Genetics // Current

Will the Duggars Inherit the Earth? Can't anyone stop them from breeding like rabbits?

The answer: Kinda-sorta.

"It's really just a little simple math," said Spencer Wells, Ph.D., Explorer-in-Residence with the National Geographic Society, working on their Genographic Project, which traces human migration patterns by studying DNA markers. "If you imagine that each of the Duggars' 19 kids has 19 kids, for only four generations--that's only going for 100 years--there would be 130,000 descendants of this one couple."

But, at the same time, it's not as easy as all that. Wells, and colleague Chris Tyler-Smith, Ph.D.,head of the Human Evolution team at The Wellcome Trust Sanger Institute, said it's too early to tell what the Duggars' genetic impact on America will be.

Let's look back at Khan again. And clarify things a bit, while we're at it. It's important to point out that nobody knows for certain that 8 percent of Asian men are descendants of the Mongol leader. What we know is that those men share a collection of genetic mutations--a haplotype--on the Y chromosome, which suggests that they all shared a common male ancestor.
Y chromosomes are passed from father to son intact, without the shake-n-bake interference of maternal DNA. So Y chromosomes don't get remixed each generation, but they do, occasionally, pick up a small change here and there from random mutation. Scientists know roughly how often those mutations happen, so they can look at a haplotype, see how different it is from the general population, and get an idea of when that family group broke off from the herd. In this case, the point of origination would have been about 1000 years ago, give or take.
Scientists associate the haplotype with Genghis Khan not because all the men who share it have a predilection for little furry hats, but because of simple logical deduction. It's a rare guy who is going to have enough children, and whose children will have enough children (and etc.) to leave such a big mark on such a large geographic area. Historically, we know that around 800 years ago, old Genghis was doing quite a bit of marrying, concubining and raping/pillaging. And we know that his immediate descendants were also powerful men who were able to have a lot of children, with a lot of different women, in a lot of different places. Chris Tyler-Smith explains it thusly,

"So we can either say that there were two separate events: One, Genghis Khan's lineage, which was present in Mongolia 800 years ago and we know was greatly amplified over the next centuries, has disappeared from the current gene pool, while another lineage that arose in the same place around the same time has reached high frequency without leaving any trace in history. Or we can say that Genghis Khan's lineage and the star cluster lineage were the same. To me, this second possibility is the simpler explanation. Indirect, but a bit more than guesswork."

To tie this whole Mongolian warlord thing back to the Duggars, just look at the kids. Genghis' sons, grandsons, and great-grandsons were privileged by his power and wealth. They had the means to support BIG families, and the social capital to acquire those families. In fact, they had the social obligation to breed it up. And, thus, did the not-exactly-meek-and-peaceful Khan inherit most of Asia.

Whether the scientists of 2800 are studying the Duggar haplotype depends on how many babies the 19 Duggar kids, and their kids, have. In this case, it's not necessarily a given that the parents' productivity will be inherited. If growing up in America's biggest TV family leaves most of the kids gun-shy, so to speak, the family could end up with no more of a long-term genetic footprint than the rest of us. On the other hand, there are certainly social and religious factors encouraging the Duggarlets to follow in their parents' footsteps. And, if a large number of them do, and if their kids carry on the family tradition...we could well be on the way to welcoming our Duggar overlords. Genetically speaking.The answer: Kinda-sorta. "It's really just a little simple math," said Spencer... more

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Judge OKs Challenge to Human-Gene Patents

http://www.wired.com/threatlevel/2009/11/genes/ The patents at issue give Myriad... more

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Shrink Yourself & Explore Innerspace!

http://learn.genetics.utah.edu/content/begin/cells/scale/

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Breakthroughs in tissue regrowth give hope to war wounded

It's science fiction turning into fact. A new Defense Department program to make... more

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Lasers Write False, Fearful Memories into Brains of Flies

It sounds like a scene from an insect version of Total Recall: Using genetically engineered fruit flies and laser beams, researchers have found a way to embed false, fearful memories in the flies.

Researchers first tested normal flies in a chamber where a jets of air on either side brought two different odors into the container. The researchers delivered an electric shock each time a fly strayed into a particular odour stream, which taught the flies to prefer the other one: the flies learned to move in the direction of the shock-related odour 30 per cent less often [New Scientist].

Next, the researchers created a strain of genetically engineered flies with certain neurons that would be activated by a laser blast. Lead researcher Gero Miesenböck explains that with this technique, called optogenetics, researchers can use light to activate particular cell types that have been genetically engineered to express a light-responsive protein. When laser pulses hit the brain, cells expressing the light-sensitive protein activate. “It’s like sending a radio signal to a city but only those houses with a radios set to the right frequency will get the signal,” says Miesenböck [Nature News].

The flies were then put back in the chamber with the two jets of air, and every time they wandered into one of the odor streams, the laser was fired. Many of the flies were unaffected, but a select group quickly learned to avoid the odor stream associated with the laser pulse. Miesenböck says these flies feared that smell as if they had been conditioned to associate an electric shock with it. “Stimulating just these neurons gives the flies a memory of an unpleasant event that never happened,” he says [New Scientist].

In the genetic engineering process, the scientists had tweaked different neurons in different groups of flies. The contingent that did react to the laser all had 12 particular light-sensitive neurons, according to the study published in the journal Cell. Those 12 brain cells may be the root of associative learning, researchers say–at least in flies.It sounds like a scene from an insect version of Total Recall: Using genetically... more

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Genetically Engineering the "Smart Rat"

Dubbed Hobbie-J after a smart rat that stars in a Chinese cartoon book, the transgenic rat was able to remember novel objects, such as a toy she played with, three times longer than the average Long Evans female rat, which is considered the smartest rat strain. Hobbie-J was much better at more complex tasks as well, such as remembering which path she last traveled to find a chocolate treat.

The report comes about a decade after the scientists first reported in the journal Nature that they had developed "Doogie," a smart mouse that over-expresses the NR2B gene in the hippocampus, a learning and memory center affected in diseases such as Alzheimer's. Memory improvements they found in the new genetically modified Long Evans rat were very similar to Doogie's. Subsequent testing has shown that Doogie maintained superior memory as he aged.

"This adds to the notion that NR2B is a universal switch for memory formation," says Dr. Joe Z. Tsien, co-director of the MCG Brain & Behavior Discovery Institute and co-corresponding author on the paper published Oct. 19 in PLoS One.

The finding also further validates NR2B as a drug target for improving memory in healthy individuals as well as those struggling with Alzheimer's or mild dementia, the scientists says.

NR2B is a subunit of NMBA receptors, which are like small pores on brain cells that let in electrically-charged ions that increase the activity and communication of neurons. Dr. Tsien refers to NR2B as the "juvenile" form of the receptor because its levels decline after puberty and the adult counterpart, NR2A, becomes more prevalent.

While the juvenile form keeps communication between brain cells open maybe just a hundred milliseconds longer, that's enough to significantly enhance learning and memory and why young people tend to do both better, says Dr. Tsien, the Georgia Research Alliance Eminent Scholar in Cognitive and Systems Neurobiology. This trap door configuration that determines not just how much but how fast information flows is unique to NMBA receptors.

Scientists found that Hobbie-J consistently outperformed the normal Long Evans rat even in more complex situations that require association, such as working their way through a water maze after most of the designated directional cues and the landing point were removed. "It's like taking Michael Jordan and making him a super Michael Jordan," Deheng Wang, MCG graduate student and the paper's first author, says of the large black and white rats already recognized for their superior intellect.

But even a super rat has its limits. For example with one test, the rats had to learn to alternate between right and left paths to get a chocolate reward. Both did well when they only had to wait a minute to repeat the task, after three minutes only Hobbie-J could remember and after five minutes, they both forgot. "We can never turn it into a mathematician. They are rats, after all," Dr. Tsien says, noting that when it comes to truly complex thinking and memory, the size of the brain really does matter.

That's one of the reasons scientists pursue this type of research: to see if increased production of NR2B in more complex creatures, such as dogs and perhaps eventually humans, gets the same results. He also is beginning studies to explore whether magnesium – a mineral found in nuts, legumes and green vegetables such as spinach – can more naturally replicate the results researchers have obtained through genetic manipulation. Magnesium ion blocks entry to the NMDA receptor so more magnesium forces the brain cell to increase expression levels of the more efficient NR2B to compensate. This is similar to how statin drugs help reduce cholesterol levels in the blood by inhibiting its synthesis in the liver.

Scientists created Hobbie-J and Doogie by making them over-express CaMKII, an abundant protein that works as a promoter and signaling molecule for the NMDA receptor, something that likely could not be replicated in humans.Dubbed Hobbie-J after a smart rat that stars in a Chinese cartoon book, the transgenic... more

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Richard Dawkins: Evolution is not a theory, it is a fact

It's been a rather big year for Charles Darwin. 2009 is the bicentennial of the man's birth and the 150th anniversary of the publication of "The Origin of Species," and the explorer and naturalist has been the subject of books (including a graphic novel adaptation of "The Origin of Species"), a movie starring Jennifer Connelly (with its own ensuing controversy), and even a viral video hit starring "Growing Pains" actor Kirk Cameron. Given that evolutionary biology is Richard Dawkins' area of expertise, it's unsurprising that the British scientist, atheist and controversial author of "The God Delusion" has also gotten on the bandwagon -- in rather ambitious fashion.

In "The Greatest Show on Earth," Dawkins has written what is essentially a layperson's primer for the theory of evolution. Dawkins aims to explain to the everyday reader why evolution isn't a "theory" but a fact and that we need only look around us to find evidence of its existence -- from continental drift to the reproductive habits of wasps. Dawkins uses simple language, elaborate metaphors and color photographs to make his point, and the result is a convincing, if occasionally dry, overview of evolutionary biology. It's also clear, from the book's first pages, that Dawkins isn't very tolerant of his creationist opponents (the book includes a memorably confrontational encounter with Wendy Wright, the creationist president of Concerned Women for America).

Salon spoke with Dawkins via Skype about creationism's popularity in America, its connection with religion, and how he feels about his own notoriety. A video excerpt of the conversation is posted below.

...................................
(excerpt)

Q: Do you think that there's any one particular piece of evidence that will change people's minds about creationism, or do you think that it's really just a question of a gradual erosion of people's belief systems?

A: I wouldn't expect their minds to be changed by fossils, really. I think the more convincing evidence is the evidence from comparison of modern animals and plants, because we have so many different species, and by comparing them with each other, particularly comparing the molecular genetics which is nowadays very easily done. All living creatures have the same genetic code, so you have an exact digital count of the similarities between every species and every other species, and if you look at that pattern of similarities it falls perfectly into a hierarchical tree. It's a family tree. And even better than that, everything you look at -- every different gene you look at -- gives you the same family tree. That's remarkably persuasive evidence to anybody who attends to it long enough to understand.It's been a rather big year for Charles Darwin. 2009 is the bicentennial of the man's... more

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Is autism genetic? Researchers Discover possible link

(Health.com) -- Alisa Rock, whose 10-year-old son Connor has autism, says parents of autistic children often align themselves with one of two camps: There are those who believe that genes cause the disorder, and those firmly convinced that environmental factors are to blame.

"Then there are people who are in the middle," says Rock, a Baltimore, Maryland, mom. She counts herself in this category, as she thinks that both genes and environment likely play a part.

She has, however, more questions than answers. "I personally am still a confused parent," she explains.

So it would seem helpful that new research on autism has just discovered a possible genetic link -- an alteration near a gene called semaphorin 5A, which is thought to guide the growth of brain-cell extensions essential for neuron-to-neuron communication. But for some parents, including Rock, the research is just a stepping stone to answering the million-dollar question: What causes autism?

"I don't think they're there yet, and I don't think that [this gene is] the answer for every single child with autism," Rock says. "Autism's just a set of symptoms. It doesn't really tell you about the child or what their disease is, really." Health.com: Kids on the run: The new trend in family-friendly fitness

And that's what the researchers say too.

"The scientific consensus now is that we're not talking about a single disorder. We're talking about a collection of disorders that are probably related," says Andy Shih, the vice president of scientific affairs for Autism Speaks, a New York City-based organization that supports autism research and advocates for people with autism and their families. "The current thinking is that there could be as many as 100 genes or more involved in autism."

In the new findings, published in the journal Nature, a team of researchers from Johns Hopkins University, Harvard, and several other institutions sifted through the genomes of 1,031 families that included at least two people with autism.

A simple change near the semaphorin 5A gene was "significantly associated with autism," they report, while dissections of brain tissue from 19 autistic individuals and 10 people without autism revealed that the gene's expression was lower in people with autism.

"That is both exciting as well as daunting," says Aravinda Chakravarti, who directs the Center for Complex Disease Genomics of the McKusick-Nathans Institute of Genetic Medicine at Johns Hopkins, in Baltimore, Maryland. If other researchers replicate the association -- meaning they do the experiment independently and get the same result, the gold standard of scientific proof -- experiments can be done to begin to unravel what environmental factors might interact with genes to contribute to the disease, he adds.

...More...(Health.com) -- Alisa Rock, whose 10-year-old son Connor has autism, says parents of... more

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Skin cancer can be inherited: studies

NEW YORK (Reuters Health) - Want to reduce your risk of skin cancer? Wear sun screen,... more

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Gene Controlling Number of Brain Cells Pinpointed

In populating the growing brain, neural stem cells must strike a delicate balance between two key processes – proliferation, in which the cells multiply to provide plenty of starting materials – and differentiation, in which those materials evolve into functioning neurons.

If the stem cells proliferate too much, they could grow out of control and produce a tumor. If they proliferate too little, there may not be enough cells to become the billions of neurons of the brain. Researchers at the University of North Carolina at Chapel Hill School of Medicine have now found that this critical balance rests in large part on a single gene, called GSK-3.

The finding suggests that GSK-3 controls the signals that determine how many neurons actually end up composing the brain. It also has important implications for patients with neuropsychiatric illness, as links have recently been drawn between GSK-3 and schizophrenia, depression and bipolar disorder.

One of the genes associated with schizophrenia appears to use GSK-3 as an intermediary to exert its effects on nerve cells. In addition, lithium, a popular treatment for bipolar disorder, acts, in part, by shutting down GSK-3. “I don’t believe anyone would have imagined that deleting GSK-3 would have such dramatic effects on neural stem cells,” said senior study author William D. Snider, M.D., professor of neurology and cell and molecular physiology, and director of the UNC Neuroscience Center. “People will have to think carefully about whether giving a drug like lithium to children could have negative effects on the underlying structure of the nervous system.”

In a study appearing online October 4th in the journal Nature Neuroscience, Snider and his colleagues created a mouse model in which both forms of the GSK-3 gene – designated alpha and beta – had been deleted. They decided to go after GSK-3 – which stands for glycogen synthase kinase 3 – because it is one of the most studied kinases or signaling molecules in all of biology.

The researchers used a “conditional knock-out” strategy to remove GSK-3 at a specific time in the development of the mouse embryo, when a type of cell called a radial progenitor cell had just been formed.

As the brain develops, neural stem cells evolve through three different stages -- neural epithelial cells, radial progenitor cells and intermediate neural precursors. The radial progenitor cells are especially important because they are thought to provide the majority of the neurons of the developing brain but also differentiate themselves to give rise to all the cellular elements of the brain. The researchers discovered that deleting GSK-3 during this second phase of development caused the radial progenitor cells to be locked in a constant state of proliferation.

“It was really quite striking,” said Snider. “Without GSK-3, these neural stem cells just keep dividing and dividing and dividing. The entire developing brain fills up with these neural stem cells that never turn into mature neurons.”

GSK-3 is known to coordinate signals for proliferation and differentiation within nerve cells through multiple “signaling pathways.” Thus, the researchers looked to see what effect deleting the molecule had on some of these pathways. They found that every one of the pathways that they studied went awry.

Snider and his colleagues now want to see if adding GSK-3 back to their genetically engineered mice can convert the proliferating stem cells into neurons, possibly resulting in three to four times as many neurons in the mutants as normal.

“I find that quite interesting because I can’t think of any other manipulation that potentially would enable you to simply dial up and down the number of neurons that are generated in the brain,” said Snider.

Funding for the studies led at UNC came from the National Institutes of Health. Study co-authors from Snider’s laboratory at UNC include lead author Woo-Yang Kim, Ph.D., postdoctoral research associate; Xinshuo Wang, graduateIn populating the growing brain, neural stem cells must strike a delicate balance... more

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Single Genetic Tweak Gives Mice Longer, Healthier Lives

By deleting a single gene from a mouse’s genetic makeup, researchers have created a... more

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Bizarre Genetic Testing of African Refugees Raises Outcry from Scientists

Scientists in the United Kingdom are outraged over a new program that seeks to... more

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Largest T-Rex Ever Discovered Died of a Throat Infection Found in Pigeons

Could the Chicago Field Museum’s mighty Tyrannosaurus Rex, a dino named Sue, have... more

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Scientists Decry "Horrifying" UK Border Test Plan

Scientists are dismayed and outraged at a new project by the UK border agency to test... more

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Ancient HIV-like Virus Discovered in Fossilized Remains

The retroviruses which gave rise to HIV first evolved around 100 million years ago –... more

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Blue-Eyed Humans Have a Single, Common Ancestor

New research shows that people with blue eyes have a single, common ancestor. A team at the University of Copenhagen have tracked down a genetic mutation which took place between 6,000 and 10,000 years ago and is the cause of the eye color of all blue-eyed humans alive on the planet today.

What is the genetic mutation

“Originally, we all had brown eyes”, said Professor Eiberg from the Department of Cellular and Molecular Medicine. “But a genetic mutation affecting the OCA2 gene in our chromosomes resulted in the creation of a “switch”, which literally “turned off” the ability to produce brown eyes”. The OCA2 gene codes for the so-called P protein, which is involved in the production of melanin, the pigment that gives color to our hair, eyes and skin. The “switch”, which is located in the gene adjacent to OCA2 does not, however, turn off the gene entirely, but rather limits its action to reducing the production of melanin in the iris – effectively “diluting” brown eyes to blue. The switch’s effect on OCA2 is very specific therefore. If the OCA2 gene had been completely destroyed or turned off, human beings would be without melanin in their hair, eyes or skin color – a condition known as albinism.

Limited genetic variation

Variation in the colour of the eyes from brown to green can all be explained by the amount of melanin in the iris, but blue-eyed individuals only have a small degree of variation in the amount of melanin in their eyes. “From this we can conclude that all blue-eyed individuals are linked to the same ancestor,” says Professor Eiberg. “They have all inherited the same switch at exactly the same spot in their DNA.” Brown-eyed individuals, by contrast, have considerable individual variation in the area of their DNA that controls melanin production.

Professor Eiberg and his team examined mitochondrial DNA and compared the eye colour of blue-eyed individuals in countries as diverse as Jordan, Denmark and Turkey. His findings are the latest in a decade of genetic research, which began in 1996, when Professor Eiberg first implicated the OCA2 gene as being responsible for eye colour.

Nature shuffles our genes

The mutation of brown eyes to blue represents neither a positive nor a negative mutation. It is one of several mutations such as hair color, baldness, freckles and beauty spots, which neither increases nor reduces a human’s chance of survival. As Professor Eiberg says, “it simply shows that nature is constantly shuffling the human genome, creating a genetic cocktail of human chromosomes and trying out different changes as it does so.”New research shows that people with blue eyes have a single, common ancestor. A team... more