Friends genetically more similar than strangers

'We Become Friends With Genetically Similar People'

‘We Become Friends With Genetically Similar People’

Our friends seem to be genetically more similar to us than strangers, according to a new U.S. scientific study led by prominent Greek-American professor of sociology and medicine at Yale University Nicholas Christakis and James Fowler, professor of medical genetics and political science at the University of California.

The researchers, who made the relevant publication in the Journal of the National Academy of Sciences (PNAS), analyzed the genome of 1,932 people and compared pairs of friends with pairs of strangers.

There was no biological affinity among all these people, but only the difference in the level of social relations between them.

The study showed that, on average, every person had a more similar DNA with his friends than with strangers. The researchers noted that this finding has to do with the tendency of people to make friends with similar racial (and hence genetic) background.

The genetic similarity between friends was greater than the expected similarity between people who share a common national and genetic inheritance. It is not clear yet by what mechanisms this occurs.

But how similar are we with our friends?

On average, according to the study, a friend of ours has a genetic affinity comparable to our fourth cousin, which means that we share about 1% of our genes our friends.

“1% does not sound a big deal, but it is for geneticists. It is noteworthy that most people do not even know who their fourth cousins ​​are, but somehow, from the countless possible cases, we choose to make friends with people who are genetically similar to us,” said Prof Christakis.

Christakis and Fowler even developed a “friendship score”, which predicts who will befriend whom with nearly the same accuracy as scientists predict, on the basis of genetic analysis, the chances of a person to obesity or schizophrenia.

Focusing on individual genes, the research shows that friends are more likely to have similar genes related to the sense of smell, but different genes that control immunity; thus friends vary genetically in their protection against various diseases.

It seems to be an evolutionary mechanism that serves the society in general, since the fact that people hang out with those who are vulnerable to different diseases constitutes a barrier to the quick spread of an epidemic from person to person. Another notable finding is that the common genes we share with our friends seem to evolve more rapidly than others.

Prof. Christakis explains that probably that is why human evolution seems to have accelerated over the past 30,000 years, as the social environment with an important role of linguistic communication is a vital evolutionary factor.

 

Source:  humansarefree.com

Humans Bred with Unknown Species

Humans Bred with Unknown Species

Humans Bred with Unknown Species

A new study presented to the Royal Society meeting on ancient DNA in London last week has revealed a dramatic finding – the genome of one of our ancient ancestors, the Denisovans, contains a segment of DNA that seems to have come from another species that is currently unknown to science. The discovery suggests that there was rampant interbreeding between ancient human species in Europe and Asia more than 30,000 years ago. But, far more significant was the finding that they also mated with a mystery species from Asia – one that is neither human nor Neanderthal. 

Scientists launched into a flurry of discussion and debate upon hearing the study results and immediately began speculating about what this unknown species could be.  Some have suggested that a group may have branched off to Asia from the Homo heidelbernensis, who resided in Africa about half a million years ago. They are believed to be the ancestors of Europe’s Neanderthals. 

However others, such as Chris Stringer, a paleoanthropologist at the London Natural History Museum, admitted that they “don’t have the faintest idea” what the mystery species could be.

Traces of the unknown new genome were detected in two teeth and a finger bone of a Denisovan, which was discovered in a Siberian cave. There is not much data available about the appearance of Denisovans due to lack of their fossils’ availability, but the geneticists and researchers succeeded in arranging their entire genome very precisely.

“What it begins to suggest is that we’re looking at a ‘Lord of the Rings’-type world – that there were many hominid populations,” Mark Thomas, an evolutionary geneticist at University College London.

The question is now: who were these mystery people that the Denisovans were breeding with?

 

Source:  ancient-origins.net

Double meaning in genetic code

Scientists discover double meaning in genetic code:

Scientists discover double meaning in genetic code

Scientists discover double meaning in genetic code

Scientists have discovered a second code hiding within DNA. This second code contains information that changes how scientists read the instructions contained in DNA and interpret mutations to make sense of health and disease.

A research team led by Dr. John Stamatoyannopoulos, University of Washington associate professor of genome sciences and of medicine, made the discovery. The findings are reported in the Dec. 13 issue of Science. The work is part of the Encyclopedia of DNA Elements Project, also known as ENCODE. The National Human Genome Research Institute funded the multi-year, international effort. ENCODE aims to discover where and how the directions for biological functions are stored in the human genome.

Since the genetic code was deciphered in the 1960s, scientists have assumed that it was used exclusively to write information about proteins. UW scientists were stunned to discover that genomes use the genetic code to write two separate languages. One describes how proteins are made, and the other instructs the cell on how genes are controlled. One language is written on top of the other, which is why the second language remained hidden for so long.

“For over 40 years we have assumed that DNA changes affecting the genetic code solely impact how proteins are made,” said Stamatoyannopoulos. “Now we know that this basic assumption about reading the human genome missed half of the picture. These new findings highlight that DNA is an incredibly powerful information storage device, which nature has fully exploited in unexpected ways.”

The genetic code uses a 64-letter alphabet called codons. The UW team discovered that some codons, which they called duons, can have two meanings, one related to protein sequence, and one related to gene control. These two meanings seem to have evolved in concert with each other. The gene control instructions appear to help stabilize certain beneficial features of proteins and how they are made.

The discovery of duons has major implications for how scientists and physicians interpret a patient’s genome and will open new doors to the diagnosis and treatment of disease.

“The fact that the genetic code can simultaneously write two kinds of information means that many DNA changes that appear to alter protein sequences may actually cause disease by disrupting gene control programs or even both mechanisms simultaneously,” said Stamatoyannopoulos.

Source:  sciencedaily.com

Ancient Humans Interbred Extensively “Unknown Population”

Genetic Analysis Suggests Ancient Humans Interbred Extensively Neanderthals, Denisovans And An “Unknown Population”:

 

Ancient Humans Interbred Extensively “Unknown Population”

Ancient Humans Interbred Extensively “Unknown Population”

Genome analysis suggests there was interbreeding between modern humans, Neanderthals, Denisovans and an unknown archaic population. Updated genome sequences from two extinct relatives of modern humans suggest that these ‘archaic’ groups bred with humans and with each other more extensively than was previously known.

The ancient genomes, one from a Neanderthal and one from a member of an archaic human group called the Denisovans, were presented on 18 November at a meeting on ancient DNA at the Royal Society in London. The results suggest that interbreeding went on between the members of several ancient human-like groups in Europe and Asia more than 30,000 years ago, including an as-yet-unknown human ancestor from Asia.

All modern humans whose ancestry originates outside of Africa owe about 2% of their genome to Neanderthals. Certain populations living in Oceania, such as Papua New Guineans and Australian Aboriginals, share about 4% of their DNA with Denisovans.

Link for Colon Cancer Discovered

Key Link Responsible for Colon Cancer Initiation and Metastasis discovered:

Key Link Responsible for Colon Cancer Initiation and Metastasis discovered

Key Link Responsible for Colon Cancer Initiation and Metastasis discovered

CXCR2- a key genetic culprit that is implicated in the tumor formation, growth and progression in a mouse model of colon cancer has been identified by scientists.
 Key Link Responsible for Colon Cancer Initiation and Metastasis discovered

“We have been trying for the past several years to understand the precise molecular links between inflammation and cancer, said DuBois. “We have demonstrated that CXCR2 mediates a critical step in the setup of the blood circulatory machinery that feeds tumor tissue. This provides an important new clue for the development of therapeutic targets to neutralize the effect of CXCR2 on colon cancer.”

The DuBois’ Laboratory for Inflammation and Cancer, which includes lead author Hiroshi Katoh, and colleagues Dingzhi Wang, Takiko Daikoku, Haiyan Sun, and Sudhansu K. Dey, published the results in the November 11 issue of Cancer Cell.

The results provide critical new clues toward the prevention of colorectal cancer, the second leading cause of cancer deaths in the U.S. Despite the availability of colonoscopy screening, the 5-year survival rate remains low, due to a large number patients presenting with advanced stages of the disease. Currently, there are no clinically available blood tests for the early detection of sporadic colon cancer.

Inflammation has long been associated with increasing one’s risk for colon cancer. For instance, more than 20 percent of patients with a form of inflammatory bowel disease (IBD) develop colorectal cancer within 30 years of diagnosis. This colitis-associated cancer has a slow progression, but a very poor response to treatment and a high mortality rate.

Researchers have known that the broad mechanisms of cancer involve an interplay with the immune system response that includes: recruiting immune cells that influence the tumor microenvironment, escaping from host immunosurveillance and suppression, shifting of the host immune response, and tumor-associated angiogenesis to establish the blood supply.

For the study, the research team first “knocked-out” or removed the CXCR2 gene in mice, and found that the signs typically associated with inflammation were prevented. Furthermore, they demonstrated that CXCR2 dramatically suppressed colonic inflammation and the colitis associated tumor formation, growth and progression in mice.

CXCR2 decorates the outer part of immune cells called myeloid-derived suppressor cells, or MDSCs, that work to block the immune response of killer CD8+ T cells. In the knockout mice, without CXCR2 present, the MDSC cells could no longer migrate from the circulatory system to the colon, dodge the killer CD8+ T cell immune response, and feed the blood supply of the tumor environment. Furthermore, when they transplanted normal MDSC cells (with normal CXCR2) into the knockout mice, tumor formation was restored.

“These results provide the first genetic evidence that CXCR2 is required for recruitment of MDSCs into inflamed colonic mucosa and colitis-associated tumors,” said DuBois.

For DuBois, who has devoted his career to unraveling the inflammatory circuitry responsible for colon cancer, the results help connect the dots between the immune system, inflammation and tumor formation and metastasis.

DuBois’ team was the first to show that colorectal tumors contained high levels of the enzyme cyclo-oxygenase-2 (COX-2), a key step in the production of pro-inflammatory mediators such as prostaglandin E2 (PGE2). PGE2 triggers production of a CXCR2 molecule that fits into CXCR2 like a baseball into a glove’s pocket and activates it. CXCR2, like the pied piper, recruits MDSCs from the bloodstream to sites of inflammation, causing the colon cancer tumors to evade the immune killer CD8+ T immune response.

“Our findings reveal not only how MDSCs are recruited to local inflamed tissues and tumor microenvironment and how local MDSCs contribute to colorectal cancer progression, but now also provide a rationale for developing new therapeutic approaches to subvert chronic inflammation- and tumor-induced immunosuppression by using CXCR2 antagonists and neutralizing antibodies,” said DuBois.

Hidden Genetic Code

A hidden genetic code for better designer genes:

 

A hidden genetic code for better designer genes

A hidden genetic code for better designer genes

 

Scientists routinely seek to reprogram bacteria to produce proteins for drugs, biofuels and more, but they have struggled to get those bugs to follow orders. But a hidden feature of the genetic code, it turns out, could get bugs with the program. The feature controls how much of the desired protein bacteria produce, a team from the Wyss Institute for Biologically Inspired Engineering at Harvard University reported in the September 26 online issue of Science.

The findings could be a boon for biotechnologists, and they could help synthetic biologists reprogram bacteria to make new drugs and biological devices.

By combining high-speed “next-generation” DNA sequencing and DNA synthesis technologies, Sri Kosuri, Ph.D., a Wyss Institute staff scientist, George Church, Ph.D., a core faculty member at the Wyss Institute and professor of genetics at Harvard Medical School, and Daniel Goodman, a Wyss Institute graduate research fellow, found that using more rare words, or codons, near the start of a gene removes roadblocks to protein production.

“Now that we understand how rare codons control gene expression, we can better predict how to synthesize genes that make enzymes, drugs, or whatever you want to make in a cell,” Kosuri said.

To produce a protein, a cell must first make working copies of the gene encoding it. These copies, called messenger RNA (mRNA), consist of a specific string of words, or codons. Each codon represents one of the 20 different amino acids that cells use to assemble proteins. But since the cell uses 61 codons to represent 20 amino acids, many codons have synonyms that represent the same amino acid.

In bacteria, as in books, some words are used more often than others, and molecular biologists have noticed over the last few years that rare codons appear more frequently near the start of a gene. What’s more, genes whose opening sequences have more rare codons produce more protein than genes whose opening sequences do not.

No one knew for sure why rare codons had these effects, but many biologists suspected that they function as a highway on-ramp for ribosomes, the molecular machines that build proteins. According to this idea, called the codon ramp hypothesis, ribosomes wait on the on-ramp, then accelerate slowly along the mRNA highway, allowing the cell to make proteins with all deliberate speed. But without the on-ramp, the ribosomes gun it down the mRNA highway, then collide like bumper cars, causing traffic accidents that slow protein production. Other biologists suspected rare codons acted via different mechanisms. These include mRNA folding, which could create roadblocks for ribosomes that block the highway and slow protein production.

To see which ideas were correct, the three researchers used a high-speed, multiplexed method that they’d reported in August in The Proceedings of the National Academy of Sciences.

First, they tested how well rare codons activated genes by mass-producing 14,000 snippets of DNA with either common or rare codons; splicing them near the start of a gene that makes cells glow green, and inserting each of those hybrid genes into different bacteria. Then they grew those bugs, sorted them into bins based on how intensely they glowed, and sequenced the snippets to look for rare codons.

They found that genes that opened with rare codons consistently made more protein, and a single codon change could spur cells to make 60 times more protein.

“That’s a big deal for the cell, especially if you want to pump out a lot of the protein you’re making,” Goodman said.

The results were also consistent with the codon-ramp hypothesis, which predicts that rare codons themselves, rather than folded mRNA, slow protein production. But the researchers also found that the more mRNA folded, the less of the corresponding protein it produced — a result that undermined the hypothesis.

To put the hypothesis to a definitive test, the Wyss team made and tested more than 14,000 mRNAs – including some with rare codons that didn’t fold well, and others that folded well but had no rare codons. By quickly measuring protein production from each mRNA and analyzing the results statistically, they could separate the two effects.

The results showed clearly that RNA folding, not rare codons, controlled protein production, and that scientists can increase protein production by altering folding, Goodman said.

The new method could help resolve other thorny debates in molecular biology. “The combination of high-throughput synthesis and next-gen sequencing allows us to answer big, complicated questions that were previously impossible to tease apart,” Church said.

“These findings on codon use could help scientists engineer bacteria more precisely than ever before, which is tremendous in itself, and they provide a way to greatly increase the efficiency of microbial manufacturing, which could have huge commercial value as well,” said Wyss Institute Founding Director Don Ingber, M.D., Ph.D. “They also underscore the incredible value of the new automated technologies that have emerged from the Synthetic Biology Platform that George leads, which enable us to synthesize and analyze genes more rapidly than ever before.”

Intelligence Linked to Ancient Genetic Accident

Origin of Intelligence and Mental Illness Linked to Ancient Genetic Accident

Origin of Intelligence and Mental Illness Linked to Ancient Genetic Accident

 

Researchers have identified the moment in history when the genes that enabled us to think and reason evolved. This point 500 million years ago provided our ability to learn complex skills, analyse situations and have flexibility in the way in which we think. Professor Seth Grant, of the University of Edinburgh, who led the research, said: “One of the greatest scientific problems is to explain how intelligence and complex behaviours arose during evolution.” The research, which is detailed in two papers in Nature Neuroscience, also shows a direct link between the evolution of behaviour and the origins of brain diseases. Scientists believe that the same genes that improved our mental capacity are also responsible for a number of brain disorders. “This ground breaking work has implications for how we understand the emergence of psychiatric disorders and will offer new avenues for the development of new treatments,” said John Williams, Head of Neuroscience and Mental Health at the Wellcome Trust, one of the study funders. The study shows that intelligence in humans developed as the result of an increase in the number of brain genes in our evolutionary ancestors. The researchers suggest that a simple invertebrate animal living in the sea 500 million years ago experienced a ‘genetic accident’, which resulted in extra copies of these genes being made. This animal’s descendants benefited from these extra genes, leading to behaviourally sophisticated vertebrates — including humans. The research team studied the mental abilities of mice and humans, using comparative tasks that involved identifying objects on touch-screen computers. Researchers then combined results of these behavioural tests with information from the genetic codes of various species to work out when different behaviours evolved. They found that higher mental functions in humans and mice were controlled by the  same genes. The study also showed that when these genes were mutated or damaged, they impaired higher mental functions. “Our work shows that the price of higher intelligence and more complex behaviours is more mental illness,” said Professor Grant. The researchers had previously shown that more than 100 childhood and adult brain diseases are caused by gene mutations. “We can now apply genetics and behavioural testing to help patients with these diseases,” said Dr Tim Bussey from Cambridge University, which was also involved in the study.

 

Cultural stereotypes rooted in Genetic’s

Why the British are freethinking and the Chinese love conformity: It’s all in the genes claim scientists:

Gene DNA

Gene DNA

Cultural stereotypes may be deeply rooted in our genetic makeup, say scientists.  Common traits like British individualism and Chinese conformity could be attributed to genetic differences between races according to a new study.  The study, by the department of psychology at Northwestern University in Illinois, suggests that the individualism seen in western nations, and the higher levels of collectivism and family loyalty found in Asian cultures, are caused by differences in the prevalence of particular genes. Common traits like British individualism and Chinese conformity could be attributed to genetic differences between races according to new research.  ‘We demonstrate for the first time a robust association between cultural values of individualism–collectivism and the serotonin transporter gene,’ said Joan Chiao, from the department of psychology at Northwestern University.  Chiao and her colleagues combined data from global genetic surveys, looking at variations in the prevalence of various genes. The findings were matched with other research which ranked nations by levels of individualism and collectivism.  The team focused their attentions on the gene that controls levels of serotonin, a chemical in the brain which regulates mood and emotions.

 
All together now: Japanese men praying
Japanese men praying.  Their studies found that one version of the gene was far more common in western populations which, they said, was associated with individualistic and freethinking behavior.  Another version of the same gene, which was prevalent in Asian populations, they said was associated with collectivism and a greater willingness to put the common good first.  People with this gene appeared to have a different response to serotonin.
 
Free-thinking: A protestor at the Occupy site in front of St Paul's in London A protestor at the Occupy site in front of St Paul’s in London.  If they are confirmed, the findings made by Chiao and her colleagues would suggest that races may have a number of inherent psychological differences — just as they differ in physical appearances.  Chiao suggests that the version of the gene predominating in Asian populations is associated with heightened anxiety levels and increased risk of depression.  She adds that such populations respond by structuring their society to ward off those negative effects.  The success of such social structures would then ensure that the gene would spread.  She added the findings showed how culture could exert a powerful influence on human genetics and evolution.