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Dead for 32,000 Years, an Arctic Plant Is Revived
By NICHOLAS WADE
Article #1
Published: February 20, 2012
Living plants have been generated from the fruit of a little arctic flower, the narrowleafed campion, that died 32,000 years ago, a team of Russian scientists reports.
The fruit was stored by an arctic ground squirrel in its burrow on the tundra of
northeastern Siberia and lay permanently frozen until excavated by scientists a few
years ago.
Enlarge This Image
Svetlana Yashina
OLD DNA A plant has been generated from the fruit of the narrow-leafed campion.
It is the oldest plant by far to be grown from ancient tissue.
This would be the oldest plant by far that has ever been grown from ancient tissue.
The present record is held by a date palm grown from a seed some 2,000 years old
that was recovered from the ancient fortress of Masada in Israel.
Seeds and certain cells can last a long term under the right conditions, but many
claims of extreme longevity have failed on closer examination, and biologists are
likely to greet this claim, too, with reserve until it can be independently confirmed.
Tales of wheat grown from seeds in the tombs of the pharaohs have long been
discredited. Lupines were germinated from seeds in a 10,000-year-old lemming
burrow found by a gold miner in the Yukon. But the seeds, later dated by the
radiocarbon method, turned out to be modern contaminants.
Despite this unpromising background, the new claim is supported by a firm
radiocarbon date. A similar avenue of inquiry into the deep past, the field of ancient
DNA, was at first discredited after claims of retrieving dinosaur DNA proved
erroneous, but with improved methods has produced spectacular results like the
reconstitution of the Neanderthal genome.
The new report is by a team led by Svetlana Yashina and David Gilichinsky of the
Russian Academy of Sciences research center at Pushchino, near Moscow, and
appears in Tuesday’s issue of The Proceedings of the National Academy of
Sciences of the United States of America.
“This is an amazing breakthrough,” said Grant Zazula of the Yukon Paleontology
Program at Whitehorse in Yukon Territory, Canada. “I have no doubt in my mind
that this is a legitimate claim.” It was Dr. Zazula who showed that the apparently
ancient lupine seeds found by the Yukon gold miner were in fact modern.
But the Russians’ extraordinary report is likely to provoke calls for more proof.
“It’s beyond the bounds of what we’d expect,” said Alastair Murdoch, an expert on
seed viability at the University of Reading in England. When poppy seeds are kept
at minus 7 degrees Celsius, the temperature the Russians reported for the campions,
after only 160 years just 2 percent of the seeds will be able to germinate, Dr.
Murdoch noted.
The Russian researchers excavated ancient squirrel burrows exposed on the bank of
the lower Kolyma River, an area thronged with mammoth and woolly rhinoceroses
during the last ice age. Soon after being dug, the burrows were sealed with
windblown earth, buried under 125 feet of sediment and permanently frozen at
minus 7 degrees Celsius.
Some of the storage chambers in the burrows contain more than 600,000 seeds and
fruits. Many are from a species that most closely resembles a plant found today, the
narrow-leafed campion (Silene stenophylla).
Working with a burrow from the site called Duvanny Yar, the Russian researchers
tried to germinate the campion seeds, but failed. They then took cells from the
placenta, the organ in the fruit that produces the seeds. They thawed out the cells
and grew them in culture dishes into whole plants.
Many plants can be propagated from a single adult cell, and this cloning procedure
worked with three of the placentas, the Russian researchers report. They grew 36
ancient plants, which appeared identical to the present day narrow-leafed campion
until they flowered, when they produced narrower and more splayed-out petals.
Seeds from the ancient plants germinated with 100 percent success, compared with
90 percent for seeds from living campions.
The Russian team says it obtained a radiocarbon date of 31,800 years from seeds
attached to the same placenta from which the living plants were propagated.
The researchers suggest that special circumstances may have contributed to the
remarkable longevity of the campion plant cells. Squirrels construct their larders
next to permafrost to keep seeds cool during the arctic summers, so the fruits would
have been chilled from the start. The fruit’s placenta contains high levels of sucrose
and phenols, which are good antifreeze agents.
The Russians measured the ground radioactivity at the site, which can damage
DNA, and say the amount of gamma radiation the campion fruit accumulated over
30,000 years is not much higher than that reported for a 1,300-year-old sacred lotus
seed, from which a plant was successfully germinated.
The Russian article was edited by Buford Price of the University of California,
Berkeley. Dr. Price, a physicist, chose two reviewers to help him. But neither he nor
they are plant biologists. “I know nothing about plants,” he said. Ann Griswold, a
spokeswoman for PNAS, as the journal is known, said the paper had been seen by
an editorial board member who is a plant biologist.
Tragedy has now struck the Russian team. Dr. Gilichinksy, its leader, was
hospitalized with an asthma attack and unable to respond to questions, his daughter
Yana said on Friday. On Saturday, Dr. Price reported that Dr. Gilichinsky had died
of a heart attack.
Eske Willerslev, an expert on ancient DNA at the University of Copenhagen, said
the finding was “plausible in principle,” given the conditions in permafrost. But the
claim depends on the radiocarbon date being correct: “It’s all resting on that — if
there’s something wrong there it can all fall part.”
If the ancient campions are the ancestors of the living plants, this family
relationship should be evident in their DNA. Dr. Willerslev said that the Russian
researchers should analyze the DNA of their specimens and prove that this is the
case. However, this is not easy to do with plants whose genetics are not well
studied, Dr. Willerslev said.
If the claim is true, then scientists should be able to study evolution in real time by
comparing the ancient and living campions. Possibly other ancient species can be
resurrected from the permafrost, including plants that have long been extinct.
This article has been revised to reflect the following correction:
Correction: February 22, 2012
An article on Tuesday about a plant generated from tissue that had been preserved
in the Siberian tundra for almost 32,000 years misidentified the organization with
which Ann Griswold is affiliated. She is a spokeswoman for Proceedings of the
National Academy of Sciences, the journal in which the work was reported, not for
the National Academy of Sciences itself.
Company Unveils DNA Sequencing Device Meant to
Be Portable, Disposable and Cheap Article #2
By ANDREW POLLACK
Published: February 17, 2012
DNA sequencing is becoming both faster and cheaper. Now, it is also becoming tinier.
A British company said on Friday that by the end of the year it would begin selling a disposable gene
sequencing device that is the size of a USB memory stick and plugs into a laptop computer to deliver its results.
The device, expected to cost less than $900, could allow small sequencing jobs to be done by researchers who
cannot afford the $50,000 to $750,000 needed to buy a sequencing machine.
It might also help doctors to sequence genes at a patient’s bedside, wildlife biologists to study genes in the field,
or food inspectors to identify pathogens.
“You don’t need to buy instruments,” Clive G. Brown, the chief technology officer of the company, Oxford
Nanopore Technologies, said in an interview. “It’s pay-as-you-go sequencing.”
Oxford presented details of the device, as well as of a new, somewhat larger sequencer that it also plans to begin
selling late this year, at the Advances in Genome Biology and Technology conference in Marco Island, Fla.,
which has become the sequencing industry’s annual boast-fest.
Both the tiny MinIon and the larger GridIon look likely to be the first sequencers to use nanopore sequencing, in
which a strand of DNA is read as it is pulled through a microscopic hole, sort of like a noodle being slurped
through rounded lips.
Outsiders have not tried the machines, and there can be a big difference between rosy specifications and how
well a machine works when it finally reaches the market. Some other sequencers that initially dazzled the field
have faltered in the marketplace.
Still, many experts at the conference were dazzled anew.
“If it does work, it will be a game-changer,” said Elaine Mardis, co-director of The Genome Institute at
Washington University in St. Louis. Chad Nusbaum of the Broad Institute in Cambridge, Mass., called it
“impressive, credible, possibly amazing.”
Isaac Ro, an analyst at Goldman Sachs, said in a note Friday that the Oxford technology had “impressive
performance specs” that suggested it would be a “significant competitor” to Illumina and Life Technologies, the
leaders in the sequencing business.
Illumina has a bit of a hedge. In 2009, it invested $18 million in Oxford Nanopore, and owns a 15 percent share.
But Illumina does not have the marketing rights to the machines unveiled Friday. Rather, it has the rights to an
alternative Oxford technology that is further back in development.
Illumina shares fell nearly 4 percent Friday to $51.82, while Life shares dropped nearly 8 percent to $45.92.
Sequencing involves determining the order of the chemical units of DNA, which are known as bases and are
usually represented by the letters A, C, G and T. The order of these bases helps determine inherited traits, like
susceptibility to some diseases.
As the cost plummets, sequencing is moving from research laboratories into patient care. Some cancer centers,
for instance, sequence genes to determine the best drugs to use.
The growing importance of sequencing in medical care is what motivated Roche to make its current $5.7 billion
hostile bid to acquire Illumina. Known mostly for pharmaceuticals, Roche also has a large diagnostics business.
Nanopore sequencing is easy to envision but has been deceptively difficult to carry out, despite two decades of
research by universities and companies.
Oxford, which is privately held and based on technology developed by a professor at Oxford University, uses
pores made from bacterial proteins. An electric current flows through the pore. The bases interrupt the current
in different ways as they go through.
The initial GridIon machines will have 2,000 pores. A machine due in 2013 will have 8,000 pores.
One big advantage of the nanopore sequencing, Dr. Mardis of Washington University said, is that preparing the
sample is quick and easy. The technology also offers the promise of being able to read tens of thousands of
bases in a stretch. Most sequencers read from around 30 to a few thousand bases at a stretch, and these small
fragments then have to be pieced together.
A drawback is that the Oxford machine has a 4 percent error rate, too high for many applications, including
diagnosis.
The MinIon, while entailing no capital cost for a machine, can be used only once and will sequence up to one
billion bases. That is a cost of up to $1,000 per billion bases.
A GridIon might cost around $30,000, Oxford executives said. The company said that if 20 of the secondgeneration GridIons were used together, a human genome could be sequenced in 15 minutes at a cost of around
$1,500.
By then, however, rival machines might be able to do genomes for that cost or even less. Ion Torrent, a
subsidiary of Life Technologies, last month announced it was developing a machine that could do a human
genome in a day for $1,000.
“We’re not losing sleep,” Jonathan M. Rothberg, chief executive of Ion Torrent, said Friday. “But they
definitely have the Twitter airwaves today.”
#3# MOUNTAIN VIEW, Calif. — In Silicon Valley, the line between computing and biology has begun to
blur in a way that could have enormous consequences for human longevity.
Enlarge This Image
Ramin Rahimian for The New York Times
Complete Genomics has produced more than 3,000 sequences at about $5,000 each this year.
Bill Banyai, an optical physicist at Complete Genomics, has helped make that happen. When he began
developing a gene sequencing machine, he relied heavily on his background at two computer networking startup companies. His digital expertise was essential in designing a factory that automated and greatly lowered the
cost of mapping the three billion base pairs that form the human genome.
The promise is that low-cost gene sequencing will lead to a new era of personalized medicine, yielding new
approaches for treating cancers and other serious diseases. The arrival of such cures has been glacial, however,
although the human genome was originally sequenced more than a decade ago.
Now that is changing, in large part because of the same semiconductor industry manufacturing trends that
opened up consumer devices like the PC and the smartphone: exponential increases in processing power and
transistor density are accompanied by costs that fall at an accelerating rate.
As a result, both new understanding and new medicines will arrive at a quickening pace, according to the
biologists and computer scientists.
“For all of human history, humans have not had the readout of the software that makes them alive,” said Larry
Smarr, director of the California Institute of Telecommunications and Information Technology, a research
center that is jointly operated by the University of California, San Diego, and the University of California,
Irvine, who is a member of the Complete Genomics scientific advisory board. “Once you make the transition
from a data poor to data rich environment, everything changes.”
Complete Genomics, based in Mountain View, is one of more than three dozen firms hastening to push the cost
of sequencing an entire human genome below $1,000. The challenge is part biology, part chemistry, part
computing, and in Complete Genomics’ case, part computer networking.
Complete Genomics is a classic Silicon Valley start-up story. Even the gene sequencing machines, which are
housed in a 4,000-square-foot room bathed in an eerie blue light, appear more like a traditional data center than
a biology lab.
In 2005 ,when Clifford Reid, a successful Silicon Valley software entrepreneur, began to assemble his team, he
approached Dr. Banyai and asked if he was interested in joining a gene sequencing start-up. Dr. Reid, who was
also trained in physics and math, had spent a year as an entrepreneur-in-residence at the Massachusetts Institute
of Technology, where he had become a convert to bioinformatics, the application of computer science and
information technologies to biology and medicine.
Dr. Banyai had even less experience in biology.
Formerly with the Internet networking start-ups GlimmerGlass and Silicon Light Machines, he in turn began by
reading a pioneering 2005 article in the journal Science in which a group of researchers in George Church’s
genetics laboratory at Harvard describe a new technique intended to speed gene sequencing.
Today Dr. Banyai is finishing the second generation of a machine that blends robotics, chemistry, optics and
computing. It is emblematic of the serendipitous changes that take place when a manufacturing process is
transformed: performance increases and cost falls at an accelerating rate.
“Genomes are now being sequenced incredibly cheaply,” said Russ B. Altman, who is a founder of Personalis, a
start-up based in Palo Alto, Calif., that is developing software to interpret genomes. “On the discovery and
science side we will be able to do clinical trials. We’ll be able to check the entire genome.”
Recently, on the company’s Web site, Dr. Reid predicted that the cost of gene sequencing could eventually be
as low as that of a blood test: “I believe that the impact on the medical community of whole human genome
sequencing at a cost comparable to a comprehensive blood test will be profound, and it will raise a host of
public policy issues (privacy, security, disclosure, reimbursement, interpretation, counseling, etc.), all important
topics for future discussions,” he wrote.
Dr. Banyai said he had found that Silicon Valley start-up ideas tracked well. “There is this remarkable thing that
happens in start-ups. You make up this plan and then you step off a cliff and magically a little bridge appears,”
he noted, as new technologies appear in the nick of time.
In the case of Complete Genomics, the company is riding in part on big advances being made in industrial
digital cameras that are capable of capturing the fluorescent molecules that are used to “read” small sequences
of DNA.
In the last half-year, a new generation of cameras, more frequently used for factory inspection systems, has
made it possible to speed up the Complete Genomics sequencing process tenfold. That, the company has said,
will drive its capacity to 100,000 genomes annually from 10,000.
The parallels between the evolution of the nascent gene sequencing industry and the Valley’s chip makers are
striking. By placing more circuits on a silicon wafer at an exponentially increasing pace since the early 1960s,
the semiconductor industry transformed the cost of computing. As a result, today the world’s most powerful
supercomputer from the 1980s nestles comfortably in your hand and costs several hundred dollars.
Complete Genomics’ competitors are also exploiting designs to drive costs down. For example, Life
Technologies, based in Carlsbad, Calif. uses a direct approach to read the bases in the genome from an array of
sensors on the surface of a semiconductor chip. As more sensors are packed onto each successive generation of
technology, the cost of sequencing will also fall sharply.
Last month, Oxford Nanopore Technologies created an industry sensation when it introduced a machine that
sequenced genes using an alternative approach called nanopore sequencing, in which a strand of DNA is read as
it is pulled through a microscopic hole.
The system is scheduled to be available later this year. However, it has an error rate much higher than that of
the Complete Genomics system, which has independently been given high marks for accuracy.
Because there is no clear winner yet, all of the companies are pushing hard to get down the cost curve as fast as
possible
In 2011, Complete Genomics became one of the market leaders. This year, it has produced more than 3,000
sequences at a cost of about $5,000 each. Dr. Banyai’s higher capacity second generation system is now being
installed and will begin production during the first half of this year. A third generation design has been
completed.
What initially set Complete Genomics apart from the field was its strategy of offering gene sequencing as a
service, rather than selling a machine to laboratories. More recently, Illumina, one of its crucial competitors, has
also begun offering sequencing as a service, in addition to selling its machines.
“Our competitors have to supply kits that can be executed by a graduate student rolling out of bed with a
hangover,” said Dr. Reid. “We don’t live with that standard, and that can be tremendously liberating. Ours can
be horrifically complex as long as it can be executed by a robot.”
The company also began with the business intent of sequencing only the human genome, rather than those of
other species, too — a strategy that was heresy in 2005, when the founders set out to raise money. At that time,
only two human genomes had been sequenced. However, Complete Genomics founders argue that focusing just
on the human genome has given them a leg up.
“You make a whole bunch of decisions that don’t work well for corn or bacteria, but they work very well for
humans,” Dr. Reid said.
The Texas Tribune
#10 Putting Pieces Together in Decades-Old Cases
Evan Lewis/Texarkana Gazette
Delma Banks Jr. is on trial again for the 1980 murder of Richard Whitehead, 16,
whose parents are in the front row.
By BRANDI GRISSOM
Mark Norwood will be led into a Georgetown courtroom Wednesday to face capital
murder charges for a killing that took place more than 25 years ago.
If Mr. Norwood, 57, goes to trial in the 1986 beating death of Christine Morton,
prosecutors and defense lawyers will have to piece together a decades-old crime.
That was what lawyers did for the trial of Dennis Davis last year, when he was
convicted of the 1985 murder of his former girlfriend.
With the advent of DNA science and other technological advancements, it is no
longer unusual for juries to see evidence from crimes that happened as long ago as
the 1970s. But old cases present unique challenges for prosecutors and defense
lawyers: Key witnesses may have moved or died, documents could have
disappeared, and evidence collection standards are now much stricter.
“The farther back in time you’re talking about, the more those things fray and
disintegrate,” said Rob Owen, a University of Texas School of Law professor who
specializes in death penalty cases.
Mr. Norwood was arrested in November for the Aug. 13, 1986 murder of Mrs.
Morton. Michael Morton, Mrs. Morton’s husband, was convicted of her murder in
1987 and spent 25 years in prison. But he was cleared last year after DNA testing
was performed on a bandanna found about 100 yards from the Mortons’ North
Austin home, where she had been beaten to death in bed. Tests showed the
biological material on the bandanna was not Mr. Morton’s, and a national database
search revealed the DNA matched Mr. Norwood’s.
His DNA was also linked to a similar Austin murder that happened on Jan. 13,
1988. Like Mrs. Morton, Debra Masters Baker was beaten to death in her bed, and
Mr. Norwood is a suspect in that cold case.
Russell Hunt Jr., Mr. Norwood’s lawyer, expects the judge to delay this week’s
hearing to allow him and state prosecutors more time to investigate.
“People change over time. People’s memories change over time,” Mr. Hunt said,
adding, “Physical evidence gets moved. Physical evidence is stored in different
ways.”
Mr. Hunt said that verifying other information and determining its relevance to Mr.
Norwood could be a challenge. For example, other evidence that recently came to
light in the Morton case includes a check cashed after Mrs. Morton’s death with her
forged signature and a report that her credit card was fraudulently used days after
her death.
“We don’t know if it’s possible to go back and find people involved or records
involved,” he said. “Things get lost, and people get lost.”
When Mr. Davis was convicted last year of murdering his former girlfriend, he was
represented by Wade Russell, an Austin lawyer.
“There’s just myriad problems” mounting a defense in a two-decades-old case, Mr.
Russell said.
Natalie Antonetti was beaten in the head while she slept on her couch on Oct. 13,
1985. The case was cold until 2006, when Mr. Davis’s estranged wife told the
police her husband had said that he had “sinned against God and man.”
She later reconciled with Mr. Davis, and refused to cooperate with police. But
investigators reopened the case and focused on Mr. Davis.
The woman Mr. Davis told police he was with the night of the murder told
investigators who reopened the case that she did not have an entry in her journal
noting that she was with him when the police called, and it was something she
would have recorded.
A quarter-century after the murder, Mr. Russell began digging through the old
police file to investigate his client’s case. The original police investigator had died.
The police case file was incomplete and unorganized, he said. “I would find
handwritten notes from various people,” he said. “You have a lot of sketchy
information, and you don’t know how it fits into the picture.”
A neighbor had told police that shortly before the murder he saw a large man
carrying a bat wearing a T-shirt with a band logo. The neighbor refused to testify.
He originally described a man who was larger than Mr. Davis. A police sketch of
the man made in 1985 based on the neighbor’s description was missing. And Mr.
Russell said finding other witnesses to challenge the credibility of those who
testified against Mr. Davis was tough. “I couldn’t track them all down,” he said.
“They were scattered so far.”
Mr. Davis was found guilty and sentenced to 36 years in prison.
Efrain De La Fuente, a Travis County assistant district attorney who worked on the
Davis case, said compiling evidence was just as challenging for prosecutors.
There was no DNA linking Mr. Davis to the crime, but prosecutors found other
women who testified about abusive relationships with him, and one said he had
confessed to her. Friends of Mr. Davis said he owned a bat and had a screaming
match with Ms. Antonetti hours before the murder.
“The crime scene speaks to us that it was someone known to her and that it was
personal,” Mr. De La Fuente said, adding that nothing was stolen. “He took a bat
and just inflicted numerous blows to her head.”
Old cases do not come to court based only on new charges, though. Delma Banks
Jr. was sentenced to death for the 1980 murder of Richard Whitehead, 16, in
Texarkana. Mr. Banks, who was 21 when the crime was committed, was convicted
of killing Mr. Whitehead to steal his car.
In 2004, the United States Supreme Court overturned his sentence, finding that
prosecutorial misconduct had led the jury to give Mr. Banks the death penalty.
This year, Mr. Banks is scheduled to face another trial to determine whether his
death sentence should be reinstated. Mr. Banks’s lawyers must try to find mitigating
evidence, information that might prompt jurors to consider a more lenient sentence.
Typically, that comes from family members or others who know about the
defendants’ past.
In Mr. Banks’s case, though, many who knew him before he went to prison are
dead. Others have moved away.
“It’s hugely problematic that the state would pursue the death penalty in a situation
like that,” said Mr. Owen of the University of Texas School of Law, who has
worked on Mr. Banks’s case in the past. “The jury is inevitably going to be
presented an incomplete set of facts.”
James Elliott, a prosecutor on the case for more than 30 years, has maintained that
he will pursue Mr. Banks until he “gets what he deserves.”
In the Norwood case, however, prosecutors have not indicated whether they will
seek the death penalty. Lisa Tanner, a special prosecutor in the Texas attorney
general’s office, will lead the state’s case. She declined to speak specifically about
Mr. Norwood, but she discussed the challenges in trying old cases.
She prosecuted two men in the so-called KFC murders. In 1983, five people at a
Kentucky Fried Chicken restaurant in Kilgore were robbed and killed. The crime
went unsolved until DNA evidence linked two cousins to the scene. They were
arrested in 2005; each was sentenced to five consecutive life sentences.
In old cases, Ms. Tanner said, DNA evidence is often the key to convincing a jury
of a person’s guilt.
“We are able to do things that were utterly inconceivable back in the ’70s, ’80s or
even the early ’90s,” she said. “In cold cases, it seems like that is the difference.”
Spotted Horses in Cave Art Weren’t Just a Figment,
DNA Shows ARTICLE #4
French Ministry of Culture and Communication
SEEING SPOTS Drawings of horses from the Chauvet cave in France, right, and a horse from the Lascaux
cave, also in France.
By HILLARY ROSNER
Enlarge This Image
Thomas Hackmann
A modern horse with leopard spots like those seen in France's Pech-Merle cave. Comparing DNA from the
present and the Stone Age convinced scientists that those spotted depictions were based on existing animals.
Today, the art at the Pech-Merle cave, and in hundreds of others across Europe, is a striking testimony to human
creativity well before modern times.
But what were these cave paintings, exactly? Were prehistoric artists simply sketching what they saw each day
on the landscape? Or were the images more symbolic, diverging from reality or representing rare or even
mystical creatures? Such questions have divided archaeologists for years.
Now, a group of researchers has used distinctly modern techniques to help decipher the mystery, at least in the
case of Pech-Merle’s famous spotted horses. By comparing the DNA of modern horses and those that lived
during the Stone Age, scientists have determined that these drawings are a realistic depiction of an animal that
coexisted with the artists.
The research, published online on Monday in the journal Proceedings of the National Academy of Sciences,
grew out of an effort to discern the coat colors of ancient horses to help figure out when the animals were
domesticated, a pivotal moment in the development of human societies. In general, domesticated species exist
in a far greater variety of colors than wild ones, so understanding color variation in fossil animals can help
pinpoint the timing.
Previous research on DNA from the bones and teeth of horses that lived 7,000 to 20,000 years ago showed that
those animals were either black or bay (a brown coat with a black mane and tail). That work was published in
the journal Science in 2009. Since then, geneticists have deciphered the underlying code for the spotted pattern,
known as leopard, in modern horses. So the scientists went back to their samples, looking for the leopard
sequence in horses that lived in Europe 11,000 to 15,000 years ago.
“There is a striking correspondence between the coat-color patterns of horses painted in Paleolithic caves of
France with what geneticists found in the genotypes” — the specific genetic sequences — “of color genes,” said
Hopi E. Hoekstra, an evolutionary biologist at Harvard who studies pigmentation. Dr. Hoekstra was not
involved in the study but called it “very convincing.”
An author of the study, Michael Hofreiter, an evolutionary biologist at the University of York in England, said:
“Why they took the effort making these beautiful paintings will always remain a miracle to us.
“It’s an enigma, but it’s also nice to see that if we go back 25,000 years, people didn’t have much technology
and life was probably hard, but nevertheless they already endeavored in producing art. It tells us a lot about
ourselves as a species.”
Extracting DNA from such old material is a complex process, and the potential for contamination is huge. Early
studies of Neanderthal DNA were marred by contamination from humans, and led to skepticism about the
field’s future.
Since then, researchers have adopted strict procedures to ensure they are not contaminating ancient samples
with modern-day DNA. The procedures include analyzing ancient and contemporary material in physically
separate facilities and replicating results multiple times.
“This is a whole different level of clean,” said Jessica L. Metcalf, a postdoctoral researcher at the University of
Colorado who also works with the Australian Center for Ancient DNA in Adelaide, where the labs that work on
ancient and modern DNA are more than half a mile apart.
“We have sealed rooms with HEPA filter air flow, UV lights that sterilize when you come in,” she said. “We
spend over half our time cleaning. We use a lot of bleach. You’re in this ridiculous-looking clean suit with a
face shield on.”
In fact, Dr. Hofreiter said, researchers who work with ancient horse genes should not even go horseback riding.
“Traces of DNA,” she said, “they just stick to people.”
Dr. Hofreiter, 38, began his career working with a pioneer of ancient DNA research, Svante Paabo. Though he
intended to study taxonomy, he was so intrigued by the idea of extracting DNA from ancient material that he
switched his focus. “You have this 30,000-year-old piece of feces in your hand,” he said, adding: “Well, you
should wear gloves. And you can actually get to the genetic code from the animal. And I thought, this is so
fascinating.”
He and his colleagues did not set out to study cave art. They were simply continuing their work on coat color in
prehistoric horses. Only after they found the spotted horse gene in their ancient samples did they realize they
could say something about archaeology.
“What we found is that there were really only these three color patterns — spotted or dappled; blackish ones;
and brown ones,” he said. “These are the three phenotypes we find in the wild populations. And then we
realized these phenotypes are exactly the ones you see in cave paintings.”
Terry O’Connor, an archaeologist at the University of York who collaborated on the study, said spotted horses
in particular had been used to argue that cave art was more symbolic than realistic, and that as a result the
finding could cause a stir. But now it is clear that some horses had a gene for that coat color. “People drew
spotty horses,” he said, “because they saw spotty horses.”
Last summer, exploring a cave in the Dordogne region, Dr. O’Connor said he became transfixed by a series of
line drawings of mammoths. “They were absolutely superb, some using contours of the cave itself, capturing
the size and shape and movement,” he said. “You look at that and say, ‘These guys know what the animals
looked like, and they can draw.’ ”
As techniques for working with ancient DNA have matured, scientists are now using it to answer an increasing
variety of questions about the past — from what happened to a species’ genetic variation as its environment
changed to how humans recolonized Europe after the last ice age to what type of microbes lived in the guts of
people and animals thousands of years ago.
“One of the things that most pleases me about this paper as a piece of ancient DNA science,” Dr. O’Connor
said, “is it kind of begins with a question. These spotty horses, were they magical or real?
“And then science answers that. It’s not just, ‘Let’s rip the DNA out of ancient bones and see what it tells us.’ ”
Why Has the Black Death Paled? Article #5
Published: October 25, 2011
The Black Death killed 25 million people — roughly half of Europe — between 1347 and 1351. In Britain
alone, 1.5 million died, including the victims whose teeth and bones yielded the DNA used in the
reconstruction. The cause, as suspected, was a strain of the bacterium Yersinia pestis, the ancestor of all modern
strains of the plague.
Behind this research, which was published in Nature, lie two basic questions. How is the medieval plague
related to other plague epidemics, like the one that ravaged the eastern Mediterranean in the 6th century? And
why is the modern plague, which kills some 2,000 people a year, so much less virulent than its medieval
ancestor?
The answers are important contributions to epidemiology. In fact, there is no link between the Black Death and
earlier plagues. They were caused either by an extinct strain of Yersinia or by something else entirely. And
there is nothing in the genetic code of the medieval Yersinia that makes it inherently more lethal than modern
strains, even though, as the scientists write, the epidemics they cause “have their origins in the medieval era.”
In other words, the origins of the Black Death are not the result of a killer bacterium alone. They may lie in the
complex interaction of any number of factors, including climate, social conditions, the genetics of its victims
and interactions with other diseases. The plague still with us — which is treatable with modern antibiotics —
lacks its medieval virulence because the conditions we live in are not medieval. We have our own plagues, but
Yersinia, at least, has outlived its time.
Scientists Solve Puzzle of Black Death’s DNA
By NICHOLAS WADE
Published: October 12, 2011
After the Black Death reached London in 1348, about 2,400 people were buried in East Smithfield, near the
Tower of London, in a cemetery that had been prepared for the plague’s arrival. From the teeth of four of those
victims, researchers have now reconstructed the full DNA of a microbe that within five years felled one-third to
one-half of the population of Western Europe.
Enlarge This Image
Museum of London
A draft sequence of the Yersinia pestis genome has been reconstructed using DNA extracted from victims of the
Black Death.
Museum of London
Advancing science: the remains of plague victims in a 14th-century London cemetery.
The bacterium that causes plague, Yersinia pestis, is still highly virulent today but has different symptoms,
leading some historians to doubt that it was the agent of the Black Death.
Those doubts were laid to rest last year by detection of the bacterium’s DNA in plague victims from mass
graves across Europe. With the full genome now in hand, the researchers hope to recreate the microbe itself so
as to understand what made the Black Death outbreak so deadly.
So far, the evidence points more toward the conditions of the time than to properties of the bacterium itself. The
genome recovered from the East Smithfield victims is remarkably similar to that of the present-day bacterium,
says the research team, led by Kirsten I. Bos of McMaster University in Ontario and Johannes Krause of the
University of Tübingen in Germany.
This is the first time the genome of an ancient pathogen has been reconstructed, opening the way to tracking
other ancient epidemics and how their microbes adapted to human hosts.
The bacterium’s genome consists of a single chromosome, about 4.6 million DNA units long, and three small
rings of DNA called plasmids. In the 660 years since the Black Death struck, only 97 of these DNA units have
changed and only a dozen of these changes occur in genes and therefore would affect the organism’s physical
properties, the researchers report in Wednesday’s issue of the journal Nature. Dr. Krause and others reported the
DNA sequence of one of the plasmids in August. The changes in the genome will be studied one by one to see
how each affects the microbe’s virulence.
The researchers hope eventually to modify a living plague bacterium so that its genome is identical to that of the
agent of the Black Death. Such a microbe could be handled only in special secure facilities. But even if it did
infect a person, the bacterium would be susceptible to antibiotics, like its living descendants, said Hendrik
Poinar of McMaster University, a team member.
If the microbe’s genome is so little changed, the deadliness of the Black Death may reflect the condition of its
medieval victims. Harsh as the economic stresses assailing Europe today may be, they are a breeze compared
with problems in the mid-14th century. The climate was cooling, heavy rains rotted out crops and caused
frequent famines, and the Hundred Years’ War began in 1337. People were probably already suffering from
malnutrition and other diseases when the plague arrived like the fourth horseman of the apocalypse. “People
honestly thought it was the end of the world,” Ms. Bos said.
Recovery of the medieval plague bacterium’s full genome is a technical tour de force. The DNA had been
degraded into millions of small fragments that were overwhelmed in number by DNA from the human host and
from the bacteria that consumed the body after death. Dr. Krause’s team fished out the plague DNA by using
DNA from the modern bacterium, relying on the fact that DNA strands bind to DNA of complementary
sequence.
“This is a major technological step forward, a great advance for the entire field of DNA and pathogens,” said
Mark Achtman, an expert on ancient plague at University College Cork in Ireland.
But Dr. Achtman disagreed with one issue in Dr. Krause’s findings, that of whether Yersinia pestis also caused
the outbreak in the sixth century known as the Justinian plague. When the full genome of the medieval
bacterium is compared with DNA recovered from other known human outbreaks, a tree of descent can be
constructed. The Black Death genome lies so close to the root of the tree that the human pathogen probably did
not exist much earlier or, if it did, has vanished without any descendants, Dr. Krause’s team says. This implies
that the Justinian plague was caused by some other agent.
Dr. Achtman said this conclusion was incorrect because the Krause team had omitted DNA from several human
cases that place the root of the tree much further back in time. Dr. Krause said he had left these cases out
because they seemed unreliable.
The modern plague bacterium changes its DNA units slowly, but it does quite often rearrange the order of its
genes. Some experts believe gene order can affect pathogenicity. Dr. Krause had available only tiny fragments
of DNA, so although he was able to reconstruct all the medieval bacterium’s genes he could not establish the
exact order in which the genes were arranged, leaving open the possibility that the bacterium was inherently
more pathogenic because its genome was differently organized.
Paul Keim, an expert on infectious bacteria at Northern Arizona University, said that work by Dr. Achtman and
Dr. Krause had shown that the Black Death “was really a series of epidemics coming out of China and sweeping
across the susceptible ecological situation” created by the culture of medieval Europe. The plague in each
outbreak probably did not persist very long and was repeatedly re-established by new infections from East Asia,
where the bacterium is still endemic in small rodents like marmots.
“We don’t have a human ecological situation comparable today, plus it is really easy to break the transmission
cycle with antibiotics and public health,” Dr. Keim said. There are still small outbreaks, like one in Madagascar
in the 1990s, but “a multiyear large human outbreak is inconceivable in this day,” he said.
Besides the Justinian plague and the Black Death, a third great wave of plague swept out of China in 1894,
causing an epidemic in San Francisco in 1900 and killing millions of people in India.
All the teeth used in the study will be returned to the skulls from which they were taken, now in a London
museum whose archaeologists excavated the East Smithfield cemetery in the 1980s.
Tracing Unscooped Dog Waste Back to the Culprit
By KATIE ZEZIMA
#6
Published: July 1, 2011
Sherlock Holmes had the case of the dog that didn’t bark, but it has taken two dozen apartment complexes and a
testing company in Tennessee to bring the art of canine detection into the “CSI” age.
Enlarge This Image
Jim Cole/Associated Press
Deborah Violette, a property manager, takes dog waste seriously.
Related

Scoop It Up or Pay: On Patrol With Enforcers of the Dog Law (June 5, 2008)
And the evidence is right underfoot.
Canine DNA is now being used to identify the culprits who fail to clean up after their pets, an offense that
Deborah Violette, for one, is committed to eradicating at the apartment complex she manages.
Everyone who owns a dog in her complex, Timberwood Commons in Lebanon, N.H., must submit a sample of
its DNA, taken by rubbing a cotton swab around inside the animal’s mouth.
The swab is sent to BioPet Vet Lab, a Knoxville, Tenn., company that enters it into a worldwide database. If
Ms. Violette finds an unscooped pile, she can take a sample, mail it to Knoxville and use a DNA match to
identify the offending owner.
Called PooPrints, the system costs $29.99 for the swabbing kit, $10 for a vial to hold the samples and $50 to
analyze them, which usually takes a week or two. The company says that about two dozen apartment complexes
around the country have signed up for the service. In 2008, the Israeli city of Petah Tikva created a dog DNA
database for the same purpose.
“It’s kind of like the F.B.I., but on a much smaller scale,” said Eric Mayer, director of franchise development
for BioPet Vet Lab, which makes the kits.
Ms. Violette said that at her complex, which opened in December and has a designated building for pet owners,
unwanted surprises have sometimes been found on lawns.
“We had a little bit of a problem,” Ms. Violette said. “Enough that I wanted to try to nip it in the bud.”
Dog owners were notified about the testing last week, and most are now taking their pets in to provide DNA
samples. But not everyone.
“I’ve had some people say it’s completely over the top and ridiculous,” Ms. Violette said. “I’m sure I’ll have a
few people who won’t come in, and I’m sure those are the people we’ll have to chase and those are the people
who are doing it.”
Tom Boyd, the founder and chief executive of BioPet Vet Lab, said the company made the kits in response to
the large of numbers of the dogs in the United States and to health concerns connected to dog feces. According
to the American Society for the Prevention of Cruelty to Animals, there are about 75 million dogs in the United
States.
“If you took 75 million Americans and said they no longer have a commode, can you imagine what would
happen in a week?” Mr. Boyd asked.
Not everyone is on board with the idea, though.
Karen Harvey of Forest Property Management in McCall, Idaho, said her company was not prepared to collect
canine samples along with the rent checks. “If you allow pets, that sort of comes with it,” Ms. Harvey said. “I
guess I would never take the issue of dog poop that far.”
Roots of Disease Found to Vary by Continent
By NICHOLAS WADE
Published: July 4, 2011
A new survey of the human genome shows that common diseases are likely to have a different set of genetic
roots in Africans, East Asians and Europeans.
The finding may represent yet another serious complication in the post-genome quest for the roots of common
disease, since it implies that each disease may need to be investigated separately in different populations.
After the human genome was decoded in 2003, biologists completed a follow-up project called the HapMap that
cataloged the genome’s common variations, meaning the sites on the DNA where one unit often differs from the
standard sequence. They then scanned the genomes of patients with common diseases to look for statistical
links between having a disease and having a particular variation.
These expensive scans, called genomewide association studies, required recruiting hundreds of patients. Many
such scans have now been done for most of the common diseases, but the results have been disappointing. With
a few exceptions, common variations account for little of the genetic risk of common disease. The basic premise
of the HapMap — that common diseases were caused by common variations — turned out to be largely
incorrect.
Back at the drawing board, biologists decided that if the genetic roots of common disease did not lie in the
common variants, they should lie in the rarer variants. With partners in England and China, the National
Institutes of Health in 2008 undertook a follow-up to the HapMap, the 1,000 Genomes Project, to catalog rare
variants in the human population.
The project is not yet complete, but a team led by Simon Gravel and Carlos D. Bustamante of Stanford
University has analyzed the data so far available and predicts the rare variants will be found to be almost
entirely different in the Chinese, European and African populations. This means that almost all of the rare
variants developed after the three populations had split apart.
“Genomewide association studies aiming to correlate common disease susceptibility with rare variants may
need extraordinarily large sample sizes,” the scientists concluded in the journal PNAS.
David B. Goldstein, a geneticist at Duke University, said that it had long been known that rare variants tend to
be specific to particular populations, but that it was too early to tell how hard it will be to find those that cause
disease. Some rare variants can greatly increase the risk of disease and should be easier to detect than others.
But the jury is still out on the catalog of rarer variants being developed by the 1,000 Genomes Project and how
useful it will be, Dr. Goldstein said. It may be more effective to decode the entire genomes of patients with a
particular disease. “We are more interested in the variants we see in patients than in a generic catalog,” he said.
These variants are so rare that even 1,000 Genomes is unlikely to pick up many of them, he said.
The Stanford study also sheds light on major aspects of human population history, like the time at which the
first modern humans emigrated from Africa. Archaeologists believe it was about 50,000 years ago, since no
modern human remains older than this have yet been found outside of Africa, but geneticists have long favored
much earlier dates. Dr. Gravel and Dr. Bustamante now calculate that 51,000 years ago, give or take several
thousand years, is the date best supported by genetic data, bringing the geneticists’ date into alignment with the
archaeologists’ favored time for the exit from Africa.
The common variations in the human genome were mostly present in the ancestral human population in Africa
and have been inherited by all the descendant populations around the world. The rare variants occurred more
recently.
“Most of the common variants hark back to pre-Out of Africa,” Dr. Bustamante said. “Most of the rare variants
come after the Neolithic revolution.” This is the event that marked the beginning of agriculture about 10,000
years ago and led to significant increases in the size of human populations.
A Blood Test Offers Clues to Longevity #7
By ANDREW POLLACK
Published: May 18, 2011
Toni Albir/EFE, Via European Pressphoto Agency
Elizabeth H. Blackburn shared a Nobel Prize in 2009 for discoveries related to telomeres.
Blood tests that seek to tell people their biological age — possibly offering a clue to their longevity or how
healthy they will remain — are now going on sale.
But contrary to various recent media reports, the tests cannot specify how many months or years someone can
expect to live. Some experts say the tests will not provide any useful information.
The tests measure telomeres, which are structures on the tips of chromosomes that shorten as people age.
Various studies have shown that people with shorter telomeres in their white blood cells are more likely to
develop illnesses like cancer, heart disease and Alzheimer’s disease, or even to die earlier. Studies in mice have
suggested that extending telomeres lengthens lives.
Seizing on that, laboratories are beginning to offer tests of telomere length, setting off a new debate over what
genetic tests should be offered to the public and what would be the ethical implications if the results were used
by employers or others.
Some of the laboratories offering the tests emphasize that the results are merely intended to raise a warning flag.
“We see it as a kind of wake-up call for the patient and the clinician to say, ‘You know, you’re on a rapidly
aging path,’ ” said Otto Schaefer, vice president for sales and marketing at SpectraCell Laboratories in Houston,
which offers a test for $290.
A company in Spain, provocatively named Life Length, has begun selling a test for 500 euros ($712), that says
that it can tell people their biological age, which may not correspond to their chronologic age.
Another company, Telome Health of Menlo Park, Calif., plans to begin offering a test later this year for about
$200. It was co-founded by Elizabeth H. Blackburn of the University of California, San Francisco, who shared a
Nobel Prize in 2009 for discoveries related to telomeres.
Calvin B. Harley, the chief scientific officer at Telome Health, said the test would be akin to a car’s dashboard
signal, a “check engine light.” He compared it with a cholesterol test, but more versatile since it can predict a
risk of various illnesses, not just heart attacks.
But among the critics of such tests is Carol Greider, a molecular biologist at Johns Hopkins University, who
was a co-winner of the Nobel Prize with Dr. Blackburn.
Dr. Greider acknowledged that solid evidence showed that the 1 percent of people with the shortest telomeres
were at an increased risk of certain diseases, particularly bone marrow failure and pulmonary fibrosis, a fatal
scarring of the lungs. But outside of that 1 percent, she said, “The science really isn’t there to tell us what the
consequences are of your telomere length.”
Dr. Greider said that there was great variability in telomere length. “A given telomere length can be from a 20year-old or a 70-year-old,” she said. “You could send me a DNA sample and I couldn’t tell you how old that
person is.”
Dr. Peter Lansdorp, a telomere expert at the British Columbia Cancer Agency, also had doubts. “If telomeres
are short for you or me, what does it mean?” he said. Dr. Lansdorp started a company, Repeat Diagnostics,
which conducts telomere testing for medical researchers only.
Recent media reports speculated on the tests and their possible implications, including ethical problems.
“You could imagine insurance companies wanting this knowledge to set rates or deny coverage,” said Jerry W.
Shay, a professor of cell biology at the University of Texas Southwestern Medical Center in Dallas, who is an
adviser to Life Length.
Test vendors say the speculation is running wild.
“It doesn’t mean we will tell anyone how long they will live,” said María Blasco, a co-founder of Life Length
and a molecular biologist at the Spanish National Cancer Research Center in Madrid. Even if a 50-year-old has
the telomere length more typical of a 70-year-old, she said, “This doesn’t mean your whole body is like a 70year-old person’s body.”
Still, she said, “We think it can be helpful to people who are especially keen on knowing how healthy they are.”
Generally tests offered by a single laboratory do not have to be approved by the Food and Drug Administration.
But the F.D.A. has been cracking down recently on some tests offered to the public, saying they may need
approval. The FDA said in a statement Wednesday that it was aware of the tests, and had not come to any
conclusions.
Executives at both Telome Health and Life Length say they will require a doctor to be involved in ordering the
test, though SpectraCell said it allowed individuals to order the
Telomeres are stretches of DNA linked to certain proteins that are at the ends of chromosomes. They are often
likened to the caps at the end of shoelaces. Each time a cell divides, the telomeres get shorter. Eventually, the
telomeres get so short that the cell can no longer divide. It enters a state of senescence or dies.
Life Length
María Blasco is a co-founder of Life Length, a company in Spain that sells a test for 500 euros ($712) that says
that it can tell people their biological age.
One study in Utah, using blood samples from 143 elderly people collected in the 1980s, found that those with
shorter telomeres were almost twice as likely to die in the ensuing years as those with longer ones.
Another study, published in The Journal of the American Medical Association last July, followed 787 people in
Italy, all initially free of cancer. Those with the shortest telomeres had three times the risk of developing cancers
in the next 10 years as those with the longest telomeres.
Still, not all studies have found such strong correlations. In any case, correlations do not prove that the shorter
telomeres are causing the problems, although experts say some animal and cell studies do suggest causality.
Some say that the telomere test might not tell people much that cannot be learned in other ways.
“You can pretty much look at people and determine their biological age,” said Michael West, who founded
Geron, the biotechnology company that sponsored and conducted some important research on telomeres. He
now runs BioTime, another biotechnology company.
It is also unclear what to do about short telomeres. At the moment, there is no drug that can lengthen telomeres,
though researchers are working on drugs and stem cell therapies.
There is some evidence, however, that stress is associated with shorter telomeres and that stress relief, exercise
or certain nutrients such as omega-3 fatty acids might at least slow the decline in telomere length. But healthy
lifestyles are already recommended for people without having to know their telomere length.
There are also disputes about how to measure telomeres. Life Length says its technique, while more expensive,
can detect not only average telomere length but the shortest telomeres in cells. The shortest telomeres cause the
health problems, said Dr. Shay, the adviser to Life Length.
Telome Health and SpectraCell use a DNA amplification technique called polymerase chain reaction, or P.C.R.,
which is cheaper but provides only an average length. And there are some questions about the accuracy.
Dr. Harley of Telome said the P.C.R. test was more relevant because virtually all the studies correlating
telomere length with disease had used that test.
For those wanting to know how long they might live, there are already some indexes that are used by
geriatricians to estimate the chances of a patient dying in anywhere from six months to nine years. A patient
with a short expected lifespan, for instance, might no longer need to undergo annual screening for cancer.
These estimates rely on factors such as person’s age, gender, smoking history, whether they have certain
diseases and whether they can perform certain functions, like walking several blocks, pushing an armchair or
managing their finances.
Dr. Sei Lee, an assistant professor at the University of California, San Francisco who developed a test that
estimates the probability of dying within four years, said he was not sure how much telomere length testing
would add. “The chance of any single factor being a great predictor is probably low,” he said.
Phys Ed: How Exercising Keeps Your Cells Young
By GRETCHEN REYNOLDS
Article #9
Chev Wilkinson/Getty Images
Recently, scientists in Germany gathered several groups of men and women to look at their cells’ life spans.
Some of them were young and sedentary, others middle-aged and sedentary. Two other groups were, to put it
mildly, active. The first of these consisted of professional runners in their 20s, most of them on the national
track-and-field team, training about 45 miles per week. The last were serious, middle-aged longtime runners,
with an average age of 51 and a typical training regimen of 50 miles per week, putting those young 45-mile-perweek sluggards to shame.
From the first, the scientists noted one aspect of their older runners. It ‘‘was striking,’’ recalls Dr. Christian
Werner, an internal-medicine resident at Saarland University Clinic in Homburg, ‘‘to see in our study that many
of the middle-aged athletes looked much younger than sedentary control subjects of the same age.’’
Even more striking was what was going on beneath those deceptively youthful surfaces. When the scientists
examined white blood cells from each of their subjects, they found that the cells in both the active and slothful
young adults had similar-size telomeres. Telomeres are tiny caps on the end of DNA strands — the discovery of
their function won several scientists the 2009 Nobel Prize in medicine. When cells divide and replicate these
long strands of DNA, the telomere cap is snipped, a process that is believed to protect the rest of the DNA but
leaves an increasingly abbreviated telomere. Eventually, if a cell’s telomeres become too short, the cell ‘‘either
dies or enters a kind of suspended state,’’ says Stephen Roth, an associate professor of kinesiology at the
University of Maryland who is studying exercise and telomeres. Most researchers now accept telomere length
as a reliable marker of cell age. In general, the shorter the telomere, the functionally older and more tired the
cell.
It’s not surprising, then, that the young subjects’ telomeres were about the same length, whether they ran
exhaustively or sat around all day. None of them had been on earth long enough for multiple cell divisions to
have snipped away at their telomeres. The young never appreciate robust telomere length until they’ve lost it.
When the researchers measured telomeres in the middle-aged subjects, however, the situation was quite
different. The sedentary older subjects had telomeres that were on average 40 percent shorter than in the
sedentary young subjects, suggesting that the older subjects’ cells were, like them, aging. The runners, on the
other hand, had remarkably youthful telomeres, a bit shorter than those in the young runners, but only by about
10 percent. In general, telomere loss was reduced by approximately 75 percent in the aging runners. Or, to put it
more succinctly, exercise, Dr. Werner says, ‘‘at the molecular level has an anti-aging effect.’’
There are plenty of reasons to exercise — in this column, I’ve pointed out more than a few — but the effect that
regular activity may have on cellular aging could turn out to be the most profound. ‘‘It’s pretty exciting stuff,’’
says Thomas LaRocca, a Ph.D. candidate in the department of integrative physiology at the University of
Colorado in Boulder, who has just completed a new study echoing Werner’s findings. In Mr. LaRocca’s work,
people were tested both for their V02max — or maximum aerobic capacity, a widely accepted measure of
physical fitness — and their white blood cells’ telomere length. In subjects 55 to 72, a higher V02max
correlated closely with longer telomeres. The fitter a person was in middle age or onward, the younger their
cells.
There are countless unanswered questions about how and why activity affects the DNA. For instance, Dr.
Werner found that his older runners had more activity in their telomerase, a cellular enzyme thought to aid in
lengthening and protecting telomeres. Exercise may be affecting telomerase activity and not telomeres directly.
In addition, Stephen Roth has been measuring telomeres and telomerase activity in a wide variety of tissues in
mice and has found, he says, the protective effects from exercise only in some tissues.
Another question is whether we must run 50 miles a week to benefit. The answer ‘‘can only be speculative at
the moment,’’ Dr. Werner says, although since he jogs much less than that, he probably joins the rest of us in
hoping not. Given his and his colleagues’ data, ‘‘one could speculate,’’ he concludes, ‘‘that any form of intense
exercise that is regularly performed over a long period of time’’ will improve ‘‘telomere biology,’’ meaning
that with enough activity, each of us could outpace the passing years.
Hello Kitty, Hello Clone #8
By ANNE EISENBERG
Published: May 28, 2005
Ordinarily it is hard to predict how a kitten will look when it is grown. But not for David Cheng, who plans to
buy a clone of his much-loved short-haired black-and-white cat Shadow. After all, the cloning company
guarantees that Shadow's successor will bear a close resemblance.
Andy Manis for The New York Times
Peaches, right, 9 months old, is a clone of Mango, 2 years old.
Forum: Gaming
Andy Manis for The New York Times
Peaches and Mango's owners are Leslie Ungerer, left, feline surrogate manager for Genetic Savings and Clone,
and Philip Damiani, the chief scientist.
When Mr. Cheng, who works as a technology auditor for a Wall Street investment bank, discovered that
Shadow had a tumor that would soon prove fatal, he had the cat's cells saved, cultured and frozen. Now, he is
preparing for the next step: paying for Shadow's cloned replacement. "I'm saving up some money," he said. "It's
a lot like buying a car."
The financing for Shadow's successor won't be trivial. Preserving the cells, a necessary beginning for anyone
interested in creating a clone, can run $300 to $1,400, not including veterinarian costs and yearly storage fees.
But these expenses pale in comparison with the cost of the clone itself: at Genetic Savings and Clone, the
company that stored Shadow's DNA, the price is $32,000 - reduced from the original $50,000, but still an
impressive sum.
Mr. Cheng said that he would pay whatever it cost - although he is waiting until the price drops a bit - because
he misses his cat so. "Shadow had two really long, funny-looking teeth like sabers," he said. "Everyone loved
him."
The cloning and sale of pets has its critics, who call it wasteful and inhumane. Some point to shelters bursting
with pets in need of homes, or remind buyers that cloning is still a relatively new process, with the health of
future generations of offspring still unknown. And the $32,000 lavished on one kitten clone would certainly pay
for the care of many a needy animal.
But Kathy Hudson, director of the Genetics and Public Policy Center at Johns Hopkins University, said
affection for lost pets was a powerful motivator. "People pay outrageous sums for unusual breeds and
purebreds, and, now, clones," she said. "Some people become adoring of a particular pet, and want another one
exactly like it."
Mr. Cheng is one of hundreds of customers of Genetic Savings and Clone in Sausalito, Calif., who have already
banked samples of pet DNA, said Ben Carlson, a company spokesman. People sign up for many reasons,
sometimes because their animals have been spayed or neutered and can't be bred, or because they were the
product of a unique genetic cocktail the company calls a breed of one. "We have many people whose pet is a
mutt with the perfect blend of characteristics," Mr. Carlson said. "That person can't go to a breeder, but he can
get what amounts to an identical twin from us."
Right now, Genetic Savings is selling only cat clones, although Lou Hawthorne, the chief executive, said the
company would probably produce its first cloned dog this year. So far, the company has sold two cat clones at
$50,000 each, and has sent out several contracts under the new, reduced price, which it plans to lower again as
the cloning process becomes more efficient.
To display its work and perhaps to help demystify its science, the company is opening an 8,000-square-foot
research site outside Madison, Wis. It will have plate-glass windows set into the U-shaped perimeter of a
laboratory so that people can view this modern version of a maternity ward.
They may also catch a glimpse of a local cat celebrity, Peaches, cloned last year from Mango, owned by Leslie
Ungerer, who oversees most of the feline projects at the lab. "They are fast friends," she said of mother and
clone, who spend part of their time at the lab and part at her home.
Mr. Hawthorne said all clones come with a one-year health guarantee. And, "We give an absolute, money-back
guarantee for physical resemblance," he said.
Dog owners can hardly wait. About 200 of them have signed up at Genetic Savings to preserve their pets' DNA.
Rebecca Alford, an opera singer who lives in Manhattan, has stored cells from her dog Missy, a Maltese mix,
now dead. Today Ms. Alford has five dogs, including two purebreds (one Shih Tzu and one Maltese) she
rescued when they were abandoned on the street. But they have not replaced Missy, she said. "I probably would
have had her bred, but I did the responsible thing and had her spayed," she said. "I won't get Missy back, but it
will be like getting her puppies."
People who want to save their pets' DNA usually start the process with a visit to a veterinarian, who collects the
tissue and mails it to Genetic Savings. Then the company cultures the cells, taking samples and growing new
cells, in a process that takes about three weeks and costs about $900, said Philip Damiani, the chief scientific
officer. Then the cells are frozen and stored in liquid nitrogen. After the first year, an annual $100 storage fee is
charged.
For a lower price, $295, customers can simply store biopsy samples, and wait until they are ready to clone to
have the culturing done. Mr. Hawthorne said business had been brisk for both the stripped-down process and
the more elaborate cell banking, and the procedures are almost always successful. "Most of the time, the tissue
grows well in culture," he said. "The marginal situations are when someone calls and says they buried their dog
three days ago."
Dr. Damiani said the procedures that people would be able to see in the display laboratory were straightforward,
and would show that the animals were treated well. The company receives cat reproductive tracts by contract
from large spay clinics. Eggs are taken from the tracts and the DNA is removed. DNA from the animal to be
cloned is placed in the egg, which is then grown into an embryo. "Once the egg is formed, we do a surgical
procedure," he said, placing the embryo inside a surrogate cat mother. "The procedure is no more invasive than
a typical spay."
That is not the view of Crystal Miller-Spiegel, senior policy analyst at the American Anti-Vivisection Society,
in Jenkintown, Pa., a Philadelphia suburb. "We are concerned about what's happening to cats in laboratories,"
she said. "They are harming animals for no reason." The society is a founding member of Californians Against
Pet Cloning, a group that supports legislation to ban the sale of genetically modified and cloned animals in
California.
Indeed, ethical issues like the treatment of animals used for cloning will need to be addressed systematically,
said Lori B. Gruen, an associate professor of philosophy at Wesleyan University, particularly as cloning grows
more efficient and therefore less expensive, and its popularity expands. "There are legitimate ethical worries
that people are expressing about the suffering of animals," she said. "But these problems can be adequately
addressed with an appropriate oversight body."
Such debates mean little to Mr. Cheng, who has a second cat named Nana that looks a lot like Shadow and is
one reason he has not opted to clone immediately. "I have to think about the other cat; she might not like having
another cat," he said of Nana, now 8 years old. "After she passes away, I may start all over again with one new
Shadow and one new Nana."