Cognitive Labs

Lindisfarne Priory Stone, 794 C.E.

"From the fury of the Northmen, O lord, deliver us!," was the chant said to have been repeated endlessly in Dark Age churches and monasteries from northern Spain to France, west to Ireland (where the Vikings founded Dublin), Greenland, Iceland, and Vinland (Canada); the whole of the British Isles except the isolated southwestern tip, the Isle of Man, whence come the tailless manx cats, which are manx-allele positive, and north to Orkney, the Faroes and Shetland.

Around the Baltic periphery of Germany and Poland they came, and down the rivers of Ukraine and Russia to the Black Sea and Constantinople, where, unable to scale the massive walls and too impatient for sieges, some Vikings took up eating Spam and became mercenaries.

DNA analysis may have solved the puzzle, at least in the UK. Taking cheek-swab samples of hundreds of men around the British Isles and the northern islands, geneticists at University of London wanted to find out the echoes of how much "Viking" is left in the population today through the footprint of the Y chromosome.

In so doing, they hoped to learn more about two earlier population groups, the so-called 'Britons' or Celts and the Angles and Saxons, tribes which started invading Angle-land (German) as early as 300 C.E., best remembered in the old English tale of Beowulf, a time of magic swords, rings, dragons, and monsters.

Were they just raiding parties, or did they settle in these areas? The king of France, tired of their incessant pillaging and vandalism, made an accommodation with Rollo, a Viking war leader, by giving him a large hereditary fief, Normandy. In return, Rollo was supposed to settle down, support the king, and most importantly, defend the coast against other Vikings. Vikings later settled in southern Italy/Sicily, Russia-playing a role in the founding of the state, and around Constantinople.

The gene analysis was supported by the BBC and presented in a BBC Learning Series, the 'Blood of the Vikings.' It is no longer posted but may appear again. The accompanying scientific publication info is here. Additional research has just been completed.

The results were quite interesting.

The Vikings that invaded the British Isles were primarily from two points of origin, Denmark and Norway, who exhibited some genetic differences. It turns out that the early population of Britain has partial affinity with the pre-bronze age Gallic peoples that inhabited a broad swath of land from Asia Minor across Europe to France and Spain, in particular the Basques.

For a time prior to 6,000 B.C.E., the English channel was a misty meadow or tidal valley, forming a land bridge with the continent. This native Briton population is echoed in the genetics of southwest Britain and central Ireland, which resisted the Angles, Saxons, Vikings, and Normans, and is still (21st century) not fully assimilated with the other parts of the British Isles, according to geneticists.


left: Genetic footprint of UK populations in the 21st century
right: The approximate extent of Old Norse and related languages in the early 10th century around the North Sea. The red area is the distribution of the dialect Old West Norse, the orange area is the spread of the dialect Old East Norse and the green area is the extent of the other Germanic languages with which Old Norse still retained some mutual intelligibility

While there is a visible genetic difference between these remote, early peoples who were isolated by geography, and the Angles and Saxons who occur throughout the remainder of England; there was an insignificant genetic difference between the Anglo-Saxons and the Danish Vikings, mainly because these tribal groups all originated in the same area, northern coastal Europe.

In fact, accounts and the archaeology of the Saxon invasions tell us that their raids were somewhat like the Viking raids 400 years later. Groups of warriors arrived by sea in boats festooned with shields. In response, the Romans created a military office to defend against these raiders, the Count of the Saxon Shore (Comes Litoris Saxonorum), who built a chain of stone fortifications along the coast to defend against the raiders and safeguard in-kind taxes.


Walls of Garrianonum fort

At least one pretender to the imperial throne, Carausius, held this office prior to seizing power and creating a Britanno-Gallic empire, so we may conclude that it was an important administrative post with ample resources. The last legions sailed away from Britain in 410 C.E. to take part in a campaign on the continent, never to return, leaving the Romanized Briton population to deal with the seafaring Saxons and Angles.

Interestingly, genetic differences occur fairly dramatically in the North Sea isles held by Britain, the north of Scotland, and parts of the coast of Western England and Ireland, where the genetic footprint of the Norwegians is evident, with some 40-60% of the population showing affinity to that of Norway in the northern islands, and pockets elsewhere.

In the U.S., you would have to go to North Dakota to see anywhere near a similar level of Norwegian ancestry, which is around 30% of the population, 17% in Minnesota and 14% in South Dakota.

Labels: angles, chromosome, dna, faroes, genetics, manx, y

Mutations relating to radiation are well-known in agriculture and have resulted in some of the recognizable advances in food science - see here in what might be considered an interesting harvest.

Labels: broad, crops, genetics, mutations, nytimes

Science moves closer to Artificial life, not just Cloning

J. Craig Venter, he-of-the-Phosphorescent-blue-eyes, works on Artificial life of a sort (research to be published in Science)


Scientists have taken a first step toward making synthetic life by transferring genetic material from one bacterium into another, transforming the second microbe into a copy of the first.

They intend to use their technique to custom-design bacteria to perform functions such as producing artificial fuel or cleaning up toxic waste, the researchers report in Friday's issue of the journal Science.

"This is equivalent to changing a Macintosh computer to a PC by inserting a new piece of software," Craig Venter, a genome pioneer who now heads his own institute in Rockville, Maryland, told reporters in a telephone briefing.

"I think eventually we could make artificial cells," Venter added. "This is a first step."

Venter has been trying for years to create a microbe from scratch. This is not quite it, but his team re-programmed one species of bacteria by adding in the genetic material from a closely related species.

They gene-engineered the replacement chromosome to resist an antibiotic and then flooded their experiment with the drug. The bacteria that survived all carried only the genes that had been spliced in.

They believe all the others simply died, but they are in fact not sure how the new DNA re-programmed some of the bacteria or what happened to the original DNA.

"I think that we don't know for certain how the donor genome takes over," Venter Institute researcher Ham Smith told reporters.

Nonetheless, Venter's team has applied for a patent on the process and they hope to exploit it industrially. Venter believes it will be relatively straightforward to build a new chromosome from scratch, one that performs the desired functions, to create a custom-made bacterium.

"What we are reporting in this Science paper is not anything about a synthetic organism," Venter said.

BOOTING UP LIFE

"It's a key enabling step so that once we have a synthetic chromosome we know it is now possible to boot that up. So synthetic biology itself and synthetic genomics is much closer to being proven," Venter added.

"We look forward to having fuels from genetically modified organisms within the next decade and perhaps in half that time."

The key to the experiment was using a very simple bacterium called Mycoplasma capricolum, which often infects goats. Bacteria do not have a nucleus as do cells from more complex organisms.

The research team injected a chromosome from a related species called Mycoplasma mycoides.

They do not know how well it worked but at least some of the M. capricolum were transformed into what looked and acted like M. mycoides.

The scientists concede it will be much more difficult to do this with more complex organisms, even bacteria, that have cell walls and all sorts of defensive mechanisms to keep out foreign

DNA.

A non-profit Canadian organization called the ETC Group expressed concern about the experiment and Venter's patent application. "We are extremely concerned about the breadth and implications of this patent and of its monopoly claims," the group's Jim Thomas said in an e-mail.

"We will be requesting that patent offices worldwide refuse this patent."

But Venter defended the patent. "At every stage of what the team has done here over the past several years, we have had to develop novel technologies and approaches that have not existed before because the field has not existed before," he said.

Labels: artificial life, craig venter, dna, genetics, ham smith, microbes, mycoplasma

Scientists have unveiled results of the largest study of the genetics of autism, involving DNA from almost 1,200 affected families worldwide. Two key clues have already been isolated.

Discoveries in two areas of the genome -- a region on chromosome 11 suspected of having links to autism, and aberrations in a brain-development gene called neurexin 1 -- could spur more targeted research, the experts noted.

"That's the real promise here," said Autism Genome Project co-researcher Dr. Stephen Scherer, director of the Center for Applied Genomics at The Hospital for Sick Children in Toronto. "When you identify certain genes, you can then develop genetic tests -- in some cases prenatal and in some cases postnatal -- because early diagnosis is crucial here."

Genetic discoveries can also further research toward a cure for autism, Scherer said.

"When we have this type of knowledge, we can actually think about designing better therapies based on what we know is not happening properly in the [brain] cell. We can try and design things to make it work better," he explained.

The Autism Genome Project was funded by the U.S.
National Institutes of Health and the nonprofit advocacy group Autism Speaks. Its findings were published in the Feb. 18 online edition of Nature Genetics.

Autism remains a real health crisis, with the U.S. Centers for Disease Control and Prevention announcing recently that one in every 150 American 8-year-olds now have some form of autistic spectrum disorder. That number is higher than prior estimates, and the debate rages as to just why the disease might be becoming more prevalent.

Experts agree that autism's causes remain cloaked in mystery, although prior research has pointed to a strong genetic component. For example, "there's about 90 percent concordance [of autism] between identical twins -- that's a significant genetic contribution," Scherer said.

So, the Autism Genome Project, which took five years to complete, sought to probe much deeper into the DNA driving the disorder. The project involved more than 120 scientists working at 50 institutions in 19 countries. They painstakingly sought out almost 1,200 families worldwide in which at least two members were affected by autism. The scientists then collected DNA samples from family members and analyzed these samples in the most advanced and standardized manner, looking for genomic "commonalities."

Those efforts have met with real success.

"First, we found several regions of the genome, particularly one region on chromosome 11, that seem to be very highly associated with the development of autism," said Scherer, who is also professor of medicine at the University of Toronto. While prior research had suggested chromosome 11 as a potential hotspot for autism-linked DNA, this study greatly strengthens that view, he said.

The researchers also used cutting-edge technologies to seek out what are known as "copy number variations" -- genes that appear not in pairs (as most genes passed down from mom and dad are), but as just a single copy, or as three or more copies.

"We found several regions of the genome -- sometimes the same region popping up in unrelated individuals -- with 3 or more copies," Scherer said. "We didn't see these in the individuals' parents, so that implies that these regions are harboring susceptibility genes for autism."

One gene in particular, called neurexin 1, appeared in some cases in just one copy. "In one family, both of the children who were autistic actually had that piece missing," Scherer said. "That's kind of a smoking gun that the gene is implicated."

It makes intuitive sense that dysfunctional neurexin 1 might play some role in autistic disorders, another expert said.

The neurexin 1 protein and its kin, "are very important in determining how properly the brain is wired up from one nerve cell to another, and in the chemical transmission of information from one nerve cell to another," said Dr. Bradley Peterson, a professor of child psychiatry at Columbia University Medical Center and the New York State Psychiatric Institute, in New York City.

Peterson, who was not involved in the project, said genes that effect early neural growth could be key to autistic disorders, since "the genetic and the non-genetic contributions to autism, by definition, have to exert their effect very early in brain development, either in utero or in the first months or couple of years of life."

Still, he and Scherer both stressed that the new study only points to potential leads for future research. Because of the study's particular methodology, no one finding reached statistical significance, Peterson said. "This is all very strong evidence, and a very good set of leads, but we can't yet say that we have proved the involvement of these regions in autism," he said.

Scherer said that, except in very rare instances, there isn't likely to be a single gene responsible for autism. Instead, a variety of genetic abnormalities may work on each other during development to create some level of autism. And experts don't discount the potential role of environmental stresses on that mix, either.

"Remember, autism is actually a grab bag of different developmental disorders. And what we show here is that many genes can be involved, and also these copy number variants," Scherer said. "And could it be that environment is contributing? Absolutely."

One thing is for sure, however: Autism research holds more promise now than ever before, the experts said.

"Anybody that's working out here can use this information now, and it really provides a great path forward as to how we need to do our experiments over the next five years or so," Scherer said. "We've now got all these new candidate genes --- the neurexins, the various copy number variants -- and we can tackle the problem in a much more focused and organ ized way."

Labels: autism, dna, genetics