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Recent advances in genetic research have allowed scientists to grow the brain of one animal inside he body of an entirely different species. Is this the dawning of a new era or a scene out of The Island of Dr. Moreau?
The idea of splicing animals together isn’t a new one The ancient Greeks fashioned a chimera out of a snake, a goat, and a lion; the Japanese made a baku out of an ox, an elephant, and a tiger. Even today, people are inventing new creatures -only now, they’re using a lot more than their imaginations.
Just ask biologist Todd Streelman. Inside his lab at Georgia Tech, Streelman successfully bred a living animal with the brain of anther species. He started with a cichlid, a type of fish found in Lake Malawai, at the southern tip of Africa’s Great Rift Valley. Over the past 500,000 years, hundreds of different species of the cichlid have evolved from a single ancestor, with each new species developing a distinct set of jaws, teeth, brain, and behaviors to fit their respective environments. Streelman took two species of cichlid fish -rock-dwelling cichlids and sand-dwelling cichlids- and figured out a way to grow a sand-dweller’s brain inside the skull of a rock-dweller. From a distance, that might seem like a simple trick in cross-pollination. But it’s no small feat when you consider that the brains of the two creatures are as different as those of chimpanzees and humans.
Todd Streelman
ANIMAL CROSSING
How’d he do it? The trick to Streelman’s success was figuring out how (and when) the brains of different species distinguish themselves during embryonic development. In the earliest stages of life, the brain of almost every animal starts out looking the same. It begins as a small sheet of rapidly dividing cells that are not yet designed for different functions. But this sheet of cells eventually rolls into a tube, and the cells turn into different types of neurons. The neurons then slowly forms connections uniquely tailored to the creature’s lifestyle. In humans, for example, the brain develops a large cerebral cortex capable of processing language and consciousness. In various species of cichlid fish, the forebrain changes and grows depending on its future environment. More specifically, the sand-dweller’s forebrain develops a large hind region for surviving in open water, while the rock-dweller’s forebrain develops a large front region to navigate Lake Malawi’s murky, cavernous bottom.
In both species, the size and shape of the forebrain is determined by the expression of a gene called Wnt1. In sand-dwellers, this gene sends out a strong signal, while in rock-dwellers, Wnt1′s signal is weak. As part of his study, Streelmen took rock-dweller embryos and placed them in water treated with lithium chloride -a salt that’s known to increase the strength of the Wnt1 signal. This caused the rear section of the rock-dweller’s brain to grow until its brain looked like that of a sand-dweller. In other words, by simply changing the expression of a single gene, Streelman was able to Frankenstein a new fish.
Cichlid embryo
OF MICE AND MEN
While Streelman has proven that he can grow one species’ brain inside another’s body, there’s no telling if his patchwork creations can survive in their natural environments. To date, most attempts to manipulate neural development in animals have led to brains that look promising in the land but fail to function in the real world. In 2002, for instance, researchers manipulated a mouse’s genetic signals to increase the size of its cerebral cortex. The cortex grew dramatically, forming folds indicative of the intelligence in high-order mammals and humans. But the mutation proved fatal, and the mouse died before it was born.
Some scientists posit that the mouse’s death may have had more to do with the complex relationship between the animal and environment and less to do with ill-suited manipulation. Georg Striedner, and evolutionary biologist at the University of California at Irvine, has found that many animals go through a phase during early development in which they’re particularly vulnerable to injury, starvation, or disease. In order for an animal to survive, something in their external world has to protect them. For instance, many species go through a prolonged period of rapid cell division before their brains become neurons. This ultimately leads to a larger brain, but it also means that the animal’s brain is not fully formed at birth. Parrots are a good example. After parrots hatch, their brains aren’t particularly developed, which forces the babies to rely on their mothers for food. That means that the mothers’ feeding behaviors must have evolved at the exact same time that parrots evolved to have larger brains. Otherwise, parrots would have never become so smart.
Cichlid fish
The process of evolving new traits is clearly complicated. Labs can create animals with shiny new traits, but that doesn’t mean the animals can handle the complexity of the world around them. As for Streelman’s fish, no one knows how their manipulated brains will affect their behavior -or, for that matter, how they’ll fare in nature. In many ways, though, that isn’t the point. The goal of Streelman’s research isn’t to grow new and funky animals; it’s to learn how animals evolve. By discovering the relationship between the animal’s genome and its brain development, scientists ultimately hope to pinpoint the genetic basis of of human thought and behavior. It just may be that, along the way, creatures like the chimera and the baku become more than the stuff of ancient folklore.
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The article above, written by Adam K. Raymond, is reprinted with permission from the March-April 2011 issue of mental_floss magazine. Get a subscription to mental_floss and never miss an issue!
Be sure to visit mental_floss‘ website and blog for more fun stuff!
Research into why Transylvanian naked neck chickens have naked necks reveals a complex balance between genes and chemicals that produce a bird’s (not just chickens) feather pattern while it is still an embryo in an egg. Once the combination was discovered, Chunyan Mou from the University of Edinburgh found that bird necks are naturally more disposed to nakedness than the rest of their bodies. This may be no benefit to poultry, but chickens are related to birds that do benefit.
Mou thinks that similar genetic tweaks have happened time and again in the evolution of birds. Many groups have lost their neck feathers independently, including vultures, the marabou stork, and large flightless birds like ostriches and emus. Naked necks allow vultures to stuff their heads into carcasses without soiling any feathers; in other cases, a naked neck probably helps its owner to keep cool in hot climates.
Whatever the benefit, it seems that it’s particularly easy for birds to evolve a naked neck, rather than another part of their body. After all, Mou found that the necks of embryonic ducks, turkeys, quails and guinea fowl all have much higher levels of retinoic acid than the rest of the body. This pattern would normally be innocuous, completely hidden from natural selection. But it allows BMP-boosting mutations to denude the neck in one fell swoop, while keeping the rest of the body covered in feathers. As Mou writes, “An underlying map within the skin provides a one-step route to a bare neck.”
The post goes into detail about how the genes initiate the production of chemical activators and inhibitors, and ends with a parable from Alan Turing that explains the concept in layman’s terms. Link
(Image credit: Demontux)
A genetic study of Icelandic natives found a genetic variation in 80 people similar to a variation found mostly in Native Americans. The genetic code was traced back to four women who lived around 1700. But the history of Iceland leads experts to believe the gene must’ve entered the population hundreds of years earlier. The simplest answer so far that fits the facts is that some Viking brought back a Native American wife from North America, who then bore the first Viking-American child in Iceland.
“We know that Vikings sailed to the Americas,” said Agnar Helgason of deCODE Genetics and the University of Iceland, who co-wrote the study with his student Sigrídur Ebenesersdóttir and colleagues. “So all you have to do is assume … that they met some people and ended up taking at least one female back with them.
“Although it’s maybe interesting and surprising, it’s not all that incredible,” Helgason added. “The alternative explanations to me are less likely”—for example the idea that the genetic trait might exist independently, undiscovered, in a few Europeans.
Link -Thanks, Marilyn!
(Image credit: Robert Harding Picture Library, Alamy)
Is schizophrenia caused by genetics or environment? The answer may be both, but in a way you’d never imagine. The culprit may be a virus! The good news is that you don’t have to worry about catching this virus. The bad news is that we all carry it in every cell of our bodies.
Sixty million years ago, a lemurlike animal—an early ancestor of humans and monkeys—contracted an infection. It may not have made the lemur ill, but the retrovirus spread into the animal’s testes (or perhaps its ovaries), and once there, it struck the jackpot: It slipped inside one of the rare germ line cells that produce sperm and eggs. When the lemur reproduced, that retrovirus rode into the next generation aboard the lucky sperm and then moved on from generation to generation, nestled in the DNA. “It’s a rare, random event,” says Robert Belshaw, an evolutionary biologist at the University of Oxford in England. “Over the last 100 million years, there have been only maybe 50 times when a retrovirus has gotten into our genome and proliferated.”
But such genetic intrusions stick around a very long time, so humans are chockablock full of these embedded, or endogenous, retroviruses. Our DNA carries dozens of copies of Perron’s virus, now called human endogenous retrovirus W, or HERV-W, at specific addresses on chromosomes 6 and 7.
This virus was long thought to be “junk DNA”, which makes up a fair amount of our genetic material, but doesn’t affect us. The new line of research says that this virus, if it is activated at a certain age under the right conditions, may cause changes to human immune systems that lead to the development of not only schizophrenia, but multiple sclerosis and possibly other diseases. The story of how this discovery came about is a fascinating read at Discover magazine. Link
(Image credit: Flickr user ynse)
Why do some people murder? Is it in their blood? Maybe so, according to scientific studies that suggest that there is a genetic basis for violent behaviors:
They’ve tested some 30 criminal defendants, most of whom were charged with murder. They were looking for a particular variant of the MAO-A gene — also known as the warrior gene because it has been associated with violence. Bernet says they found that [the defendant] Waldroup has the high-risk version of the gene.
"His genetic makeup, combined with his history of child abuse, together created a vulnerability that he would be a violent adult," Bernet explains.
Over the fierce opposition of prosecutors, the judge allowed Bernet to testify in court that these two factors help explain why Waldroup snapped that murderous night.
"We didn’t say these things made him become violent, but they certainly constituted a risk factor or a vulnerability," Bernet says.
Bernet cited scientific studies over the past decade that found that the combination of the high-risk gene and child abuse increases one’s chances of being convicted of a violent offense by more than 400 percent. He notes that other studies have not found a connection between the MAO-A gene and violence — but he told the jury that he felt the genes and childhood abuse were a dangerous cocktail.
"A person doesn’t choose to have this particular gene or this particular genetic makeup," Bernet says. "A person doesn’t choose to be abused as a child. So I think that should be taken into consideration when we’re talking about criminal responsibility."
Does that make a person less culpable of his own actions? What do you think of the "my genes made me do it" defense?
Can you live to be 100 years old? Your genes might tell the story.
A newly discovered suite of 150 “long life” variants in about 70 genes allows scientists to guess, with 77 percent accuracy, whether a person can live into their late 90s or longer, a new study says.
These long-life gene variants, the authors speculate, may suppress genes associated with ailments often linked to aging, such as dementia and heart problems.
“This is just a genetic predisposition,” cautioned study leader Paola Sebastiani, a biostatistician at the Boston University School of Public Health. “It doesn’t mean that you’re going to live to be a hundred. Many things can happen in life.”
The research may lead to longer lives, but that would be so far in the future that our best bet is still a healthy lifestyle. Link
Some animals eats algae and incorporates the algae’s chlorophyll into its own body. According to Sidney K. Pierce of the University of South Florida in Tampa, the sea slug Elysia chlorotica no longer has to, because it has incorporated enough of the plant’s genes into its own DNA to manufacture chlorophyll in its own body!
The slugs can manufacture the most common form of chlorophyll, the green pigment in plants that captures energy from sunlight, Pierce reported January 7 at the annual meeting of the Society for Integrative and Comparative Biology. Pierce used a radioactive tracer to show that the slugs were making the pigment, called chlorophyll a, themselves and not simply relying on chlorophyll reserves stolen from the algae the slugs dine on.
“This could be a fusion of a plant and an animal — that’s just cool,” said invertebrate zoologist John Zardus of The Citadel in Charleston, S.C.
Microbes swap genes readily, but Zardus said he couldn’t think of another natural example of genes flowing between multicellular kingdoms.
It looks like the tree of life has some spots where it merges as well as branches. Link
(image credit: Nicholas E. Curtis and Ray Martinez)
There has never been a documented case of cancer found in a Naked Mole Rat, which is unusual as they can live to be 30 years old. Now biologists at the Unversity of Rochester believe they have found the reason.
The findings, presented in today’s issue of the Proceedings of the National Academy of Sciences, show that the mole rat’s cells express a gene called p16 that makes the cells “claustrophobic,” stopping the cells’ proliferation when too many of them crowd together, cutting off runaway growth before it can start. The effect of p16 is so pronounced that when researchers mutated the cells to induce a tumor, the cells’ growth barely changed, whereas regular mouse cells became fully cancerous.
“We think we’ve found the reason these mole rats don’t get cancer, and it’s a bit of a surprise,” say Vera Gorbunova and Andrei Seluanov, professors of biology at the University of Rochester and lead investigators on the discovery. “It’s very early to speculate about the implications, but if the effect of p16 can be simulated in humans we might have a way to halt cancer before it starts.”
Further research might reveal whether the findings will be applicable to humans. Link -via reddit
Is there an evolutionary reason for women to undergo menopause? One theory says that it happens so they can survive long enough to be grandmothers. This is not a reward; it is another method of helping one’s genes to survive and flourish.
The grandmother hypothesis suggests that humans have “given up” their reproductive potential in later years in order to invest in the children they already have as well as their grandchildren. Naturally, this is an unconscious, biological adaptation that emerges over many generations and is not the result of individual decision-making. For such a hypothesis to be confirmed it would have to be demonstrated that children are significantly more likely to survive when a grandmother is present than when she isn’t.
Dr. Lummaa has done just that in her study published in the journal Nature, demonstrating that children are 12% more likely to survive to adulthood when they have a grandmother’s support than when they don’t.
Let’s hear it for grandmas! Link
Charles Darwin was a lifelong fan of flowers, but was unable to figure out how they evolved. There were fossils of flowering plants going back 66-100 million years, which didn’t help much because flowers evolved much earlier. Recently, however, scientists are turning to DNA analysis of contemporary plants to decode where they came from. They are also finding older fossils than ever before, as far back as 136 million years ago. Paleobotanist James A. Doyle says the fossil record is the only thing that will bring together the many theories of flower evolution.
If you could travel back to 130 million years ago, you might not be impressed with the earliest flowers. “They didn’t look like they were going anywhere,” Dr. Doyle said.
Those early flowers were small and rare, living in the shadows of far more successful nonflowering plants. It took many millions of years for flowers to hit their stride. Around 120 million years ago, a new branch of flowers evolved that came to dominate many forests and explode in diversity. That lineage includes 99 percent of all species of flowering plants on Earth today, ranging from magnolias to dandelions to pumpkins. That explosion in diversity also produced the burst of flower fossils that so puzzled Darwin.
Genetic research is providing answers to how plants can switch on genes that control how different plants parts grow, and to use sexual reproduction to increase genetic diversity. Link
