Last week, I told you about the US Supreme Court ruling that made it illegal to patent naturally occurring DNA. In that article, I talked briefly about the fact that the new ruling doesn't cover all DNA. It's still perfectly legal to patent synthetic DNA, and the court documents referred specifically to complementary DNA (aka cDNA).

This is where things get murky. Complementary DNA is a thing that can be both natural and synthetic. And, as a laboratory creation, it's an important step in a common method of replicating naturally occurring DNA. All of which leaves some holes in the idea that the Supreme Court ruling is a simple "win" for open-access science, patent activists, and patients. After all, if you can't patent a gene, but you can patent the laboratory copy of the gene, what's that mean? It's sort of like not being able to patent a novel, but being able to patent a copy of its contents that's had all the white space removed. It seems like everybody is a bit confused by this. So I wanted to take a moment to at least clarify what cDNA is and what some people, on different sides of the science/law/biotech divides, are thinking about it.

It starts with some stuff you learned back in junior high — how information from your DNA gets turned into actual working proteins.

DNA, you'll remember, is like a twisted ladder, a double helix. Split the ladder in half, add a few chemical changes, and you get RNA.* This molecule can do many things, but one of the big ones is moving genetic information from DNA to ribosomes, the cellular factories that build proteins. To do that, you need a special kind of RNA, messenger RNA (mRNA). This is basically just a condensed version of your genetic information — half a strand of DNA, but with all the bits that don't build proteins snipped out.

It's sort of like taking

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But scientists have another use for mRNA. If they want to make lots of copies of a specific gene, they can essentially put the mRNA in reverse, using it to create a whole strand of DNA. This lab-created DNA is nearly identical to the stuff that occurs naturally. The only difference is that, like the mRNA, it's lacking all the stuff that doesn't build proteins. And that is what counts as cDNA. Just to clarify, according to the ruling last week, you can't patent the DNA for

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That fact has left a lot of people with a lot of confusion about what this ruling will actually mean in the real world.

At The LA Times, Amina Kahn reported that Myriad Genetics — the company that had claimed a patent on two genes involved in breast cancer risk, and which ostensibly lost at the Supreme Court — actually saw their stock price go up in the wake of the ruling. That could be because a big, profit-affecting question (Can the company patent the genes?) got solved and, now, the company could turn around and patent cDNA versions of the genes. Sure, they lose some of their monopoly on the breast cancer industry, but they still have something special and aren't totally out of the game, financially. In fact, with a Supreme Court ruling in their pocket, Myriad's business model may now be more stable, since what they can and can't do is now more spelled out.

That seems to be a perspective shared by biotech consultant Susan Finston. The ruling, she writes, does open up the market to allow more companies to sell their own tests for breast cancer risk — but it's also not some kind of wide-scale smack down against the biotech industry.

All in all, the Myriad decision should not adversely affect the patentability of a broad swath of gene-based inventions. The ability of a patent applicant to avoid the law of nature exception, i.e, to “create or alter” DNA – whether via cDNA or through use of plasmids – limits the prospective impact of the case.

On the other hand, Myriad shouldn't get too comfortable in its new position, writes Lyle Denniston at the SCOTUS blog.

The opinion said in a footnote, however, that the Court was not actually ruling that cDNA is specifically entitled to a composition patent, and noted that the federal government had raised other objections under patent law to that phenomenon.

In fact, Justice Scalia's wrote a side note saying that he, himself, couldn't make any statements on the science beyond the simple fact that naturally occurring DNA is not something that a company creates, and thus, is not patentable. That's been interpreted by some people (including some of the commenters on the story last week) as an expression of some anti-science "I don't believe in DNA" position. But I'm not sure it is. Denniston, for instance, interprets it as something closer to Scalia saying that has absolutely no idea whether he believes DNA and cDNA should count as different things — he simply doesn't know enough about the science to say. And that's actually a pretty reasonable position to take. Especially when you consider the fact that cDNA can happen in nature, without the help of scientists. HIV, for example, can turn its own RNA into cDNA. That's how it makes copies of itself.

Taken all together, it's safe to assume that this is not the last time the Supreme Court will be talking about the patentability of cDNA. This is not a given yet.

The basic lesson that you should take away seems to be this: The Myriad Genetics ruling is really, really narrow. Yes, it prevents companies from patenting a gene that they just happened to find in the human body (or anyplace else). But it leaves plenty of room to patent genetic information — and it leaves plenty of room for future court battles over what genetic information can and cannot be patented. This is a big court case that only reduced uncertainty a tiny bit.

When James Joyce wrote in Ulysses: “A man of genius makes no mistakes. His errors are volitional and are the portals of discovery,” he meant the first part of the statement to be provocative. History has shown us that even some of the greatest scientific luminaries, towering figures such as the naturalist Charles Darwin, the twice-Nobel-Laureate chemist Linus Pauling, and the embodiment of genius — Albert Einstein — have made some serious blunders.

In Darwin’s case, he did not realize that with the theory of heredity prevailing at his time, natural selection simply could not work. Basically, the then-held belief stated that the characteristics of the two parents become physically blended in their offspring, just as in the mixing of paints, or of gin and tonic. If that were true, however, then any variation would have been inevitably lost, as all the extreme types would have vanished rapidly into some intermediate mean. Imagine, for instance, a population of one thousand white cats and one black cat. Additionally, suppose that being black confers some evolutionary advantage. In the “paint-pot theory,” the first offspring of the black cat with a white partner would be gray, and continuous mating with white cats would result in increasingly paler shades of gray. There was no way for the black cat to turn the entire population black after many generations, no matter how advantageous the black color might have been, contrary to Darwin’s vision of evolution by means of natural selection.

The solution to this problem came in the form of Gregor Mendel’s particulate genetics. In categorical contrast to blending, Mendel’s theory stated that the genes are discrete entities that are passed on unchanged to the next generation. In this sense, genetics resembles the shuffling together of two decks of cards rather than the mixing of paints — a Jack remains a Jack, no matter how many times you shuffle.

Continuing on the topic of life on Earth, Linus Pauling’s blunder concerned an ill-fated model for DNA. Having previously had enormous success in deciphering the structure of proteins, Pauling turned his attention to DNA in earnest only in November of 1952. Yet, just about one month later, he already came up with what he considered a viable model for the molecule. His model contained three helical strands (as opposed to the later, correct model by Watson and Crick, which was a double helix), was built inside-out, and was patently unstable because all the negative charges were concentrated at its center and would have driven the structure apart. How was it possible that the world’s greatest chemist would come up with such an incorrect model? There were many, fairly complex reasons for Pauling’s blunder, but largely it was hubris. Pauling fell victim to his own earlier success — a victory against a rival group of researchers — which made him feel infallible. In the words of Nobel Laureate Maurice Wilkins: “Pauling just didn’t try. He can’t really have spent five minutes on the problem himself.”

Finally, from the evolution of life we come to the evolution of the universe as a whole. Einstein’s blunder reminds us all that human logic is not mistake proof, even when exercised by a monumental genius. What was Einstein’s blunder? In 1917 Einstein first attempted to understand the entire cosmos in light of his theory of General Relativity. At the time, Einstein was convinced that the universe was unchanging and static on its largest scales. However, since he knew that every mass in the universe gravitationally attracts every other mass, he concluded that he needed to add something to prevent the universe from collapsing under its own weight. To achieve a static configuration, Einstein introduced a “fudge factor” into his equations, creating a repulsive force that precisely balanced gravity. This term became known as the “cosmological constant.” In the late 1920s, however, cosmologist Georges Lemaître and astronomer Edwin Hubble discovered that our universe is in fact expanding. Einstein realized that in an expanding universe gravity would simply slow the expansion down, just as the Earth’s gravity slows down the motion of a ball thrown upward, and no precise balance was needed. He therefore removed the cosmological constant from his equations, even though the theory definitely allowed for its inclusion, and for the rest of his life regretted having introduced it in the first place. Things took an unexpected turn in 1998, when two groups of astronomers discovered that not only is the cosmic expansion not slowing down, it is in fact speeding up. Moreover, the acceleration appears to be driven precisely by Einstein’s cosmological constant! So Einstein’s blunder was not the introduction of this term, rather it was its removal. For some geniuses, what initially appears to be a mistake can turn out to be great insight.

Despite their blunders, and perhaps even because of them, the individuals I have sketched here (and others, all of whom I describe more fully in Brilliant Blunders), have catalyzed great innovations. The impact of their ideas has been felt across all aspects of the evolution of life on Earth, of the Earth itself, of stars, and of the universe as a whole. But the blunders and the reactions of these geniuses to them have also demonstrated something that modern neuroscientists have concluded: that humans are not purely rational beings capable of completely turning off their emotions. Rather, our brains integrate emotions into the stream of rational thought.

Buy Brilliant Blunders: From Darwin to Einstein - Colossal Mistakes by Great Scientists That Changed Our Understanding of Life and the Universe

In an unanimous decision, the United States Supreme Court ruled today that companies can't patent genes, or parts of genes — at least, so long as that genetic material is identical to what occurs in nature. The lawsuit dealt specifically with Myriad Genetics, the company that isolated and has claimed a patent on BRCA 1 and BRCA 2 — genes associated with an increased risk of breast and ovarian cancers. From a practical perspective, Myriad's hold on the genes has meant that tests for genetic cancer risk are strikingly expensive — Xeni paid more than $3000 for hers. It's also meant that, if you get a positive result, there's been nowhere you could go for a second opinion.

That's a big deal. Mutations in the BRCA 1 and 2 genes mean an increased risk of cancer, but there's more than one kind of mutation that can happen. In fact, BRCA 1, alone, has hundreds of known mutations. Some increase your risk of cancer. But, even if you narrow it down to just those, they don't all increase the risk by the same amount. The health choices you make could be very different depending on whether you have an 80% risk of developing breast cancer by age 90 (the worst-case scenario for BRCA 1 mutations), or something much lower. That's the kind of situation where you might really like to have more than one lab run more than one kind of test.

This ruling opens the door for that, and the competition should (theoretically) also lower the cost.

It's worth noting that the ruling does not apply to synthetically created DNA, which, based on the Myriad context, seems to apply to lab-created genes that are different from what happens in nature, as opposed to lab-created versions of natural genes (Myriad had previously cloned BRCA 1 and BRCA 2). For a little more clarity on what does not fall under the scope of this ruling, here's a quote from Justice Clarence Thomas' description of the Court's decision. It's the cDNA Thomas describes here that would still be patentable.

DNA’s informational sequences and the processes that create mRNA, amino acids, and proteins occur naturally within cells. Scientists can, however, extract DNA from cells using well known laboratory methods. These methods allow scientists to isolate specific segments of DNA—for instance, a particular gene or part of a gene—which can then be further studied, manipulated, or used. It is also possible to create DNA synthetically through processes similarly well known in the field of genetics. One such method begins with an mRNA molecule and uses the natural bonding properties of nucleotides to create a new, synthetic DNA molecule. The result is the inverse of the mRNA’s inverse image of the original DNA, with one important distinction: Because the natural creation of mRNA involves splicing that removes introns, the synthetic DNA created from mRNA also contains only the exon sequences. This synthetic DNA created in the laboratory from mRNA is known as complementary DNA (cDNA).

Read More:
• The Washington Post on the Court decision
• The full Supreme Court decision itself
• Rebecca Skloot, who literally wrote the book on the ethics of genes and genes patents, is answering questions at Facebook.

Boldly going where nobody's gone before. In a lot of ways, that idea kind of defines our whole species. We travel. We're curious. We poke our noses around the planet to find new places to live. We're compelled to explore places few people would ever actually want to live. We push ourselves into space.

This behavior isn't totally unique. But it is remarkable. So we have to ask, is there a genetic, evolution-driven, cause behind the restlessness of humanity?

At National Geographic, David Dobbs has an amazing long read digging into that idea. The story is fascinating, stretching from Polynesian sailors to Quebecois settlers. And it's very, very good science writing. Dobbs resists the urge to go for easy "here is the gene that does this" answers. Instead, he helps us see the complex web of genetics and culture that influences and encourages certain behaviors at certain times. It's a great read.

Not all of us ache to ride a rocket or sail the infinite sea. Yet as a species we’re curious enough, and intrigued enough by the prospect, to help pay for the trip and cheer at the voyagers’ return. Yes, we explore to find a better place to live or acquire a larger territory or make a fortune. But we also explore simply to discover what’s there.

“No other mammal moves around like we do,” says Svante Pääbo, a director of the Max Planck Institute for Evolutionary Anthropology in Leipzig, Germany, where he uses genetics to study human origins. “We jump borders. We push into new territory even when we have resources where we are. Other animals don’t do this. Other humans either. Neanderthals were around hundreds of thousands of years, but they never spread around the world. In just 50,000 years we covered everything. There’s a kind of madness to it. Sailing out into the ocean, you have no idea what’s on the other side. And now we go to Mars. We never stop. Why?”

Why indeed? Pääbo and other scientists pondering this question are themselves explorers, walking new ground. They know that they might have to backtrack and regroup at any time. They know that any notion about why we explore might soon face revision as their young disciplines—anthropology, genetics, developmental neuropsychology—turn up new fundamentals. Yet for those trying to figure out what makes humans tick, our urge to explore is irresistible terrain. What gives rise to this “madness” to explore? What drove us out from Africa and on to the moon and beyond?

Read the full story

When scientists from the Leibniz Institute of Plant Genetics and Crop Plant Research in Germany sequenced the genome of barley, they were thinking primarily about the impact on food. Understanding the genetics behind certain traits could help us breed barley varieties that have built-in resistance against disease, or that contain more fiber. (Contrary to popular understanding, there's actually a lot of overlap between what we might think of as genetic engineering and what we might think of as breeding. Crop researchers can use genome maps to select specific plants to cross pollinate, enabling them to reliably breed a trait into a new variety much faster than was previously possible.)

But, this is barley. And we don't just eat barley. With this plant, sequencing the genome also has implications for the way we brew beer. At Popular Science, Martha Harbison explains what we're learning about barley's genetic code and why it matters in beer making. In particular, she says it's significant that the researchers sequenced the genomes of more than one variety of barley.

Why should aspiring homebrewers care? Because two-row and six-row barley behave slightly differently in the mash, which can have profound effects on brewing efficiency and characteristics of the finished beer (a complex phenomenon I'll get into in a future column). I figured anyone nerdulent enough to want to know about genetic differences of cultivars would be curious as to which kind of barley was used in the single-nucleotide-variation study.

Read the rest of the story at Popular Science

You can read more about the surprisingly complex world of plant breeding in two articles I wrote — one for Popular Science, and one for Discover.

The cost of genome sequencing is starting to sink into the affordable range. (In comparison to its previous cost. We're talking "within reach" the same way Design Within Reach uses the phrase.)

Companies are starting to claim that a $1000 personal genome sequence is on the horizon. But what does that mean for you? Should you save up and get one? Can it really tell you anything meaningful at all? Who is going to sift through all the information your genome represents — and how will they do it?

Tonight, starting at 7:00 Eastern, Science Online New York City is hosting a round-table to discuss these issues, especially the problems associated with collecting, making sense of, and protecting a massive new stream of personal data. The live event is sold out, but you can watch whole thing streaming online.

Panelists: Ronald Crystal, the Chairman of the Department of Genetic Medicine at Weill-Cornell Medical College, who has had his genome sequenced and analyzed it himself. Virginia Hughes, a freelance author who has written about her experience with the 23andMe genotyping service. Manish Ponda of Rockefeller University, who has experimented with other -omic type analyses.

SoNYC's livestream feed

In this case, Haskell v. Harris, the ACLU of Northern California is challenging the California law, arguing that it violates constitutional guarantees of privacy and freedom from unreasonable search and seizure.  This is the first court hearing to address DNA privacy since the research on “junk” DNA has become widely known, and in its role as amicus, EFF asked the court to consider the ground-breaking new research.  The oral argument is open to the public at the federal courthouse at 95 7^th Street in San Francisco.  The hearing starts at 10am, in courtroom 1 on the third floor.

Wednesday Hearing in 9th Circuit Tackles DNA Privacy ]]> http://boingboing.net/2012/09/19/court-to-hear-argument-on-the.html/feed 1 http://boingboing.net/2012/09/13/for-the-last-time-redheads-ar.html http://boingboing.net/2012/09/13/for-the-last-time-redheads-ar.html#comments Thu, 13 Sep 2012 16:09:51 +0000 Maggie Koerth-Baker http://boingboing.net/?p=180821 Pictured: Your great-grandchildren? As a redheaded science journalist, I hear this "fact" a lot. Reality is, though, we aren't going anywhere.]]>

As a redheaded science journalist, I hear this "fact" a lot. Reality is, though, we aren't going anywhere. Yes, as Cara Santa Maria points out at Huffington Post, redheads represent only about 1% of the world's population. And this hair color is related to a recessive gene. Both your parents have to have a copy in order for you to be a redhead, so a redheaded person can have non-redheaded babies. But that's not the same thing as going extinct. Because here's our little secret: We redheads are stealthily infiltrating the rest of humanity. Only 1% of humans are redheads, but 4% of humans carry a copy of the gene that makes redheads. You could be a carrier and not even know it. So could your spouse. Two redheads are unlikely to make a brunette, but two brunettes can make a redhead. Good luck wiping us out. *Insert evil laughter here*

You can learn more about this at Cara Santa Maria's Talk Nerdy To Me vidcast, but I'll add a little piece of anecdata, too. My parents are both brunettes. So were their parents. I am largely an anomaly on both sides of my family. In fact, besides my brother and I, the only other redhead in my Mom's entire family (that anyone remembers) was her grandfather. And yet still, we rise.

How Stuff Works also has a great debunking of the redhead extinction myth

Some more info on how redheads are in yer genome, gingerin' yer descendants from the Stanford University Tech Museum

If you've read anything in the past week about ENCODE—a group of laboratories that recently published their latest work on the human genome—then you need to read John Timmer's excellent piece over at Ars Technica.

What ENCODE has actually done, and why it matters, has been widely misrepresented in the mainstream press—largely because of misleading press releases put out by ENCODE, itself. Timmer sets the record straight. It's a long read, but a fascinating one. Highly recommended.

This week, the ENCODE project released the results of its latest attempt to catalog all the activities associated with the human genome. Although we've had the sequence of bases that comprise the genome for over a decade, there were still many questions about what a lot of those bases do when inside a cell. ENCODE is a large consortium of labs dedicated to helping sort that out by identifying everything they can about the genome: what proteins stick to it and where, which pieces interact, what bases pick up chemical modifications, and so on. What the studies can't generally do, however, is figure out the biological consequences of these activities, which will require additional work.

Yet the third sentence of the lead ENCODE paper contains an eye-catching figure that ended up being reported widely: "These data enabled us to assign biochemical functions for 80 percent of the genome." Unfortunately, the significance of that statement hinged on a much less widely reported item: the definition of "biochemical function" used by the authors.

This was more than a matter of semantics. Many press reports that resulted painted an entirely fictitious history of biology's past, along with a misleading picture of its present. As a result, the public that relied on those press reports now has a completely mistaken view of our current state of knowledge (this happens to be the exact opposite of what journalism is intended to accomplish). But you can't entirely blame the press in this case. They were egged on by the journals and university press offices that promoted the work—and, in some cases, the scientists themselves.

Read the rest of John Timmer's story at Ars Technica

Image: Micah's DNA, a Creative Commons Attribution Share-Alike (2.0) image from micahb37's photostream

When you have been diagnosed with cancer, as I have, you quickly grow accustomed to "friendly cancer spam." Friends, relatives, and well-meaning acquaintances routinely forward you a gazillion identical links to whatever this week's hot cancer news headline may be.

So it was for me with this New York Times story on Lukas Wartman, a leukemia doctor and researcher at Washington University who developed leukemia. As he faced death last Fall, his cancer genome was sequenced by his colleagues.

What was revealed then led to a treatment plan that targeted the specifics of his genetic makeup. And so far, according to Gina Kolata's report, that experimental treatment plan has been an amazing success. Snip:

Dr. Ley’s team tried a type of analysis that they had never done before. They fully sequenced the genes of both his cancer cells and healthy cells for comparison, and at the same time analyzed his RNA, a close chemical cousin to DNA, for clues to what his genes were doing.

The researchers on the project put other work aside for weeks, running one of the university’s 26 sequencing machines and supercomputer around the clock. And they found a culprit — a normal gene that was in overdrive, churning out huge amounts of a protein that appeared to be spurring the cancer’s growth.

Even better, there was a promising new drug that might shut down the malfunctioning gene — a drug that had been tested and approved only for advanced kidney cancer. Dr. Wartman became the first person ever to take it for leukemia.

And now, against all odds, his cancer is in remission and has been since last fall. While no one can say that Dr. Wartman is cured, after facing certain death last fall, he is alive and doing well.

Suffice it to say that this stuff is relevant to my interests. It is routine for breast cancer patients like me to receive genetic screening for the BRCA mutation, and sometimes a few additional known genetic factors. But there is so much that we do not know, and a growing sense that this infinite array of genetic unknowns could lead to more saved lives, and better quality of life for those of us who have been diagnosed with the disease.

I know I'm not alone in feeling like the treatment I am receiving now will one day be perceived as blunt and barbaric, when genetically-targeted therapies like the ones outlined in these stories become the norm. Those of us undergoing the brutal routine of chemo, radiation, and surgery to keep cancer at bay long for the day when more precise technologies can stop the disease without so much collateral damage.

And then, there is the greater hope that maybe one day all of this will lead to the other "c-word."

A cure.

Read the full article: "In Treatment for Leukemia, Glimpses of the Future."

Part two in the series: "A New Treatment’s Tantalizing Promise Brings Heartbreaking Ups and Downs"

And part three: "A Game Changer in Revealing a Cancer’s Prognosis."

There is a related item in the Economist. Here is the referenced study in the journal Nature from researchers at Washington University.

(image: Shutterstock)]]> http://boingboing.net/2012/07/09/nyt-series-on-genetic-targeted.html/feed 49 http://boingboing.net/2012/06/26/probably-false-article-claims.html http://boingboing.net/2012/06/26/probably-false-article-claims.html#comments Tue, 26 Jun 2012 17:01:17 +0000 Cory Doctorow http://boingboing.net/?p=167691 Melbourne Herald-Sun, quoting an unlinked article in the UK Mirror (a truly awful tabloid) claims that Madonna has a DNA cleanup crew who sterilize all the surfaces and vacuum all skin cells and hair follicles after Madonna uses a dressing room, to prevent fans from getting hold of her genetic material.]]> An report in the Melbourne Herald-Sun, quoting an unlinked article in the UK Mirror (a truly awful tabloid) claims that Madonna has a DNA cleanup crew who sterilize all the surfaces and vacuum all skin cells and hair follicles after Madonna uses a dressing room, to prevent fans from getting hold of her genetic material. Given the stupid provenance, it's almost certainly not true, but it's a great plot-point for some future science fiction story.

Madonna thinks fans want her DNA | Herald Sun (via Kottke) ]]> http://boingboing.net/2012/06/26/probably-false-article-claims.html/feed 47 http://boingboing.net/2012/06/04/open-source-human-genomes.html http://boingboing.net/2012/06/04/open-source-human-genomes.html#comments Mon, 04 Jun 2012 16:05:47 +0000 Maggie Koerth-Baker http://boingboing.net/?p=164618 a World Science Festival panel on human origins and why our species outlasted other species of Homo, geneticist Ed Green mentioned that there were thousands of sequenced human genomes, from all over the world, that had been made publicly available.]]> Yesterday, during a World Science Festival panel on human origins and why our species outlasted other species of Homo, geneticist Ed Green mentioned that there were thousands of sequenced human genomes, from all over the world, that had been made publicly available. Our code is open source.

But where do you go to find it? Several folks on Twitter had great suggestions and I wanted to share them here.

The 1000 Genomes Project—organized by researchers at the Wellcome Trust, the National Institutes of Health, and Harvard—is working on sequencing the genomes of 2500 individuals. The data they've already collected is available online. Read a Nature article about The 1000 Genomes Project: Data management and community access.

The Personal Genome Project is interactive. Created by a researcher at Harvard Medical School, the program is aimed at enrolling 100,000 well-informed volunteers who will have their genomes sequenced and linked to anonymized medical data. Everything that's collected will be Creative Commons licensed for public use.

The University of California Santa Cruz Genome Browser is a great place to find publicly available genomes and sequences.

"My Favorite Museum Exhibit" is a series of posts aimed at giving BoingBoing readers a chance to show off their favorite exhibits and specimens, preferably from museums that might go overlooked in the tourism pantheon. I'll be featuring posts in this series all week. Want to see them all? Check out the archive post. I'll update the full list there every morning.

From Australia's McLeay Natural History Museum at Sydney University comes ... dun dun dun ... the Cyclops!

Sorry. I've got a bit of THE TRIUMPH OF MAN stuck in my head. Actually, this skull belonged to a foal, says Justin Cahill, who sent in the photos. It's part of a long, natural history museum tradition of exhibiting the weird and often grotesque, preserving them as examples of how the natural way isn't always ideal. The same forces that shape evolution can also seriously screw you up. So much of what we call "normal" is based on chance.

Nobody ever actually saw this foal alive, by the way. The skull was found in the Hawkesbury River in 1841. But there have been attempts to reconstruct what the horse might have looked like during it's brief time alive. You can see that photo after the cut:

National Geographic has a really interesting story on what we can learn about human biology and human culture from studying the lives of twins. (Last week, Mark blogged about some of the photos in the story.) The story explains the chance beginnings of the now-massive Minnesota Study of Twins Reared Apart; introduces you to twin girls from China who were adopted by two different Canadian families that now work to keep the girls in each other's lives; and delves into what we know and don't know about why some identical twins are different from each other in very conspicuous ways.

One example of this last bit is the story of Sam and John, identical twin brothers. Both are on the autism spectrum, but they appear to be on entirely different parts of that spectrum, with John experiencing much more severe symptoms that led the boy's parents to enroll him in a special school. Why would identical twins, raised in the same family, have such an obvious difference in the expression of characteristics that are probably mostly inherited? That's where epigenetics comes in.

A study of twins in California last year suggested that experiences in the womb and first year of life can have a major impact. John's parents wonder if that was the case with him. Born with a congenital heart defect, he underwent surgery at three and a half months, then was given powerful drugs to battle an infection. "For the first six months, John's environment was radically different than Sam's," his father says.

Shortly after Sam and John were diagnosed, their parents enrolled them in a study at the Kennedy Krieger Institute in Baltimore. Blood samples from the boys were shared with a team at nearby Johns Hopkins University looking into the connection between autism and epigenetic processes—chemical reactions tied to neither nature nor nurture but representing what researchers have called a "third component." These reactions influence how our genetic code is expressed: how each gene is strengthened or weakened, even turned on or off, to build our bones, brains, and all the other parts of our bodies.

If you think of our DNA as an immense piano keyboard and our genes as keys—each key symbolizing a segment of DNA responsible for a particular note, or trait, and all the keys combining to make us who we are—then epigenetic processes determine when and how each key can be struck, changing the tune being played.

A study at Nanjing University in China found that ingested "microRNA" (very small pieces of ribonucleic acid, or RNA) from plants were able to survive digestion and influence the function of human cells.

Food columnist Ari Levaux has a piece digging into the implications, in The Atlantic. The basic idea: if this research stands up to the rigors of scientific scrutiny, it could prove that when we eat food, we consume not just fuel and nutrients, but information that changes us on a cellular level, and influences health.

Snip:

Monsanto's website states, "There is no need for, or value in testing the safety of GM foods in humans." This viewpoint, while good for business, is built on an understanding of genetics circa 1950. It follows what's called the "Central Dogma" (PDF) of genetics, which postulates a one-way chain of command between DNA and the cells DNA governs.

The Central Dogma resembles the process of ordering a pizza. The DNA knows what kind of pizza it wants, and orders it. The RNA is the order slip, which communicates the specifics of the pizza to the cook. The finished and delivered pizza is analogous to the protein that DNA codes for.

We've known for years that the Central Dogma, though basically correct, is overly simplistic. For example: Pieces of microRNA that don't code for anything, pizza or otherwise, can travel among cells and influence their activities in many other ways. So while the DNA is ordering pizza, it's also bombarding the pizzeria with unrelated RNA messages that can cancel a cheese delivery, pay the dishwasher nine million dollars, or email the secret sauce recipe to WikiLeaks.

Monsanto's claim that human toxicology tests are unwarranted is based on the doctrine of "substantial equivalence." This term is used around the world as the basis of regulations designed to facilitate the rapid commercialization of genetically engineered foods, by sparing them from extensive safety testing.

via The Very Real Danger of Genetically Modified Foods - The Atlantic. You'll also want to read the actual study, and make up your own mind.

Update: Here's a critical take on the linked-to Atlantic piece. Ari responds here.

(via @coopportunity)