and are genuinely interested in how ethanol precipitation works, try these much better explanations:

Bitesize Bio: How ethanol precipitation of DNA and RNA works (requires registration)

Paul Zumbo: Ethanol precipitation (PDF)

(note added May 25, 2013).

Curiosity killed the parrot? My guest post at Scientific American blogs

There’s too much to say about kea, those playful, destructive and slightly obsessive-compulsive snow parrots from New Zealand. I wrote a guest post at Scientific American Blogs this week on the problem of lead poisoning in wild kea populations, but there were a million things I had to leave out for fear of boring people with kea overload. If I ever finish my homework, maybe I’ll  write more about them, in the meantime please enjoy:

Wheelie bin raids

The Kea Conservation Trust

The 1993 documentary Kea: Mountain Parrot

Kea - Mountain Parrot

Update (24th Jan):

Just plain ol’ footage of kea flying around:

No, squeezing breasts does not cure cancer

You may have seen reports that squeezing breasts cures cancer.

You may have seen these reports a few days ago, at such esteemed British purveyors of science news as the Daily Mail and Huffington Post UK (no, I haven’t linked to the articles). If you looked today, you may have seen similar reports, along with similarly tacky stock images of boobs being squeezed, at news sites and blogs all over the world.

You are probably not surprised to learn that squeezing breasts, pleasant as it might be, will have absolutely no effect on anybody’s cancer.

This is yet another case of the UK media finding a jokey angle on a small science story that sends it viral overseas. I’ve seen it happen many times (which is why I enjoyed this slightly bewildered article about the phenomenon), but this time it really bothered me. That’s because usually this cycle starts with research that was already a joke (or publicity stunt) to begin with, but in this case the story was about some real science.

I suppose I also took it a bit personally because I was involved in publicising the particular nugget of research at the center of the boob squeezing madness. I’m an associate of the Public Information Committee of the American Society for Cell Biology, which means I help pick out which research from the society’s annual meeting we will promote to the press. This story, presented at the ASCB meeting by Berkeley grad student Gautham Venugopalan, was an easy choice because the science is new, interesting and medically relevant.

And no, he did not squeeze breasts and then measure cancer regression rates – that would be pointless and weird. What he actually did was compress breast cancer cells that were growing in the lab. Remarkably, a brief squeeze prompted the cancer cells to arrange themselves into highly organized spherical structures that are usually only formed by non-cancerous breast cells. The finding is intriguing because these well-behaved cells presumably still had the same cancer-causing genetic mutations that they started with. Venugopalan and his colleagues had somehow blocked the effects of those mutations.

This is precisely the kind of effect that Mina Bissell’s group, who collaborated in the research, searches for. Bissell argues that an important reason why cancer mutations do not always lead to cancer is that a cell’s behavior is strongly regulated by its “microenvironment” – its immediate surroundings, including neighboring cells and a gel-like goo called the extracellular matrix. You can see her discussing this idea in a TED talk in which she describes the experimental system that Venugopalan used. This system simulates the breast cell microenvironment using a gel enriched with extracellular matrix proteins and signaling factors. Bissell’s lab has previously shown that they can force cancerous cells to behave like normal cells by manipulating the signals that come from this simulated microenvironment.

Venugopalan took the system in a different direction, however. He is a member of Daniel Fletcher’s group, who study (among other things) the tiny mechanical forces that cells experience within their microenvironment. Neighboring cells push and pull each other in many ways as they do their various jobs; some cells are compressed as they slide between others, some cells are tugged around because they are stuck together into networks of interlocking cells. But cells are not just passively buffeted, they treat mechanical forces as sources of information, signals about what is going on around them, and in turn manipulate those signals to change their microenvironment. Such mechanical signals can influence the development and spread of cancers in a variety of ways that are still being unravelled.

The Berkeley experiments have contributed to this growing field by demonstrating that signals generated by compression can override certain cancer mutations. Understanding those signals might one day lead to drugs that could control cancers in people, not just in dishes. We even have a clue for where to look for the signals – the effects of compression disappeared when the researchers blocked the function of E-cadherin, a protein that helps glue neighboring cells together.

This work is preliminary. It hasn’t been peer reviewed yet and there’s no guarantee that the findings will translate from the dish to the clinic, but the results were still newsworthy enough for some publications that ignored the boob squeezing angle (like NatureScienceNews, Medical Daily and ironically, the Huffington Post US). You might wonder what is so bad about research being mentioned by publications that would normally not bother to cover it. You might argue that it’s a good thing for people who are hooked in by the pictures of breasts to end up reading about some science, given that most of the earlier articles described the science relatively accurately (ignoring the headlines and leads).

My response would be this travesty from MsnNOW (a tip of the hat to Ankur Chakravarthy, who found this first):

Squeezing breasts could prevent cancer, best study ever says

Getting to second base, the holy grail for hormonal boys, is now science: New research has shown that squeezing breasts could prevent malignant breast cells from causing cancer. This doesn’t give pervy dudes license to grope you on the subway, ladies, but it does mean boob-grabbing should be a regular part of your self-care routine (yes, absolutely try it DIY-style). Experiments found that physical pressure led cells back to normal growth patterns, and that even after compression was no longer applied, the malignant cells stopped growing. Spread the word, boob-lovers of the world.

This is the Chinese whisper effect of viral news, with each new aggregator leaving out more and more context until you’re left with only an echo of the original science.

Counting fish

Update: December 10 – I won a travel award! I’m going to ScienceOnline! A hearty thanks to NESCent, and you should all go read the other awesome winning posts – on bed bug ground zero, bee housekeeping, and evolutionary escapes from environmental toxins.

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I’m entering this post in the 2012 NESCent evolution blog contest. The winners get a travel award to attend ScienceOnline 2013!

Pink salmon, Bear Creek by K.Yasui/2011 USFWS Alaska Fish Photo Contest. Shared under this Creative Commons license.

Pink salmon spend two salty years in the ocean before they return to their birthplace to spawn and to die. If that birthplace was Auke Lake, near Juneau, Alaska, then a returning salmon can only reach its final destination by passing through a narrow opening in the weir at Auke Creek, which drains the lake into Auke Bay. Every year, thousands of pink salmon pass through the weir’s trap, both adults fighting upstream and juveniles coasting the other way. Each one of those fish is counted by researchers who stand thigh deep in the cold water, monitoring the trap every day between March and October. This marathon fish count stretches back to the 1970s, and has provided one of the most detailed records of a salmon population anywhere in the world. Combined with a fortuitous little genetic experiment performed at the weir in 1979, the Auke Creek data have also given us some long-sought evidence that the annual rhythms of the natural world are evolving in response to climate change.

Auke Lake is the body of water on the left  and Auke Bay is on the right. Migratory fish that need to move between the two must travel the short creek in between. Photo by Gillfoto, used under this Creative Commons license.

Many things have changed in the decades since the fish counting started. Average stream temperatures are higher by more than one degree celcius, the salmon are returning to the lake nearly two weeks earlier, and the entire migration season falls within a narrower window of time. Although we can’t say for sure that the migration shifts are caused by the temperature change, it falls into a pattern that has been observed for many other organisms all over the world. Birdsbutterflies, frogs, flowers, plankton – to name just a few – are slightly shifting the timing of their big, seasonal life events, all consistent with a response to a warming climate.

But do these timing shifts count as evolution? Without evidence of genetic change in a population, such shifts might be just the result of individuals adjusting within their normal range of behaviors. Genetic evidence to the contrary is extremely hard to come by – so even though biologists have long believed that the many examples of shifting seasonal traits must include some examples of rapid evolution, they haven’t had the hard genetic data to show it.

Luckily, some three decades ago, fisheries biologist Anthony J Garrett started an obscure little experiment at Auke Creek. Recently, that experiment was extended and repurposed by Ryan P Kovach, a graduate student from University of Alaska, Fairbanks, and David A Tallmon of University of Alaska, Southeast, to confirm that the Auke Creek salmon have indeed evolved.

In the 1979 experiment, Garrett tinkered with the genetics of late-migrating salmon just enough to let him trace their fortunes. Historically, the fish counters could distinguish between two relatively distinct populations that migrated about twenty days apart – the “early run” and the “late run.” Interested in these sub-populations, Garrett looked for a gene variant to use as a genetic “marker” for the late-run fish. The genetic marker he chose was naturally present at low levels in the population, but seemed likely to be selectively neutral – neither harming nor helping the fish that bore it. He captured all of the very last migrating pink salmon of the season and only spawned those that carried the genetic marker. The offspring of those fish rejoined the naturally spawned population, and by the time the next generation returned, late-run salmon had a five-fold increased frequency of the genetic marker compared to the early run.

Because all those diligent Auke Creek fish counters in waders were also taking DNA samples throughout the spawning seasons, we know that the frequency of the late-run marker stayed constant for about a decade, confirming that the marker was indeed selectively neutral. The “marked” fish and their descendants kept turning up reliably late until 1989, when stream temperatures during the spawning season reached the second highest on record.

By 1991, the late-run marker had faded back to the low natural levels found in the early-run fish, and in parallel, the fish counters saw a dramatic decrease in the number of salmon turning up late. In a single generation, the distinct late-migrating subpopulation had practically disappeared, making the average migration time of the entire population significantly earlier. In 2011, twenty years later, the data looked much the same as in 1991 – which means the Auke Creek salmon population is probably still dominated by descendants of the 1989 early run.

So this is interesting news for biologists looking for evidence of climate change-driven evolution. But what does it mean for salmon? Today, Auke Creek pink salmon are as abundant as ever, and thanks to that hot 1989 summer, the population is now adapted to a slightly warmer climate. But because of that adaptation process, they are also less genetically diverse and less behaviourally diverse, which means they might not be so lucky when up against other natural selection events in the future. There is also a limit to how early a salmon can spawn. If temperatures continue to rise, at some point Auke Lake could cease to be a viable salmon spawning ground, with effects that would ripple through the region, both ecologically and economically. It would also bring an end to the salmon counting.

Auke Creek Salmon Research. Photo by Alaska Fisheries Science Center, NOAA Fisheries Service (Public domain).

Genetic change for earlier migration timing in a pink salmon population

Ryan P. Kovach, Anthony J. Gharrett and David A. Tallmon

Proc Biol Sci. 2012 Sep 22; 279 (1743):3870-8

Fierce Trees vs. Terrible Birds

This is a story about why lancewoods look more like umbrella carcasses than trees.

Fierce lancewood (Pseudopanax ferox) juvenile in its natural habitat, an NZ Dept. of Conservation carpark. Photo by me.

See what I mean?

This is also about why, after an awkward adolescence of 10-15 years they undergo an ugly-duckling transformation into much more elegant trees with bushy mop-tops.

Mature lancewood (probably the more common species, P. crassifolius). Photo by me.

But first, let’s take a closer look at the juvenile lancewood’s umbrella spines/leaves:

P. ferox juvenile leaf. Photo by Mike Hudson.

That is one unappetising leaf, given that lancewoods evolved in the complete absence of mammals that could eat it.

Part of the reason why New Zealand has such an odd assemblage of plants and animals is because until recently, mammals were never much of a success there. Until 800 years ago, when humans and their beloved pigs and rats arrived, the islands experienced many blissful millions of years of mammal-less natural selection. There were no deer-like browsing animals, or rat-like opportunists, or wolf-like predators. It was this lack of ground predators that led to New Zealand’s most distinctive quirk, the prevalence of flightless birds. Like the Moa.

Giant moa (Dinornis novaezealandiae) skeleton and Richard Owen (he’s the short one in the velvet cape).

There were nine moa species, ranging from a modest, turkey- rhea-sized species, to the giants that inspired paleontologist Richard Owen to name them Dinornis (‘terrible bird’). Giant moa could reach over 3 m (10 ft) and could get about as heavy as a baby grand piano.

The preserved foot of a moa in the genus Megalapteryx, apparently held in the Natural History Museum. Photo by Ryan Baumann.

Despite their nasty-looking claws, moas were herbivores, eating the leaves, fruit, seeds and twigs of many different kinds of plants. They probably exerted a formidable selective pressure on the plants they ate and on the other herbivores they competed with. In other words, all kinds of plants and animals in New Zealand were adapted to life with moas, and one possible example is that scrappy lancewood.

You calling me scrappy? P. crassifoliusjuvenile. Photo by me

The moa/lancewood hypothesis goes like this:

The weirdness of the leaves of lancewood saplings was an adaptation that discouraged moas from eating them. The juvenile leaves would make an awkward meal, even for a giant bird, because they are long, inflexible and have pointy edges. Birds don’t have teeth, don’t chew and have to angle elongated objects down their throats before swallowing, so the whole operation of eating the umbrella carcass phase would have been extremely annoying. To help moas recognise just how annoying, lancewoods have pale patches that highlight each spine, and a racing stripe down the length of each leaf.

Here’s the cool part. Since moas could fly about as well as a baby grand piano, the leaves of a fully-grown lancewood would be permanently out of reach for even the giant moa species. So the strange adaptations that were beneficial to the juvenile were useless to the adult plant, and adult leaves could revert to the ancestral shape and colouration. Adult lancewood leaves are indeed broader, softer, much less spiky and lack the spine ‘highlights’.

But how can we test this idea? Sadly, there are no moas left alive that could be subjected to feeding preference trials. No-one will ever get to see the result of a moa vs. lancewood wrestling match because they were hunted to extinction within a few hundred years of humans arriving. I doubt we will ever get hard evidence supporting/rejecting the hypothesis, but here’s some circumstantial evidence:

  1. Fadzly et al. (2009) found that the spine highlighting should have been quite visible to moas, based on the visual sensitivities of ostriches and other living birds.
  2. Chatham Island was never occupied by moas, but has a native species of lancewood that evolved from the mainland lancewood. However, the island lancewood has mostly lost the umbrella carcass phase. The juvenile leaves don’t have the distinctive stiff, elongated shape and they also don’t have the highlight colours.
  3. The only other hypothesis I consider plausible is that the juvenile leaf form is better adapted for life in the shaded understory, and the adult leaf form is better adapted for life in the canopy. But a comparison of juvenile lancewoods with a related species that lacks the umbrella carcass form found that the spiky lancewoods actually do worse in shady environments (Someone more qualified than me would be a better judge of whether the comparison species they picked was a fair choice – do tell me if you know).

So it seems that the lancewood looks like an umbrella carcass to avoid being eaten by a herbivore that has been dead for 500 years. One of the reasons that I like this story is that it is a visual reminder of one fact about natural selection that we should remember more often. No organism is adapted to its environment; it is adapted to its ancestors’ environment. Just like us.

July was the hottest month on record in the US. Image from NOAA.

We were here

In the early hours of a Monday morning in July 1945, the world’s first atomic bomb test lit up a remote corner of New Mexico. Several weeks later, two more atomic bombs were dropped on large urban centres in Japan. These events marked the beginning of the ‘atomic age,’ but they also marked another beginning, a brief pulse that an experimental biologist would call Time Zero.

Since my post on the ‘natural’ genetics experiment on rescue workers at the World Trade Center site, I’ve been thinking more about the unintentionally brilliant experiments that can emerge from disasters and accidents. One of the most remarkable examples is the so-called bomb-pulse, which is the global isotopic signature left by the atomic bomb tests of the 1950s and 1960s. That signature is found in every living thing on the planet and can now be read back like a ticking clock. It can tell us the birth year of an unidentified murder victim, a vintage wine, your brain cells, fat cells or even the molecules of fat themselves. But it also left an enduring message for future scientists in the geological record. The message says: We were here.

Dog 2 – 19kt, Nevada Test Site, May1951. Image Public Domain, with many thanks to Trinity Atomic Web Site. Click on the photo to visit this fascinating archive of historical documents and media on nuclear weapons.

Before 1945, the global levels of naturally-occurring radioactive isotopes were steady. Between 1955 and 1963, an intense period of cold war-fueled nuclear weapons development caused a sudden increase in the levels of certain isotopes in the atmosphere. This increase came to a sharp end with the signing of the 1963 Partial Test Ban Treaty (PTBT), an agreement that dramatically reduced the number and power of such tests. Bomb pulse testing makes use of the spike in atmospheric levels of the harmless isotope carbon-14 (14C), which doubled between 1945 and 1963. 14C is normally produced at a low rate by the action of cosmic rays in the upper atmosphere, but 99% of the carbon on earth is in the non-radioactive 12C form. The ratio between 14C and 12C levels in living things reflects that of the atmosphere. Plants take up the 14C and 12C in the form of carbon dioxide, convert it into sugars, are eaten by animals, who in turn may be eaten by other animals.

We can estimate the ‘birth date’ of molecules within a living thing because the levels of 14C have been decreasing at a steady rate since 1963. This regular decrease is due to the gradual dissipation of the isotope into the ocean and into living things, as well as dilution due to the burning of fossil fuels (which are rich in 12C). By comparing the historical records of atmospheric  14C ratios to the ratios in say, a vintage bottle of Australian red, we can determine the year in which the grapes were grown. Similarly, the 14C ratio of the tooth enamel of an unidentified body can tell us their year of birth to an accuracy of less than two years. We can do this because the enamel is only formed at very specific times in childhood.

But most of our bodies are not made of permanent structures like tooth enamel.  We are each a colony of different kinds of cells that are constantly growing, dying, and renewing. The bomb pulse allows us to measure the birth and lifespans of these different kinds of cells, giving us an average ‘age’ for the different cells of our body. To do this, we measure the 14C ratio of the DNA molecules in each cell, since DNA is made only at the time the cell is first formed (during cell division). Many of the discoveries made using this technique have settled acrimonious debates or overturned long-held models. For instance, it showed that the neurons of your neocortex (the ‘brainiest’ bit of our brain) have the same birthday as you do.  In other words, you’re stuck with the neurons you were born with (you can read a summary at Not Exactly Rocket Science.) Another (of many) high profile findings of the same group was that you are not stuck with the fat cells you are born with – most fat cells die and are replaced by a new cell about once a decade. Last month, a new study was published that looked at the molecules of fat within those fat cells, and found that their average age was about 1.6 years. They also found that the average age of fat molecules in obese people is about 50% higher than in non-obese people, probably because the rate of fat removal is slower.

As interesting and useful as all these methods are, we are probably only going to be able to use them for another generation or two, since atmospheric 14C levels should be back to their pre-cold war levels by about 2020.  However, there will also be a more long-lived legacy of the bomb pulse: the sudden spike of isotopes in the geological record. The sediments being laid down today will contain organic matter with higher levels of 14C. Will this become a distinct ‘event boundary’ like the iridium-rich K-T boundary that records the arrival of an asteroid and the extinction of (many) dinosaurs? Geologists are currently arguing about that possibility as part of the wider debate about whether to formally recognise a new geological epoch – the Anthropocene. Informally, the Anthropocene designates the modern age, under the hypothesis that human activity has changed the planet as profoundly as many other major geological events. Some geologists argue that the bomb pulse would be the best candidate for the official stratigraphic boundary of the Anthropocene. It’s unambiguous, global, and sharp.

To have a debate about how geologists in the future should classify the evidence of our existence is a charmingly human activity. I look forward to the squabble continuing for some decades. But whatever the outcome of the debate, no matter how long our civilization lasts, whether it flares magnesium bright or fades into the darkness, it will be much, much longer before all traces of our existence are gone. We were definitely here.

Assorted additional information about atomic bombs, atomic bomb tests and atomic bomb pulse testing:

For mere mortals:

An archive of historical material related to nuclear weapons, including an eerie gallery of mushroom cloud photos. And another one at The Atlantic, with more variety and bigger pictures.

An interesting article from Gareth Cook about whether the bombing of Hiroshima and Nagasaki was responsible for the end of WWII: Why did Japan Surrender?

Elizabeth Kolbert explores the Anthropocene in National Geographic.

For mere mortals with access to fancy academic journals beginning with ‘S’:

At Science, read about how Kirsty Spalding, an Australian postdoc, developed the ‘bomb pulse’ dating method by collecting horses heads from the abattoir and analysing the brains with very sensitive isotope detectors.

Also at Science, the Anthropocene debate continues amongst geologists.

The dangers of mongrel viruses

Jim Pipas is a professor in my department and the co-mentor of Sandlin, one of the graduate students in my lab. Because his lab is two floors above ours, I’ve never had much to do with him, but sometimes the things Sandlin says in passing pique my interest.

“No, Jim’s not even here this week. He’s still in Siberia.”

or

“Jim’s having trouble importing his tiger poop.”

Jim studies cancer in the lab using the tumor-causing virus SV40 and I couldn’t figure out why that meant he was always in Borneo or China or Malawi.

Another time, our lab manager was driving us home and started singing along to the CD she was playing.

“I’ve got those SV40 Lab-ratory, undesirous adenovirus, polyoma – Take me homa Blues!”

“What the hell?” I asked.

“It’s Jim and his brother’s band,” she explained.

“What the hell?” I asked again, since I’m never satisfied by explanations.

So when I decided that I should write about someone in my department to give me some practice interviewing people and writing on topics that I have no clue about, I figured this was a good excuse to find out what Jim was up to.

Jim Pipas, Department of Biological Sciences, University of Pittsburgh

Figuring out what he was up to took several interviews and some adventures in suburban bars, but I think I got a good story for The Original. In the process, the editor became so enthusiastic about Jim and his stories that she ended up writing a companion piece about his musical persona, ‘Dr Space’. In fact, we got so many good stories I’m going to have to use this post as the ‘Supplementary Data’ section, to give the full science story.

Let’s start by thinking about your body as a viral landscape. Right now, you are playing host to billions of viruses. If you’re unlucky, you might have the sniffles or some horrific intestinal disease, but more likely you don’t. These viral guests are living quietly in your guts, on your mucus membranes, inside your cells and inside your genome. They live inside the countless bacteria and fungi that have colonized every nook and cranny of your body, as well as the plant cells you are digesting after eating that salad. Some of your viral guests may even be playing host to their own viruses.

And yet you are not the most complex viral landscape in the world. By one estimate, there are a few thousand kinds of viruses in a typical human, compared to a million kinds in a kilogram of seafloor. Jim has started taking stock of this dizzying viral diversity, sampling everywhere from Barcelona sewers to Phillipino bat caves, because he has a radical idea about one way that dangerous new viruses can arise. He thinks that all those millions of kinds of viruses are continually engaged in a haphazard game of gene mix-n-match, in which every so often, one hits the viral jackpot that lets them infect a new kind of host, wreaking havoc on that host’s defenses.

Jim’s radical idea was born from his decades of studying how viruses manipulate hosts. Specifically, he studies how SV40 interacts with its host cells, inadvertently causing them to become cancerous. SV40 is a monkey virus that you might have heard of because millions of people were exposed to it from contaminated polio vaccines in the ’50s. I really wish the top Google hit for “SV40 polio vaccine” was this CDC site, rather than all the conspiracy theory sites. Despite the hysteria, it turns out to be unlikely to cause cancer in humans, although it is quite effective at doing so in non-primate hosts like rodents.

Jim’s specialty is the veritable swiss-army-knife of a protein (T-antigen), that SV40 uses to manipulate its host into replicating the tiny virus genome. Recently, he has branched out to look for proteins in other viruses that are also used to manipulate the host.  Actually ‘other viruses’ is an understatement; what I meant was all other viruses. They have searched all of the several thousand known virus genomes for clues as to which genes encode proteins that interact with host biology. They call these proteins ‘Host Interacting Proteins’ or HIPs, and the possession of certain host-specific HIPs is what allows a virus to infect its chosen host.

But in the process of searching thousands of viral genomes for HIPs, they kept finding evidence for the exchange of HIPs between completely unrelated viruses.

“Gene recombination across different virus families makes no sense, we don’t know how it happens,” he says. This phenomenon is nothing like the relatively orderly process of gene shuffling that gives the flu virus a new edge every year. This is more like genome butchery, with random bits of DNA from one virus being pasted into another’s genome. The strangest thing was that they saw evidence for this process even between viruses that cannot infect the same host cells. Contrary to what is normally assumed, Jim realized that in such gene exchange events, some of the DNA could come from an inactive virus.

“Only one virus has to be able to grow in the cell, the other one just has to be in the cell.”

This means that the viruses of all kinds of different hosts could, in theory, be exchanging genes all the time, until one virus suddenly gains the ability to jump between hosts.

“Is this a mechanism for the emergence of new viruses? And where in nature does this mixing happen?” To answer these questions, Jim and his colleagues are preparing to take environmental samples, isolate all the viral DNA, then sequence everything that comes out. This will give a comprehensive overview of the viral genomes present.

The reason why Sandlin’s accounts of Jim’s travels were always so bizarre was because he used computational prediction to select environments that will favour his ability to detect any viral gene exchange. Because the computational algorithm takes into account features like biodiversity, species density, endemism and animal migration, the list of sites it generated tended towards the exotic. Like Siberia.

“You think of Sibera as frozen tundra,” he says. “I know that’s what you’re thinking. And most of it is.”

But not all of it – in the alpine areas of the South, Siberia offers hot summers followed by bitter cold winters. One of the potential sites in Siberia is Lake Chany, an enormous shallow marsh that is a summer destination for migratory birds arriving from Africa and Asia. The area swarms with biting insects that feed on the summer visitors, as well as the local wildlife, all of which conveniently defecate into the waters of the lake. In contrast, another of their potential Siberian sites is much more biologically isolated; Lake Baikal is the largest freshwater lake in the world, but 40% of the species found there are found nowhere else. By choosing a variety of sites with different kinds of hosts, they hope to more easily spot gene exchange between very different kinds of viruses. Jim has spent several years visiting the sites, establishing collaborations with local scientists that can help collect and process the samples.

But even once the samples start arriving, the most challenging aspect will still be ahead of them: analyzing all the sequence data to find evidence for gene exchange. To test their sampling methods and start developing the computational tools for analysis, Jim and his lab have sequenced raw sewage from Ethiopia, Barcelona and Pittsburgh. So far they have identified 234 known viruses, which is almost 10% of all viruses ever detected previously. But they also found between 10,000 and 50,000 times as many kinds of unknown viruses. Most of them are viruses that infect bacteria, and 90% of the rest are plant viruses. Yes, that’s right, plant viruses. Apparently, animal stools typically contain enormous numbers of plant viruses from the animal’s diet. But because Jim thinks that gene exchange between different virus families doesn’t require infection, these plant viruses are fair game for their hunt for evidence of these events. What kind of evidence might he find?

Eastern Barred Bandicoot, Australia. Wikimedia commons, http://www.noodlesnacks.com/

Take the virus that has been ravaging a cute, but endangered, Australian marsupial called the Bandicoot. Efforts to protect the dwindling Bandicoot population have been hampered by the rapid spread of a viral disease that results in debilitating skin cancer-like masses. When scientists isolated the virus causing all the trouble they found a curious mongrel between a papillomavirus and a polyomavirus. Papillomaviruses, like the human virus linked to cervical cancer, are sometimes associated with cancer-like diseases. In contrast, polyomaviruses are mostly well-behaved house guests, only causing disease in hosts with compromised immune systems. The splicing of new combinations of genes in the Bandicoot virus gave it the structure of a papillomavirus, but also bestowed it with a protein closely related to SV40′s T-antigen, the protein that causes cancer in SV40-infected mice.

To understand why such mixed-up viruses might be so dangerous, you need to consider how viruses make their host sick. If you remember your high school biology, you might be tempted to say it’s because viruses lyse the cells in which they reproduce in order to escape and spread to new cells and new hosts. But in most cases the loss of these cells is insignificant; the real culprit behind the wooziness/snot/tingles/headaches/what-have-you is your own body’s response to invasion.

So in the case of a virus that has been co-evolving with its host, its ability manipulate the biology of the host has been finely tuned; some viruses benefit from disease symptoms like coughing and sneezing, but most do best by keeping their heads down and escaping immune system surveillance. A virus that has suddenly been bestowed with a magical new HIP that allows it to infect a new host has evolved for a totally different environment, and is likely to cause all kinds of problems as it starts interacting with host biology in all kinds of new ways.