Tag Archives: gene

mouse brain

Big-brained mice engineered using human DNA

In the quest to understand what are the crucial differences between human and chimpanzee brains, scientists have isolated a stretch of DNA, once thought to be “junk”, near a gene that regulates brain development in mice. The engineered mouse embryos grew significantly larger brains. Those which received human brain DNA strands had 12% larger brains than those bred with chimp brain DNA. Research like this, though ethically controversial, might help identify which DNA sequences give a brain human characteristics, but also aid in findings treatment or cures for brain diseases like Alzheimer’s.

mouse brain

Image: Current Biology

It’s a common fact thrown about that humans and chimps, often called our cousins, share 95% of their DNA. Though it’s easy to see a piece of you in the eyes of a chimp, we humans and chimps are quite different. Basically, we’re more complex,  something that can be easily interpreted from brain size. Depending on the specimen, chimp brains are two to four times as small as the human kind. Debra Silver, a neurobiologist at Duke University Medical School, is studying DNA code that is different between the two or unique to each species in an attempt to piece those pieces of DNA that made humans the dominant species on Earth. For, make no mistakes, we owe it all to our superior intellect.

“We went through those and picked out ones that seemed to be likely to be regulating gene activity in a developing brain,” explains Silver.

The researchers focused on a particular DNA stretch which looked promising since it was located near a gene known to be involved in brain development. So, to see what could happen, the researchers added the chimp version of the DNA to mouse embryos. Then, in other mouse embryos, they added the human DNA.

“What we discovered is that the human DNA turned on gene activity in neural stem cells, and these are cells which produce the neurons of our cerebral cortex,” says Silver.

current biology -

Image: Current Biology

All the mice grew bigger brains than they would have normally, but those embryos infused with the human DNA had a significantly bigger brain than the rest – 12% larger than those bred using the chimp variety of the DNA, according to the paper published in Current Biology. What’s interesting is that this particular DNA code was thought to be “junk”, a slag for DNA that doesn’t code proteins. Evidently, discoveries like these overthrow this common assumption that see “useless” DNA as serving no purpose. The genome – the entire DNA sequence of an organism – is made up of a small number of genes. The rest or bulk of it is comprised of DNA that regular gene expression. Code that turns a gene on or off, and more often than not it’s gene expression that make all the difference between a human, chimp or mouse, and not the presence of a gene itself.

“We have very little scientific information about the actual functions of those regions,” says Katie Pollard, who studies human and chimp DNA at the Gladstone Institutes and the University of California, San Francisco.

Most of the genetic differences between humans and chimps are actually found in the so-called junk DNA, Pollard notes. “While it’s now pretty easy to find the genetic differences, it’s very challenging to figure out exactly whether those differences made a change in a trait, and why.”

This new study, says Pollard, “is helping to try to bridge that gap.”

But will the big-brained mice be smarter? It’s very difficult to gauge this kind of cognitive enhancement, but the researchers are most excited about probing this idea once the pups reach adulthood. Ideally, the best results would be seen if scientists would tinker with switching off and on genes in human and chimpanzee embryos, but this would be dubiously unethical. Instead, Pollard and colleagues are keeping their eyes on petri dishes.

“We can now actually generate the equivalent of embryonic brain cells and tissues that are human or chimpanzee,” says Pollard. “And, using genome engineering techniques, we can start to study the effects of switching the human and the chimp sequences in these primate cell lines.”

Could this sort of research render super animals with human-like cognition? Well, according to those involved something out of Planet of the Apes is why too far ahead, if not impossible. But while we won’t make mice that can speak any time soon, this sort of tinkering with the brains of nonhuman primates or other reasonably intelligent animals, like pigs, is seemingly unethical and merits particular attention.

“The prospect of, sort of, tearing down the barriers between humans and other nonhuman species in ways that really threaten our sense of ourselves as special is disturbing,” Ruth Faden points out, who directs the Johns Hopkins Berman Institute of Bioethics.

Would you clone your dog for $100,000?

We’ve come a long way since the first mammal, a sheep named Dolly, was cloned. Now, a lab in South Korea will clone your dog for around $100,000; so far, they’ve cloned 400 pets since 2006.

Los Angeles businessman Peter Onruang cloned his dog, Wolfie.

Cloning is still tabu in many parts of the world, but it’s a process which is no longer reserved for the future – it’s happening now. It took 434 attempts before researchers managed to clone Dolly, and the sheep only lived for six years, but now, the Sooam Biotech Research Foundation laboratory in South Korea can clone your dog pretty with relative ease. They’re using the same technology through which Dolly was cloned, and the price is somewhere around $100,000.

The technology is called ash nuclear transfer. It starts by taking a few cells from your beloved pet and then reprogramming them to stop growing. They then take an egg from a different female dog, and with a straw-like device they remove its nucleus. With a similar device, they take the nucleus from your dog and place it in the egg. The cell nucleus contains most of the cell’s genetic material, organized as multiple long linear DNA molecules. They then zap the resulting cell with electricity to fuse it together and ensure that it can divide again, and then they reimplant the egg in a surrogate mother dog. If everything else works out fine, the surrogate mother will give birth to a dog which will look exactly like your dog. I say “look exactly like your dog” because it won’t exactly be your dog… it’s something more like a perfect twin of your dog.

“The dog will not be 100 percent the same – the spots on a Dalmatian clone will be different, for example – but for breeds without such characteristics it will be very hard to tell them apart,” Sooam biologist Insung Hwang told The Guardian last year.

So, doesn’t this mean that you’re technically not getting your pup? Indeed, Hwang admits that this is the case – people are “not getting their old dog back”, but a new one that looks just like it. It will also likely have the same temperament, but it won’t be the same dog. There are also many risks associated with this procedure, and often times it goes wrong.

“Things can go wrong. In 2005, when Snuppy, our first cloned dog, was born, we had a 2% pregnancy rate. Now it is about 30%. Some traits go wrong. Dogs can be born unhealthy. For example, they can be born with thickened necks or tongues, and experience breathing difficulties. But we guarantee a healthy puppy for our clients, so we will try again. Often the client will take both puppies in this situation. We never put a dog down.”

Hwang poses with the recently uncovered woolly mammoth, whom the researchers named Buttercup. He hopes to be able to clone this wooly mammoth. Image via Business Insider.

Technologically, this is a laudable achievement. It also serves the purpose of improving and further developing the technique. But what about the ethics? Is it ethical to create life like this – especially when there’s a good chance of the puppy suffering from defects? Oh, and technically you’re not getting your dog back, you’re just getting a really good surrogate… so one could argue that there is little point in doing this. There is also another big problem with this laboratory. As Erin Brodwin writes for Business Insider:

“Eight years after winning international acclaim for cloning the world’s first dog in 2005, Sooam founder and veterinarian by training Woo Suk Hwang was publically disgraced for falsifying research on human embryo cloning. Hwang (no relation to Insung Hwang) was expelled from Seoul National University, where he did the research, and is still facing criminal charges.”

Despite public outrage, Hwang was able to raise funding and start this laboratory, and these days, they’re producing about 15 pups a month. For some people, it’s just a way to ease the pain, and a good replacement. As someone who dearly loves animals, I can understand that. I’m not sure I agree with it, but I can understand it.

Cloning can be very useful in bringing back to life extinct species, as some scientists are already planning. Hwang also believes that, together with Russian researchers he can bring back to life a wooly mammoth – though many doubt that possibility. All in all, the technique can be very valuable, but I still feel that we need to set a very clear ethical framework. With this, the question remains: would you clone your dog ?


Genome duality: chromosome sets sequenced separately reveal magic ratio

Genetic diversity is essential to our survival, but its exactly the huge variance in genetic information that makes all so sought for personalised treatment so difficult. And you don’t need to look at an entire population or even two different people to experience the power of diversity. It’s enough to look inside your own, personal genome since you carry two versions of a gene – one for each parent. Now, for the first time, scientists at the Max Plank Institute for Molecular Genetics in Berlin have decoded the genetic information on the two sets of chromosomes separately.

A dual nature

Image: louisdietvorst.wordpress.com

This may be a breakthrough moments for genetics. While the team led by Margret Hoehe used a small sample size based on the decoded maternal and paternal parts of the genome in 14 people, an amazing discovery was made: the two paternal chromosome sets are distributed in the same ratio in everyone. This ratio held so closely in all the sequenced genomes  – with supplemented genetic material gathered from 372 Europeans from the 1000 Genomes Project – that it is very likely that the findings hold true no matter how many genomes are sequenced.

“Fourteen people may not sound like a lot, but given the technical challenge, it is an unprecedented achievement,” says Hoehe.

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Using novel molecular genetic and bioinformatic methods, the team found that most genes have many different forms. On average, 250 different forms of each gene exist and some four million different genes were found in just the 400 or so genomes that were sequenced. Considering 85 percent of all genes have no predominant form which occurs in more than half of all individuals, we can safely say that around 9,000 of all the 17,500 gene occur uniquely in that one person.

“We need to fundamentally rethink the view of genes that every schoolchild has learned since Gregor Mendel’s time. Moreover, the conventional view of individual mutations is no longer adequate. Instead, we have to consider the two gene forms and their combination of variants,” Hoehe explains.

A magic ratio

Every human being possesses a cis and trans mutations in a 60:40 ratio. In the cis configuration two mutations occur in one and the same genetic copy. The corresponding protein becomes incapacitated, but the second copy and the protein remain unaffected. In the trans configuration, however, both copies of the gene are mutated and produce two -damaged proteins. © Art 4 Science

Every human being possesses a cis and trans mutations in a 60:40 ratio. In the cis configuration two mutations occur in one and the same genetic copy. The corresponding protein becomes incapacitated, but the second copy and the protein remain unaffected. In the trans configuration, however, both copies of the gene are mutated and produce two -damaged proteins.
© Art 4 Science

It’s not enough anymore to look at a mixed gene to retrieve information, like a predisposition to developing a disease like cancer – something doctors today are most interested as far as the benefits of genomic identity is concerned. The findings show that the genome is truly dual, and scientists need to extract both chromosome sets if a more accurate picture is to be painted. Of course, the effects of both forms as a pair shouldn’t be overlooked. The issue right now is that current analytical methods “are ignoring an essential property of the human genome. However, it’s important to know, for example, how mutations are distributed between the two chromosome sets,” according to Hoehe.

The key findings is that gene mutations aren’t randomly distributed between the parental chromosomes. Instead, 60 percent of mutations affect the same chromosome set and 40 percent both sets – cis and trans mutations, respectively. By the looks of it, this formula is essential to the survival of the organism.

 “It’s amazing how precisely the 60:40 ratio is maintained. It occurs in the genome of every individual – almost like a magic formula,” says Hoehe. The 60:40 distribution ratio appears to be essential for survival. “This formula may help us to understand how gene variability occurs and how it affects gene function.”

Overall, this highly significant study (Nature Communications) proves that medicine today, and especially that of the future, can not ignore the “dual nature” of human genomes.

“Our investigations at the protein level have shown that 96 percent of all genes have at least 5 to 20 different protein forms. This results in tremendous individual diversity in possible interactions between genes, and shows how daunting the challenge is to develop individually tailored therapies,” says Hoehe.


Study that looked at 409 pairs of Gay Brothers confirms Chromosome X link to Homosexuality

A massive independent genetic survey sought to replicate the findings of a 20 year old controversial study which identified a stretch on the X chromosome as being linked with homosexuality. The latest findings, which took into account the genetic makeup of a staggering 409 pairs of gay siblings, confirm the initial reports and further boost the idea that homosexuality is also influenced by genes, and not environmental cues only. Not everyone is convinced though. Opponents have been quick to criticize the report, citing outdated analysis methods and a lack of more solid arguments. Namely, what everyone is waiting for is a gene or set of genes that define homosexuality, yet where we stand now we only have a region of a chromosome to work with, which can contain hundreds if not thousands of genes.

Is this proof that homosexuality is genetic?

When Dean Hamer published his groundbreaking research in 1993, while working as a molecular biologist at the U.S. National Institutes of Health (NIH) in Bethesda, Maryland, he was quickly met with skepticism and prejudice by the scientific community. His genomic study revealed that a specific stretch of the X chromosome called Xq28 holds a gene or set of genes that predispose a man to being gay. Because of his low study group comprised of only 38 pairs of gay brothers and the fact that attempts to replicate his results have turned out mixed results, many voices in the field have generally dismissed Hamer’s work.

Replicating Hamer’s research isn’t only challenging from a scientific perspective, however. Few scientists venture in this line of work, since they risk scrutiny. One, there’s little funding and, two, researching homosexual genes isn’t politically correct. Imagine if gay genes were positively identified; what would this mean for the gay community and the world at large, for that matter? We’d then have the basis to genetically screen a baby and even a fetus for gay genes. Some would be quick to say – and maybe rightfully so – that people would become discriminated even before they’d been born. It’s a really tense environment, but for Alan Sanders of the NorthShore Research Institute in Evanston, Illinois this made little difference.

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Sanders and colleagues sought to replicate Hamer’s findings using the same methods he used in 1993, but only this time with a much larger sample focus: 409 pairs of gay brothers versus the original 38 pairs. The researchers collected blood and saliva samples from each family member then looked at the locations of genetic markers called single nucleotide polymorphisms (SNPs) – differences of a single letter in the genetic code – and measuring the extent to which each of the SNPs were shared by the men in the study. This took them five years, plus an addition two years until their work was published in Psychological Medicine.

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The only trait common between the 818 men was being gay. Things like hair colour, weight, height or skin colour varied more or less between each individual. Therefore, any SNPs consistently found in the same genetic locations across the group would most likely be associated with sexual orientation. Five SNPs stood out, which could be found in the Xq28 and 8q12 regions on the X chromosome and chromosome 8 respectively.

“It erodes the notion that sexual orientation is a choice,” says study leader Alan Sanders of the NorthShore Research Institute in Evanston, Illinois.

What’s next

This doesn’t mean they’ve found gay genes , though. Instead, they’ve identified what seems like a block of genes that may be linked with homosexuality. This broad estimation is due to the researchers’ use of an outdated technique called genetic linkage. Nowadays, scientists in the field use genome-wide association (GWA) studies to identify the association of a specific gene with a certain trait in the population. Of course, Sanders was interested in replicating Hamer’s results (which he confirmed), and as such he was forced to use a technique popular two decades ago. Next, the researchers plan on making a GWA study, which includes genetic data from the just-published work plus DNA samples from more than 1000 additional gay men. Hopefully, this will help them identify individual genes that may or not be associated with homosexuality.

[RELATED] Female mice turned lesbian after altering gene. An answer to genetic homosexuality?

“The most pleasing aspect is that the confirmation comes from a team that was in the past somewhat sceptical and critical of the earlier findings,” says Andrea Camperio Ciani of the University of Padua in Italy.

“This study knocks another nail into the coffin of the ‘chosen lifestyle’ theory of homosexuality,” says Simon LeVay, the neuroscientist and writer who, in 1991, claimed to have found that a specific brain region, within the hypothalamus, is smaller in gay men. “Yes, we have a choice in life, to be ourselves or to conform to someone else’s idea of normality, but being straight, bisexual or gay, or none of these, is a central part of who we are, thanks in part to the DNA we were born with.”

“Much hard work now lies ahead to identify the specific genes involved and how they work, as well as to find equivalent genes in women,” he adds.

Hamer, now retired from science and working a documentary film maker, is delighted to see his life’s work back in the spotlight.

“Twenty years is a long time to wait for validation, but now it’s clear the original results were right,” he says. “It’s very nice to see it confirmed.”

Sanders and colleagues stress, however, that even if they find a gay gene, it’s unlikely that these would make too much of a difference. Homosexuality is a highly complex trait, one that can’t be explained by genes or environmental cues alone. It’s a mix, and as such it’s very difficult to pinpoint which of the two is dominant.


Genes that Define How Tall You Grow Identified

It’s common knowledge that babies born out of tall parents will most likely grow to be just as tall, but it’s only recently that scientists report finding most of the genes responsible for height. Information like this could prove to be useful in diagnosing genetic growth deficiencies or, in the not so distant future, genetic manipulation to enhance growth in height.

Short and tall genes


Researchers at the GIANT (Genetic Investigation of Anthropometric Traits) project studied the DNA of about 250,000 Europeans and more than 2 million genetic factors. Mining the data helped reveal that height is determined by the different variations in DNA sequences. From this, they identified 697 genetic variants located in 424 genetic regions that were linked to height. A while ago, ZME Science reported how men’s average height has risen by 11 centimeters since the industrial revolution. This astonishing growth was made possible through better nutrition, yet diet only accounts for a fifth of the growth spurt, the researchers report.

Surprisingly, the team also found some genes that they never would have thought would be involved in height. One of which is a gene that has always been known to be related to cell growth, but not skeletal functions.

“It’s a mix ranging from completely known things, to those that make sense to things that are completely surprising and things we don’t even know what to think about them,” said Dr. Joel Hirschhorn, the leader of the GIANT consortium at Boston Children’s Hospital, Broad Institute of MIT.

Now it is possible to make reliable genetic tests that screen for diseases that have to do with height, including osteoporosis, at a very early age. In the meantime, treatments may dampen the disease’s advance.

“It’s also a step forward towards a test that may reassure parents worried that their child is not growing as well as they’d hoped – most of these children have probably simply inherited a big batch of ‘short genes,” Hirschhorn said.

This isn’t a full, comprehensive list, though. By enhancing their database, more genes that influence height will be discovered. Even so, the GIANT team made an impressive leap forward in this field of research.

“In 2007 we published the first paper that identified the first common height gene, and we have now identified nearly 700 genetic variants that are involved in determining height,” says co-senior investigator Timothy Frayling, PhD, of the University of Exeter in the UK. “We believe that large genetic studies could yield similarly rich lists in a variety of other traits.”

Findings were reported in Nature Genetics.

The normal mouse thymus (left) contains only a small fraction of B-cells (red). If the gene FOXN4 is activated, a fish-like thymus with many B-cells develops. Image: Max Planck

Resetting the immune system back 500 million years

Researchers at the Max Planck Institute of Immunobiology and Epigenetics (MPI-IE)  re-activated the expression of an ancient gene in mice. To their surprise, the gene in question which is dormant in all mammalian species caused the mice to develop  fish-like thymus. The thymus is an organ of paramount importance to the adaptive immune system, but in this particular instance, the thymus produced not only T cells, but also served as a maturation site for B cells – a property normally seen only in the thymus of fish. So, what we’re seeing is a resetting of the immune system to a state similar to what it was like 500 million years ago, when the very first vertebrates began to emerge. By closely following how these gene works, the scientists hope to build a model that will explain how the thymus evolved during the past hundreds of millions of years.

An ancient immune system, today

T-cells are a type of white blood cell that circulate around our bodies, scanning for cellular abnormalities and infections, and are essential to human immunity. These are matured by the epithelial cells in the thymus, but genetically-wise it’s the FOX1 gene that triggers their development. FOX1’s evolutionary ancestor is FOX4, an ancient gene that lies dormant in most vertebrates except jawed fish, such as cat sharks and zebra fish.

The team led by Thomas Boehm, director at the MPI-IE and head of the department for developmental immunology, activated FOX4 in mice. When both FOX1 and FOX4 are simultaneously activated, the researchers found the mouse thymus exhibited properties similar to those found in a fish. Coupled with previous findings, the results suggest that that thymus as we know it today in most vertebrates evolved from and was prompted by the FOX4 gene.  Through  an evolutionary gene duplication FOX1 was born. Initially  both genes must have been active, until finally only FOXN1 was active in the thymus.

The normal mouse thymus (left) contains only a small fraction of B-cells (red). If the gene FOXN4 is activated, a fish-like thymus with many B-cells develops. Image: Max Planck

The normal mouse thymus (left) contains only a small fraction of B-cells (red). If the gene FOXN4 is activated, a fish-like thymus with many B-cells develops. Image: Max Planck

A surprising find was that not only T-cells developed in the thymus of the mice, but also B-cells. Mature B-cells are responsible for antibody production. In mammals, they normally do not mature in the thymus, but in other organs, such as the bone marrow.

Boehm says that it’s not yet clear whether the B-cell development is based on the migration of dedicated B-cell precursors to the thymus, or to maturation from a shared T/B progenitor in the thymus itself.  Nevertheless, it’s remarkable how the researchers have uncovered a particular evolutionary innovation that occurred in an extinct species. Retracting evolutionary steps in our collective ancestral background might provide insights we dare not dream of.

Effects of Alzheimer's. Image: healthbenefitstimes.com

Chemical switch found in Alzheimer’s and stroke victims’ brains kills neurons

Effects of Alzheimer's. Image: healthbenefitstimes.com

Effects of Alzheimer’s. Image: healthbenefitstimes.com

Researchers at the Sanford-Burnham Medical Research Institute (Sanford-Burnham) have found a chemical switch that both regulates the generation of new neurons from neural stem cells and the survival of existing nerve cells in the brain. Postmortem examination of the brains of Alzheimer’s patients and stroke victims found the switch that shuts off the signals was in abundance. With this in mind, it’s possible that a drug that targets the switch, called MEF2, might prevent neuronal loss in a variety of neurodegenerative diseases, such as Alzheimer’s, Parkinson’s and autism.

“We have shown that when nitric oxide (NO)—a highly reactive free radical—reacts with MEF2, MEF2 can no longer bind to and activate the genes that drive neurogenesis and neuronal survival,” said Stuart Lipton, M.D., Ph.D., director and professor in the Neuroscience and Aging Research Center at Sanford-Burnham, and a practicing clinical neurologist. “What’s unique here is that a single alteration to MEF2 controls two distinct events—the generation of new neurons and the survival of existing neurons,” added Lipton, who is senior author of the study.

Switching new neurons on and off

Transcription factors are proteins that control which genes are turned on or off in the genome. They do so by binding to DNA and other proteins. Once bound to DNA, these proteins can promote or block the enzyme that controls the reading, or “transcription,” of genes, making genes more or less active. In the brain, the transcription factors are paramount to linking external stimuli to protein production, enabling neurons to adapt to changing environments. Previous research showed that the MEF2 family of transcription factors plays an important part in the neurogenesis and neuronal survival, as well as in the processes of learning and memory. On the opposite side, MEF2 mutations have been linked with neurodegenerative disorders, including Alzheimer’s and autism.

The NO-protein modification process mentioned by Lipton earlier was first described him and his collaborators some 20 years ago (S-nitrosylation). S-nitrosylation involves the covalent incorporation of a nitric oxide moiety into thiol groups, to form S-nitrosothiol (SNO). S-nitrosylation of MEF2 controlls neuronal survival in Parkinson’s disease and has important regulatory functions under normal physiological conditions throughout the body.

“Now we have shown that this same reaction is more ubiquitous, occurring in other neurological conditions such as stroke and Alzheimer’s disease. While the major gene targets of MEF2 may be different in various diseases and brain areas, the remarkable new finding here is that we may be able to treat each of these neurological disorders by preventing a common S-nitrosylation modification to MEF2.”

“The findings suggest that the development of a small therapeutic molecule—one that can cross the blood-brain barrier and block S-nitrosylation of MEF2 or in some other way increase MEF2 transcriptional activity—could promote new brain cell growth and protect existing cells in several neurodegenerative disorders,” added Lipton.

“We have already found several such molecules in our high-throughput screening and drug discovery efforts, so the potential for developing new drugs to attack this pathway is very exciting,” said Lipton.

The study was published in Cell Reports.

A gene mutation for excessive alcohol drinking found


  • Mice in the control group refused to drink alcohol
  • When a certain gene was deactivated, they started preferring alcohol over water
  • Researchers stress that human alcoholism depends much more on environmental and personal factors

Researchers have discovered a gene that regulates alcohol consumption; when this genes becomes faulty, it makes humans more prone to excessive drinking. They have also identified the mechanism underlying this phenomenon. However, it should be kept in mind that this is only a small cog in the great system of biological and psychological machinery that determines the extent to which a person will use, abuse, or become addicted to alcohol.


photo credit: AutumnRedux</a

photo credit: AutumnRedux

Normal mice don’t really like alcohol; when given a choice between a bottle of water and a bottle of diluted alcohol, they rarely chose any alcohol at all. The same goes for pretty much all mammals. However, mice with a mutation in a gene called Gabrb1 overwhelmingly preferred drinking alcohol over water – choosing to consume about 85% of their daily fluids with alcohol (about as strong as wine).

Furthermore, researchers showed mice carrying this mutation were willing to work to obtain the alcohol-containing drink by pushing a lever and, unlike normal mice, did this relentlessly over large periods of time. They would then drink until they got intoxicated and could barely coordinate their movements.

The gene has a significant impact in humans as well:

“We know from previous human studies that the GABA system is involved in controlling alcohol intake. Our studies in mice show that a particular subunit of GABAA receptor has a significant effect and most importantly the existence of these mice has allowed our collaborative group to investigate the mechanism involved. This is important when we come to try to modify this process first in mice and then in man.”

However, the team of researchers from five UK universities – Newcastle University, Imperial College London, Sussex University, University College London and University of Dundee – and the MRC Mammalian Genetics Unit at Harwell published their results in Nature Communications, and they stress that human alcoholism depends much more on environmental and personal factors than on genes.

“It’s amazing to think that a small change in the code for just one gene can have such profound effects on complex behaviours like alcohol consumption. We are continuing our work to establish whether the gene has a similar influence in humans, though we know that in people alcoholism is much more complicated as environmental factors come into play. But there is the real potential for this to guide development of better treatments for alcoholism in the future.”

Journal Reference:

Anstee, Q. M. et al. Mutations in the Gabrb1 gene promote alcohol consumption through increased tonic inhibition. Nat. Commun. 4:2816 doi: 10.1038/ncomms3816 (2013).

Evidence that RMST is necessary for neuronal differentiation: overexpression of RMST led to a 3-fold increase in neuron-specific beta tubulin (bottom) compared to control (top). Scale bars represent 100 microns. (Credit: Shi-Yan Ng et al./Molecular Cell)

Gene key in neuron generation discovered

Scientists have discovered an atypical gene that is thought to be crucial for the generation of new neurons in the brain, a process called neurogenesis. The discovery and further study of the gene might help scientists better understand how neurodegenerative diseases such as Alzheimer’s affect the brain and, in term, how to address them.

Evidence that RMST is necessary for neuronal differentiation: overexpression of RMST led to a 3-fold increase in neuron-specific beta tubulin (bottom) compared to control (top). Scale bars represent 100 microns. (Credit: Shi-Yan Ng et al./Molecular Cell)

Evidence that RMST is necessary for neuronal differentiation: overexpression of RMST led to a 3-fold increase in neuron-specific beta tubulin (bottom) compared to control (top). Scale bars represent 100 microns. (Credit: Shi-Yan Ng et al./Molecular Cell)

New neurons are born through a complex temporal and spatial control of hundreds of genes. The expression of these genes is controlled by regulatory networks, usually involving proteins, indispensable for the well functioning of the central nervous system. When one or some of these genes are inhibited or over expressed,  neurological disorders develop. Understanding the mechanisms that govern neurogenesis becomes thus of the utmost importance when developing treatments for such serious diseases.

A major breakthrough in this respect was recently made by scientists at A*STAR’s Genome Institute of Singapore (GIS), who discovered a key component within a gene regulatory network that controls the birth of new neurons, called RMST. This component isn’t a protein like most people, even the researchers involved in the study, thought. RMST is an atypical, long non-coding RNA, a newly discovered class of RNA whose functions remain largely unknown

In this latest study, one of the components in this new class has been at least demystified. They found that RMST acts directly within a gene regulatory network.

“Stanton and colleagues show how RMST, a human lncRNA, directly regulates SOX2, a key transcription factor protein that is instrumental for directing the birth of new neurons,” said Associate Prof Leonard Lipovich, from the Center for Molecular Medicine and Genetics at the Wayne State University and a member of GENCODE. Even more intriguingly, they highlight that RMST controls SOX2 by directly interacting with the protein.

Their work is important not only because it sheds light on the process of neurogenesis, but also new insight into how lncRNA works together with protein components to regulate the important biological processes of gene expression.

“The paper is therefore an important advance in the still nascent and controversial field of riboregulators, or RNAs that regulate proteins in our cells. DNA-binding proteins that turn genes on and off were traditionally thought to be distinct from RNA-binding proteins. Stanton et al, however, illuminate the cryptic, yet crucial, RNA-binding roles for DNA-binding transcription factors: lncRNAs just might be the definitive regulatory switch that controls these factors’ activity.”

Findings were reported in the journal Molecular Cell.

[via KurzweilAI]

GM ‘hybrid’ fish poses threat to natural populations

A study has shown that genetically modified salmon that breed with wild trout can produce a fast-growing, competitive fish that not only screws around with the local ecosystem, but because it also alters the fish genome in ways which cannot be anticipated.

Two same-age salmon, a GM salmon, rear, and a non-GM salmon, foreground. Photograph: Anonymous/AP

Two same-age salmon, a GM salmon, rear, and a non-GM salmon, foreground. Photograph: Anonymous/AP

What do you get when you cross a genetically modified salmon and wild brown trout? Well, something which is much faster growing and competitive than each of his parents and non GMO cousins. In the study, a natural environment was simulated, and the offspring suppressed the growth of GM salmon by 82% and wild salmon by 54% when all competed for food in a simulated stream.

“To the best of our knowledge, this is the first demonstration of environmental impacts of hybridisation between a GM animal and a closely related species,” wrote the scientists from Memorial University of Newfoundland. “These findings suggest that complex competitive interactions associated with transgenesis and hybridisation could have substantial ecological consequences for wild Atlantic salmon should they ever come into contact [with GM salmon] in nature.”

Study lead author, Krista Oke, said:

“These results emphasise the importance of stringent regulations to ensure GM animals do not escape into nature.”

Salmon and brown trout are closely related anyway and can create hybrids, though usually less than 1% of offspring are hybrids. But these natural hybrids are not really perturbing the environment, unlike the offspring which come from GMO fish.

The study raises more questions and concerns about genetically modified organisms altering ecosystems. But here’s another take on the problem: during millions and billions of evolution, nature has created a complex, specialized, sustainable genetic system of species. If genetically modified organisms start swimming in the gene pool, and contaminate it with human created genes, we don’t really know what will happen. We don’t even know the direct effects, let alone the indirect ramifications. These genes will forever remain in the gene pool, there is nothing we will be able to do to remove them – and we have no idea what effects this will have. There’s some food for thought.

Controversial study claims humans are slowly losing their intellectual abilities

According to a new study conducted by Professor Gerald Crabtree, who heads a genetics laboratory at Stanford University in California, humans have peaked their intellectual capacities thousands of years ago, and now we are in a slow, but certain, state of decline.

The provocative theory comes from one of the leading minds in genetics, and it relies on the fact that human intelligence, in order to function at its finest, needs optimal functioning of a large number of genes, which in turn requires enormous evolutionary pressures to maintain. Since there are no such major pressures at the moment (and haven’t been, for millennia), we cannot function to the best of our capacities.

“The development of our intellectual abilities and the optimization of thousands of intelligence genes probably occurred in relatively non-verbal, dispersed groups of peoples before our ancestors emerged from Africa,” says the papers’ author, Dr. Gerald Crabtree, of Stanford University. In this environment, intelligence was critical for survival, and there was almost certainly an immense selective pressure focused around intelligent folk.

Basically, it boils down to this: for over 99 percent of our Homo Sapiens history, we have survived as hunter-gatherer societies, relying greatly on our wits, developing into bigger and bigger brained creatures. However, that process has stopped the moment we established ourselves as the dominant species on the planet, natural selection on our intellect practically halting.

“I would wager that if an average citizen from Athens of 1000BC were to appear suddenly among us, he or she would be among the brightest and most intellectually alive of our colleagues and companions, with a good memory, a broad range of ideas and a clear-sighted view of important issues,” Professor Crabtree says in a provocative paper published in the journal Trends in Genetics.

But it’s not all about intelligence – he believes they would be emotionally superior to us as well.

“Furthermore, I would guess that he or she would be among the most emotionally stable of our friends and colleagues. I would also make this wager for the ancient inhabitants of Africa, Asia, India or the Americas, of perhaps 2,000 to 6,000 years ago,” Professor Crabtree says. “The basis for my wager comes from new developments in genetics, anthropology, and neurobiology that make a clear prediction that our intellectual and emotional abilities are genetically surprisingly fragile,” he says.

So what about now? Is there no intellectual selection for humans nowadays? There is, but it is nowhere near as fierce as it was in ancient times.

“A hunter-gatherer who did not correctly conceive a solution to providing food or shelter probably died, along with his or her progeny, whereas a modern Wall Street executive that made a similar conceptual mistake would receive a substantial bonus and be a more attractive mate,” Professor Crabtree says.

However, the study was met with skepticism, to say the least. Some researchers dispatched the study as amateurish, while some just labeled it as speculation.

“At first sight this is a classic case of Arts Faculty science. Never mind the hypothesis, give me the data, and there aren’t any,” said Professor Steve Jones, a geneticist at University College London. “I could just as well argue that mutations have reduced our aggression, our depression and our penis length but no journal would publish that. Why do they publish this?” Professor Jones said.

Indeed, while the study scores heavy points in terms of circumstantial evidence and creativity, it doesn’t score where it matters the most: hard data.

“I am an advocate of Gradgrind science – facts, facts and more facts; but we need ideas too, and this is an ideas paper although I have no idea how the idea could be tested,” he said.

So what do you think about it? Have we in fact regressed to the point where we become couch potatoes, unable to fend for ourselves, declining generation after generation? Are we in fact much superior to the ancient man? Or is the truth totally different?


Science explains why supermarket tomatoes are less tasty than garden grown


(c) S. Zhong and J. Giovannoni

A newly published researchers by scientists at University of California Davis and Cornell University explains why beautiful, perfectly ripped tomatoes, that one can typically pick up from a local supermarket, are ironically less tastier than homegrown tomatoes, which look less appetizing.

I had the good fortune of spending most of my early childhood in the countryside, where my grandfolks took care of me. There, besides your usual farm animals, they also catered to a beautifully lush fruit and vegetable garden – they’re still caring to it to this day. There’s no secret to anyone that homegrown veggies are tastier, and now that I’m looking back at . Some say they taste better because they’ve been grown with love. I think that, plus simple genetics.

Heirloom tomatoes are harder to grow than the commercial alternative. This is because they take longer to turn from green to red near the stem as they ripen, causing difficulties in mass production, besides the obvious marking downturn of not being uniformly red. For the past 70 years or so, tomato breeders have been growing a naturally-occurring type that ripens uniformly, turning into a beautiful red from top to bottom. These are now almost unanimously present in supermarkets and are extensively used for producing pasta sauces and ketchup. However, they’re sensibly less testier.

In their study, the scientists, lead by Ann Powell of University of California David, discovered the precise genetic change that causes a tomato to ripen almost perfectly, which also offers a viable explanation for why they’re less tastier.

When the first breeders came by the back then inactive gene, which causes tomatoes to turn an uniform luscious scarlet when ripe, everybody was ecstatic. However, the researchers found that the gene GLK2, causes a tomato’s chloroplasts, which turn the sun’s energy into sugar, to be smaller, fewer, and dispersed evenly throughout the fruit. This means a lower sugar concentration in commercial tomatoes – 10-15 percent less sugar actually. It also reduces the amount of lycopene and other compounds that give a tomato its color, aroma, and nutritional benefits such as antioxidants.

The discovery “is one piece of the puzzle about why the modern tomato stinks,” said Harry Klee, a tomato researcher at the University of Florida in Gainesville who was not involved in the research. “That mutation has been introduced into almost all modern tomatoes. Now we can say that in trying to make the fruit prettier, they reduced some of the important compounds that are linked to flavor.

Klee is undoubtedly referring to the other conditions under which commercial tomatoes are currently bred and transported. Typically, tomatoes are picked when still green, and then frozen for shipping. Frost/defrost causes a loss in taste and texture.

The researchers hope he findings will get breeders interested in the subject, and tempt some to change the strain to heirloom tomatoes or some wild species.

The study was published in the journal Science.


Lab uses skin cells to help repair heart muscle

Another breakthrough in biology and medicine was reported, as scientists were able, for the first time, to take skin cells from patients who had suffered heart failure and make them repair the cardiac muscle.

The technique had been tested only on rats and it seemed decades could pass until it would become suitable for humans, but in lack of anything better, doctors applied it, and it worked out remarkably fine, marking the beginning of a new era in the quest for replacement cells to treat tissue affected by disease, Israeli researchers declared.

Image source

The research relies on a technique called human-induced pluripotent stem cells, or hiPSCs, a recently-discovered source which can be a good replacement for the much more controversial stem cells technique. Basically what you do is take cells from the patient and inject new genes into their nucleus, along with a ‘chemical cocktail’. Basically, these new elements reprogram the cells to their youthful stage, and teach them to do other things as well. The major advantage here is that if the body sees its own cells, it will recognize them as friendly cells and the immune system will not attack.

The bad thing is that so far, studies have only shown hiPSCs from younger (under 60 years) and healthy people who are able to adapt to this new situation and transform their cells. So far, this doesn’t seem to work out for elderly and diseased patients. But scientists are confident in this technique, and believe it can be used in many more exciting cases.

“What is new and exciting about our research is that we have shown that it’s possible to take skin cells from an elderly patient with advanced heart failure and end up with his own beating cells in a laboratory dish that are healthy and young,” said Lior Gepstein, a professor of cardiology at the Technion-Israel Institute of Technology and Rambam Medical Center in Haifa, Israel.

Basically, it is the equivalent to the stage of his heart cells when he was just born.

Solomon Islands blond hair

Dark skin and natural blond hair genetic mystery solved

Solomon Islands blond hair

Skin and hair color are most inherited from parents, and usually hint pretty accurately to a person’s ethnicity. Dark skin and hair are most common in the regions around the Equator, however natives of the Solomon Islands, an archipelago east of Papua New Guinea, seem to defy common expectations, as around 10% of the population here has strikingly natural blond hair, despite being dark skinned.

An explanation for this rather atypical occurrence has been attempted in the past, ideas ranging from excess sun exposure, to the fish-rich diet, to ultimately the plausible blond hair genetic inheritance from European traders and explorers. Now, even the latter explanation has been debunked after researchers at Bristol University have found that the gene responsible for blond hair in the islanders is unique to any other genome in the world.

“For me it breaks down any kind of simple notions you might have about race,” said Carlos Bustamante, a geneticist at Stanford University. “Humans are beautifully diverse, and this is just the tip of the iceberg.”

The researcher analyzed saliva samples from more than 1,000 islanders, looking closely at a subset of the samples — from 43 blond and 42 dark-haired islanders. Looking at the data, the researchers have identified the single genetic mutation that causes the islanders to have such contrasting pigmentation of their skin and hair. A variation of the TYRP1 gene, typically responsible for influencing pigmentation in humans, is what causes blond hair in Solomon Islanders, as described in the journal Science.

Dr Nic Timpson, one of the leaders of the project, said: “Naturally blond hair is a surprisingly unusual trait in humans which is typically associated with people from Scandinavian and Northern European countries.
“Whether this genetic variation is due to evolution or a recent introgression (the introduction of a new gene from another population) requires further investigation, but this variant explains over 45 per cent of the variance in hair colour in the Solomons.”

source: Telegraph

Men’s Y chromosome stands its ground – men aren’t going extinct!

Good news for men, and especially women: the Y chromosome, which holds the male sex determining genes in most mammals, including humans, is not going extinct, as some claim, as a new research found that the diminishing gene numbers have come to a halt and will remain this way.

Sex chromosomes come in pairs, such men have X-Y and women have X-X. Around 320 million years ago when the first Y male determining chromosome appeared, both the X and Y chromosomes had roughly the same number of genes, actually sharing 800 genes. In time, the Y chromosome has lost 1,393 of its 1,438 original genes over the course of its existence. With a rate of genetic loss of 4.6 genes per million years, the Y chromosome may potentially lose complete function within the next 10 million years, or so some scientists claim. Currently, the human Y carries a mere 19 of its ancestral genes shared with the X chromosome, out of a once 800 strong, bringing the total number of genes in the human Y to 27.

This would mean that in a few million years, the world would be dominated by women alone, leaving only artificial reproduction as an exclusive option – highly practical, not all that fun. Fear not, for Jennifer Hughes at the Whitehead Institute for Biomedical Research in Cambridge, Massachusetts, along with colleagues, have found that the Y chromosome is here to stay.

The researchers sequenced the Y chromosome of the rhesus macaque, a very close relative of humans, from which it diverged paths some 25 million years ago. It was found that the monkey’s Y has 20 genes shared with its X, of which 19 are shared with the human Y. This suggests that the human Y chromosome has lost only one gene since humans and macaques last shared a common ancestor. The research, thus, provides direct evidence that the linear extrapolation model is flawed.

“We finally have empirical data that the Y chromosome has held steady over the last 25 million years,” says Hughes. “Most of the Y chromosome’s gene loss happened almost immediately after it stopped recombining with the X chromosome.” The 19 surviving genes probably have vital biological functions, she says, and so aren’t going anywhere anytime soon.

Here’s to men!

The research was published in the journal Nature. Image credit.

Ozzy Osborne’s genome reveals why he is still alive

The lead singer, rock legend bat beheader has done pretty much anything you can do in this life. He played in front of thousands, ate/drank/smoked/injected pretty much everything that can be, had motorcycle accidents, never ate right, and yet, at the proud age of 61 he’s alive and kicking just as he ever was. Researchers wanted to find out why this is happening (not that anybody would have something against it), analyzed his genome and found some interesting mutations.

Ozzy Osborne joined DNA co-discoverer James Watson and Harvard University professor Henry Louis Gates in having his genome analyzed by Cofactor Genomics, a Saint Louis–based company and Knome, Inc. At first, he said he was a bit skeptical, but after a while thought he actually has something to give to science.

[read this in his voice]”I was curious,” he wrote in his column. “Given the swimming pools of booze I’ve guzzled over the years—not to mention all of the cocaine, morphine, sleeping pills, cough syrup, LSD, Rohypnol…you name it—there’s really no plausible medical reason why I should still be alive. Maybe my DNA could say why.”

It is in fact pretty curious how he managed to survive after such a lifestyle, and researchers were interested in finding out how he metabolized things, and how this was affected by his substance use; they also found some interesting mutations regarding the way the brain processes dopamine. Here are just a few questions Scientific American asked Jorge Conde, co-founder and chief executive as Knome:


Is Ozzy the first rock star to have his full genome sequenced?

Conde: Yes, as far as I know. I can definitely tell you he’s the first prince of darkness to have his genome sequenced and analyzed.

Can we see in his genome any traces of his legendary rock-and-roll lifestyle—or evidence of his body’s efforts to repair any damage?

Conde: We cannot find the “Ozzy Osbourne” gene. But what we did see, as one of our scientists refers to it, is a lot of interesting smoke—but not any specific fire. We found many variants—novel variants—in genes associated with addiction and metabolism that are interesting but not quite definitive.

So can his genomes tell us anything about his ability to survive so many years of hard partying?

Pearson: I talked with Ozzy, and we looked at the genome with an eye toward the nerves. If you think about what makes Ozzy unusual, it’s that he’s a world-class musician, he has an addictive personality, he has a tremor, he’s dyslexic, he gets up very early in the morning. And many of these can be traced back to the nervous system.

One variant involves a gene that makes CLTCL1, which is a really interesting protein. When a cell takes in things from the outside membrane, it pulls itself in like a basket to pull things in. It does this in all kinds of cells, including nerve cells. He has two copies of an unusual variant that makes a grossly different version of the protein than most people produce. Here’s a gene that’s central to how nerve cells communicate with each other, so it’s curious to us to see a grossly different protein variant. It’s thought provoking.

We didn’t find anything that can explain to you from point A to point B why Ozzy can think up good songs or why he is so addicted to cocaine, but we found some things that would be interesting to follow up on.

Such as?

Pearson: Alcohol dehydrogenase genes. They’re involved in breaking down alcohol when you drink. Ozzy has an unusual variant near one of his alcohol dehydrogenase genes, ADH4, that help regulate how much of the protein gets made. Given his troubles with alcohol in the past, obviously we would like to clarify why his body responds differently than other people’s.

What can we learn from Ozzy’s genome?

Pearson: I think one lesson is understanding music. It’s a pretty interesting thing we do at humans—that some of us can synchronize to a beat, that we like to sing songs. But we don’t understand it well genetically, so one of the open questions is we’ll get a better understanding of what makes a good musician, what kinds of variants help us keep a beat, make a good tune. I think looking ahead, sequencing the genomes of more musicians would be a good idea.

If you could sequence any other celebrity genomes, whose would you choose?

Pearson: Ozzy suggested Keith Richards. Our partners who did the sequencing suggested we sequence Ozzie Smith, the baseball player, as a control. He’s always been a good teetotaler.

Full interview here

Homer Simpson gene limits memory and learning ability ?

Researchers at Emory University School of Medicine have conducted a study showing that the deletion of a particular gene makes mice smarter by unlocking a mysterious part of the brain, thought to be totally unflexible until now. When the gene, RGS14, is disabled, mice learn how to figure out mazes faster and more effective than regular mice. They also show signs of better memory and improved overall mental abilty.

Since RGS14 seems to hold mice down, John Hepler, PhD, professor of pharmacology at Emory University School of Medicine have nicknamed it the “Homer Simpson” gene. The gene is located in one particular part of the brain, the CA2, which is a part of the hippocampus, a region known to be involved in learning and the forming of new memories. However, the CA2 area is still an unknown area for researchers.

What makes this whole study even more interesting is the fact that the RGS14 gene is also in humans, and probably has the same use as it does for mice.

“A big question this research raises is why would we, or mice, have a gene that makes us less smart – a Homer Simpson gene?” Hepler says. “I believe that we are not really seeing the full picture. RGS14 may be a key control gene in a part of the brain that, when missing or disabled, knocks brain signals important for learning and memory out of balance.”

Some of our sources have reported that Homer Simpson doesn't like this study

What’s even better is that there didn’t seem to be any negative side effects to the deactivation of the gene, but there are still some possibilities that have to be investigated before definitive conclusions are drawn.

“The pipe dream is that maybe you could find a compound that inhibits RGS14 or shuts it down,” he adds. “Then, perhaps, you could enhance cognition.”

Mad genius reddux: study suggest link between psychosis and creativity

History is just teeming with examples of brilliant artists that acted in very peculiar ways – to put it lightly. They were absolutely brilliant, and they were absolutely mad; how can this be? Well, according to a new study published in Psychological Science the two traits often go hand in hand.

mad genius

In order to gather information on this, Szabolcs Kéri of Semmelweis University in Hungary directed his search on ‘neuregulin 1’, a gene responsible for strengthening and communication between the neurons and other brain processes. They were especially interested in a variant of this gene associated with a greater risk of developing mental disorders.

The way they conducted this study was quite interesting; they recruited volunteers who think of themselves as being very creative and they moved on to assessing their creativity (and intelligence). I was unable to find the full tests they used, but evaluating someone’s creativity seems to be quite a task; they used questions such as “Just suppose clouds had strings attached to them which hang down to earth. What would happen?”, and volunteers were rated based on the flexibility of their answers. They were also asked to note their lifetime creative achievements (which may or may not be relevant, if you ask me).

The results showed a clear link between neuregulin 1 and creativity, as volunteers with the specific variants of the gene had a way bigger chance of scoring higher in the creativity assessment and also their lifetime achievements were more significant. Hungarian researchers also note that this study can also have some beneficial functions, explaining that “molecular factors that are loosely associated with severe mental disorders but are present in many healthy people may have an advantage enabling us to think more creatively.”. If accurate, this study can also show that certain genetic variations with negative effects can bypass evolutionary selection if they also have some beneffic effects.

Dead gene is resurrected in humans

This is what researchers believe to be the first true comeback of a gene in the human/great ape lineage; the study was led by Evan Eichler’s genome science laboratory at the University of Washington and the Howard Hughes Medical Institute, and they pointed out that the infection-fighting human IRGM is (as far as we know) the first doomed gene to make a comeback in our own species.

Medical interest sparkled for this gene when scientists discovered that IRGM mutations can lead to an inflammatory digestive disorder known as Crohn’s disease. Also, in the animal world there are significant variations of this gene; for example, mice have 21 Immune-Related GTPases, and most mammals have several. The truncated IRGM gene is one of only two genes of its type remaining in humans.

In this latest study, they reconstructed the evolutionary history of this gene, and they found out that it was eliminated by going to multiple copies to only a single copy in primates, about 50 million years ago. By comparing Old World and New World monkey species suggest that the gene dissappeared in their common ancestor.

Everything went according to plan and the inactive gene was inherited through millions and millions of years of evolution. But then, something totally unexpected happened: the gene started to produce proteins once more. The only evidence they could find for this relied on a retrovirus that was somehow inserted in this ancient genome.

“The IRGM gene was dead and later resurrected through a complex series of structural events,” Eichler said. “These findings tell us that we shouldn’t count a gene out until it is completely deleted.”

Language is defined by culture, not biology

How and why language appeared has been a subject of countless studies and hours of research, but the results haven’t been always clear and as a matter of fact, they’ve sometimes been contradictory. Still, according to a recent study conducted by Professor Nick Chater (UCL Cognitive, Perceptual and Brain Sciences) and his colleagues, one thing’s for sure: it’s culture that defines a language.

They came to this conclusion by creating models of genes to find out which genes would evolve as language evolves to; they came to the conclusion that such an evolution is extremely improbable, because gene modifications are much more slower than language modifications. Still, a cultural modifications take place much more faster than genetic ones, and with a margin, they coincide with language alterations.

According to what is called today “the Baldwin effect” what is learned in a lifespan gets slowly encoded into your genes (we’ll get in more details in a later article), but the biology behind our language preceeds the actual appearance of the language.

Professor Nick Chater, UCL Cognitive, Perceptual and Brain Sciences, said:

“Language is uniquely human. But does this uniqueness stem from biology or culture? This question is central to our understanding of what it is to be human, and has fundamental implications for the relationship between genes and culture. Our paper uncovers a paradox at the heart of theories about the evolutionary origin and genetic basis of human language – although we have appear to have a genetic predisposition towards language, human language has evolved far more quickly than our genes could keep up with, suggesting that language is shaped and driven by culture rather than biology.”