Scientists create organism with ‘Alien’ DNA

organism with 'alien' DNA

organism with ‘alien’ DNA

Scientists have created the first “semi-synthetic” micro-organism with a radically different genetic code from the rest of life on Earth.

The researchers believe the breakthrough is the first step towards creating new microbial life-forms with novel industrial or medical properties resulting from a potentially massive expansion of genetic information.

The semi-synthetic microbe, a genetically modified E. coli bacterium, has been endowed with an extra artificial piece of DNA with an expanded genetic alphabet – instead of the usual four “letters” of the alphabet its DNA molecule has six.

The natural genetic code of all living things is based on a sequence of four bases – G, C, T, A – which form two sets of bonded pairs, G to C and T to A, that link the two strands of the DNA double helix.

The DNA of the new semi-synthetic microbe, however, has a pair of extra base pairs, denoted by X and Y, which pair up together like the other base pairs and are fully integrated into the rest of the DNA’s genetic code.

The scientists said that the semi-synthetic E. coli bacterium replicates normally and is able to pass on the new genetic information to subsequent generations. However, it was not able to use the new encoded information to produce any novel proteins – the synthetic DNA was added as an extra circular strand that did not take part in the bacterium’s normal metabolic functions.

The study, published in the journal Nature, is the first time that scientists have managed to produce a genetically modified microbe that is able to function and replicate with a different genetic code to the one that is thought to have existed ever since life first started to evolve on Earth more than 3.5 billion years ago.

“Life on earth in all its diversity is encoded by only two pairs of DNA bases, A-T and C-G, and what we’ve made is an organism that stably contains those two plus a third, unnatural pair of bases,” said Professor Floyd Romesberg of the Scripps Research Institute in La Jolla, California.

“This shows that other solutions to storing information are possible and, of course, takes us closer to an expanded-DNA biology that will have many exciting applications, from new medicines to new kinds of nanotechnology,” Professor Romesberg said.

Expanding the genetic code with an extra base pair raises the prospect of building new kinds of proteins from a much wider range of amino acids than the 20 or so that exist in nature. A new code based on six base pairs could in theory deal with more than 200 amino acids, the scientists said.

“In principle, we could encode new proteins made from new, unnatural amino acids, which would give us greater power than ever to tailor protein therapeutics and diagnostics and laboratory reagents to have desired functions,” Professor Romesberg said.

“Other applications, such as nanomaterials, are also possible,” he added.

The researchers emphasised that there is little danger of the new life-forms living outside the confines of the laboratory, as they are not able to replicate with their synthetic DNA strand unless they are continuously fed the X and Y bases – synthetic chemicals called “d5SICS” and “dNaM”, that do not exist in nature.

The bacteria also need a special protein to transport the new bases around the cell of the microbe. The transporter protein comes from algae and if it, or the X and Y bases, are lacking, the microbial cells revert back to the natural genetic code, said Denis Malyshev of the Scripps Institute.

“Our new bases can only get into the cell if we turn on the “base transporter” protein. Without this transporter or when the new bases are not provided, the cell will revert back to A, T, G, C and the d5SICS and the dNaM will disappear from the genome,” Dr Malyshev said.

 

Source:  independent.co.uk

Chemists produced artificial plastic cell

First Plastic Cell With Working Organelle:

chemists have successfully produced an artificial cell

Chemists have successfully produced an artificial cell

It is hard for chemists to match the chemistry in living cells In their laboratories.  In a cell many complex reactions are taking place in an overfull Simultaneously , small container , in various compartments and incredibly efficiently. This is why chemists attempt to imitate the cell in various ways. In doing so , they hope to learn more about the origin of life and the transition from chemistry to biology.

Jan van Hest and his PhD candidate. Their organelles Ruud Peters created by tiny spheres filling with chemicals and placing these inside a water droplet . They then cleverly covered the water droplet with a polymer layer – the cell wall . Using fluorescence , They were able to show the planned cascade of reactions, it did in fact take place . This means that they are the first polymer chemists to create a working cell with organelles . Just like in the cells in our bodies , the chemicals are able to enter the cell plasma following the reaction in the organelles , to be processed elsewhere in the cell .

Creating cell-like structures is currently very popular in the field of chemistry , with various methods being tried at the Institute for Molecules and Materials (IMM ) . Professor Wilhelm Huck, for example , is making cells from tiny droplets of solutions very similar to cytoplasm , and Van Hest ‘s group is building cells using polymers .

Competing groups are working closer to biology , making cells from fatty acids. We would like to do the same in the future . Another step would be to make cells produce their own energy supply . Also we are working on ways of controlling the movement of chemicals within the cell, organelles towards . By simulating these things , we are able to better understand living cells. One day we will even be able to make something that looks very much like the real thing.

Red Blood Cells Take On New Geometry During Clotting

Red Blood Cells Take On Many-Sided Shapes:

Red Blood Cells Take On Many-Sided Shape During Clotting

Red Blood Cells Take On Many-Sided Shape

 

 

 

 

 

 

 

 

 

 

 

Red blood cells are real levers of change in body shape, perhaps the most malleable of all cell types , transformation – among other forms – in compressed discs able to pass through capillaries with diameters less than the cell itself blood . While the study of how blood clots John W. contract Weisel , Ph.D. , Professor of Cell and Developmental Biology at the Perelman School of Medicine at the University of Pennsylvania, and his colleagues discovered a new geometry that red blood cells are supposed to when compressed during clot formation .

Although red blood cells were visualized for the first time in the mid-17th century and studied extensively since then , this new study , published online ahead of print in the journal Blood, describes a previously unknown and new function potential of red blood cells . The Penn team found that red blood cells can be compressed into multifaceted structures close together – polyhedral – instead bi – concave , free-flowing form of the disc.

What is more , contrary to expectations , the fibrin and platelet aggregates which form highly clots are mainly employed on the outside of clots , with red blood cells crowded into the clot , while the content of clots are more homogeneous before shrinkage occurs .

Hired clots can form a watertight seal and help prevent vascular obstruction, but confer resistance to penetration of drugs that break down fibrin, the structural component of blood clots , one common treatment option for heart attacks and strokes.

” When I first saw this, he thought :” This can not be biological , ‘”says Weisel . The team first saw the red blood cells shaped polyhedron – when the coagulation process of contraction is studied using a novel MRI technology , with the co -authors of T2 Biosystems, along with co -author Douglas Cines , MD , director of the Coagulation Laboratory and Professor of Pathology and Laboratory Medicine at Penn. They observed a signal indicating tight red blood cells.

The clot network clots are dimensional network of fibers , mainly consisting of the blood protein fibrinogen , which is converted to fibrin during coagulation , and platelets , which aggregate by binding to fibrin once activated . A blood clot must have the proper degree of rigidity and plasticity to stop the flow of blood when tissue is damaged , however , be flexible enough that it does not block the blood flow .

After a clot forms , actin and myosin in platelets initiate the contraction process and cause the clot is reduced to about one third of its original size. This is an important step to stop bleeding , to reduce the blockage in the blood vessel , and to provide a matrix for the migration of cells involved in wound healing . Red blood cells are involved in the contraction process , especially in the venous system , and get pulled by platelets into the clot, blood and the study indicated .

Little is known about the structure of the contracted clots or the role of red blood cells in the contraction process . “We found that the contracted blood clots develop a remarkable structure with a mesh of fibrin and platelet aggregates outside the clot and close packing , tiled matrix of polyhedral erythrocytes compressed inside ,” says Weisel .

The team also saw the same morphology of compacted clots after initiating coagulation activators and also with several clots formed from reconstituted human blood cellular components and blood plasma and mouse . Such matrices polyhedral packing of erythrocytes or polyhedrocytes as researchers dubbed them , were also observed in human arterial thrombi taken from patients who had heart attacks . This form is likely taken up by the red blood cells when contracted or compressed together when platelets clot in order to decrease the volume , surface energy , or the energy of bending , the authors assume .

Cines notes that these findings may have clinical implications . Doctors need to inject tPA as thrombolytic agents to quickly break thrombi , clots that obstruct blood flow , for example, in the coronary arteries to treat a heart attack or arteries leading to the brain to treat stroke. It is well known that thrombi develop time be broken , which is one reason why early intervention resistance is important . The nearly impermeable barrier formed by the red blood cells within contracted clots was observed in the study of the blood can help explain why . Clot contraction could be a target of intervention to prevent the formation of densely packed array polyhedrocytes .

Scientists Grow Human Brain

Scientists Grow Human Brain From Stem Cells:

Scientists Grow Human Brain From Stem Cells

Scientists Grow Human Brain From Stem Cells

Ear, eye, liver, windpipe, bladder and even a heart. The list of body parts grown from stem cells is getting longer and longer. Now add to it one of the most complex organs: the brain.

A team of European scientists has grown parts of a human brain in tissue culture from stem cells. Their work could help scientists understand the origins of schizophrenia or autism and lead to drugs to treat them, said Juergen Knoblich, deputy scientific director at the Institute of Molecular Biotechnology of the Austrian Academy of Sciences and one of the paper’s co-authors.

The advance could also eliminate the need for conducting experiments on animals, whose brains are not a perfect model for humans.

To grow the brain structures, called organoids, the scientists used stem cells, which can develop into any other kind of cell in the body. They put the stem cells into a special solution designed to promote the growth of neural cells. Bits of gel interspersed throughout the solution gave the cells a three-dimensional structure to grow upon. In eight to 10 days, the stem cells turned into brain cells. After 20 days to a month, the cells matured into a size between three and four millimeters, representing specific brain regions such as the cortex and the hindbrain.

Growing brain tissue this way marks a major advancement because the lab-grown brain cells self-organized and took on growth patterns seen in a developing, fetal brain.

Currently, the organoids are limited on how big they can get because they do not have a circulatory system to move around nutrients.

Knoblich’s team didn’t stop at growing the brain organoids, though. They went a step further and used the developing tissue to study microcephaly, a condition in which the brain stops growing. Microcephalic patients are born with smaller brains and impaired cognitive development. Studying microcephaly in mice doesn’t help because human and mouse brains are too different.

For this part of the study, the researchers used stem cells from a microcephalic patient and grew neurons in a culture. They found that normal brains have progenitor stem cells that make neurons and can do so repeatedly. In microcephalic brains, the progenitor cells differentiate into neurons earlier, said Madeline A. Lancaster, the study’s lead author. The brain doesn’t make as many neurons and a child is born with a much smaller brain volume.

Yoshiki Sasai, a stem-cell biologist at the Riken Center for Developmental Biology in Kobe, Japan, garnered headlines last year by growing the precursors to a human eye.

“The most important advancement is that they combined this self-organization culture with disease-specific cells to model a genetic disease of human brain malformation,” he said.

“Everything we have done with other organs starts with this stage,” said Dr. Anthony Atala, the director of the Wake Forest Institute for Regenerative Medicine, who has done years of research on using 3D printers to build organs. Atala was not involved in this study, but he noted that before he could build organs, he needed to grow the pieces in order to get the cells to differentiate in just the right way. So though it’s unlikely anyone will print brains the way he did a kidney, this kind of experiment is where organ regeneration starts.

Knoblich said the next step is studying other brain disorders, but it will take some time to grow enough brain tissue. One factor is maximum size and how far the brain can develop in the culture. Brain cells develop in layers, and there are several by the time a baby is born. The cortical cells Knoblich’s team grew only had one such layer. Another factor is getting blood vessels inside the tissue. That problem could be solved some time in the future, though he said he couldn’t predict when.

It is tempting to think one day there will be whole brains in vats, but that isn’t likely to happen.

“Aside from the severe ethical problem, I do not think this will be possible,” Knoblich said. To form actual functioning neural circuits, a brain needs sensory input. “Without any sensory input, the proper organization may not happen.”

New light on how Genes turn off and on

New insights into how genes turn on and off:

New insights into how genes turn on and off

New insights into how genes turn on and off

 

Researchers at UC Davis and the University of British Columbia have shed new light on methylation, a critical process that helps control how genes are expressed. Working with placentas, the team discovered that 37 percent of the placental genome has regions of lower methylation, called partially methylated domains (PMDs), in which gene expression is turned off. This differs from most human tissues, in which 70 percent of the genome is highly methylated.

While PMDs have been identified in cell lines, this is the first time they have been found in regular human tissue. In addition to enhancing our understanding of epigenetics, this work could influence cancer research and help illuminate how environmental toxins affect fetal development. .

Since it was unraveled more than ten years ago, the human genome has been the focus of both popular interest and intense scientific focus. But the genome doesn’t act alone; there are many factors that influence whether genes are turned on or off. One of these is an epigenetic process called methylation, in which a group of carbon and hydrogen atoms (a methyl group) attaches to DNA, adjusting how genes are expressed.

“I like to think of epigenetics as a layer on top of your genetic code,” said senior author Janine LaSalle, professor of medical microbiology and immunology. “It’s not the DNA sequence but it layers on top of that — and methylation is the first layer. Those layers provide a lot of information to the cells on where and when to turn on the genes.”

How and when genes are activated (or inactivated) can have a profound impact on human development, cancer and the biological legacy of environmental toxins. Prior to this research, PMDs had only been found in cultured cell lines, which led some scientists to wonder if they existed outside the test tube. This study confirms they exist in placental tissue, a critically important window into fetal development.

“The placenta is the interface between mother and fetus,” said LaSalle, who is a researcher affiliated with the UC Davis MIND Institute. “It’s a time capsule from when a lot of important methylation events occurred.”

In addition, placental tissue was interesting to study because it has a number of invasive characteristics often associated with cancer. In fact, a number of cancers, such as breast and colon, have widespread PMDs. LaSalle notes that anti-cancer epigenetic therapies that adjust methylation could be refined based on this improved understanding of PMDs.

This work could also enhance our ability to detect genetic defects. Methylation, and other epigenetic data, provides information that cannot be found in the genome alone. For example, the vast majority of cells in the body contain identical genetic code. However, the added information provided by methylation allows scientists to determine where specific DNA came from.

“Methylation patterns are like fingerprints, showing which tissue that DNA is derived from,” LaSalle said. “You can’t get that information from just the DNA sequence. As a result, methylation studies could be a very rich source for biomarkers.”

In the study, PMDs encompassed 37 percent of the placental genome, including 3,815 genes, around 17 percent of all genes. When found in low-methylation regions, these genes were less likely to be transcribed into proteins. Researchers also found that PMDs also contain more highly methylated CpG islands (genomic areas with large numbers of cytosine-guanine pairs), which are often associated with gene transcriptional silencing of promoters.

Because the placental PMDs contained many genes associated with neuronal development, and specifically autism, LaSalle notes that future research could investigate how epigenetics impacts autism genes at birth.

“We are looking for biomarkers that predict neurodevelopmental outcomes,” LaSalle said. “Now we have a series of snap shots from a critical period where we think environmental factors are playing a role in the developing brain.”

Nutrition and Health based on flimsiest evidence.

The Surprising Reason People Get Fat:

 

The Surprising Reason People Get Fat

The Surprising Reason People Get Fat

 

“I want to convince you that the conventional wisdom about weight gain is wrong,” declared Gary Taubes. The idea that eating too much and exercising too little is the culprit is, he said, “as obsolete as the belief that the sun rotates around the earth.” Thus began the most revolutionary presentation in the five-year history of the Nutrition and Health Conference, an annual three-day event co-sponsored by the Arizona Center for Integrative Medicine (founded by Dr. Weil in 1994). Held most recently in Phoenix, Arizona in April of 2008, it attracted some 500 health care professionals from around the world, and the packed house at Arizona Grand Resort made it clear that Taubes was a headliner. The writer, trained in applied physics at Harvard and aerospace engineering at Stanford, specializes in parsing hot science controversies in articles and books (such as 1993’s Bad Science: The Short Life and Weird Times of Cold Fusion). He is widely credited with kicking off the national low-carb diet trend with his July 2002 New York Times Magazine article, What If It’s All Been a Big, Fat Lie? In 2007, he published Good Calories, Bad Calories: Challenging the Conventional Wisdom on Diet, Weight Control and Disease, a book that led the New York Times to assert that “Gary Taubes is a brave and bold science journalist” who shows that “much of what is believed about nutrition and health is based on the flimsiest evidence.” Taubes’ message: political pressure and sloppy science over the last 50 years have skewed research to make it seem that dietary fat and cholesterol are the main causes of obesity and heart disease, but there is, in fact, little or no objective data to support that hypothesis. A more careful look (Taubes researched his book for five years, its 450 pages include 60 pages of footnotes) reveals that the real obesity-epidemic drivers are increased consumption of refined carbohydrates, mainly sugar and white flour. Further, as he stated in his conference presentation, obesity is not “a disorder of energy imbalance,” in which weak-willed people eat too much and exercise too little, but rather “a disorder of excess fat accumulation” in which the body, not the brain, is the primary culprit. Eating too much and exercising too little are side effects, not causes, of the active role of carbohydrate-driven hormones on the whole organism, including the brain. Much of Taubes’ presentation was devoted to illustrating the central role that glucose and insulin – both of which are products of carbohydrate metabolism – play in fat deposition. A chemical compound derived from glucose, he said, turns fatty acids – the “burnable” kind of fat – into triglycerides, the “storable” form of fat. Consequently, “Anything that works to transport glucose into fat cells works to deposit fat.” And what transports glucose into fat cells? Insulin. “When insulin is secreted or chronically elevated, fat accumulates in fat tissue,” he said. “When insulin levels drop, fat escapes from fat tissue and the fat depots shrink.” Bottom line: “Carbohydrate is driving insulin is driving fat deposition.” So when it comes to accumulating fat, carbohydrates are indeed “bad calories,” as they are the only ones that boost insulin and make fat accumulation possible. Highly refined carbohydrates are even worse, as they lead to insulin surges and subsequent drops, which creates a hunger for more – hunger so voracious that, for most people, it can’t be overcome by willpower. Refined carbohydrates, Taubes contends in his book, are literally addictive. So what’s the scientific weight-loss solution? Taubes asserted that since the fewer carbohydrates we eat, the leaner we will be, our diets should emphasize meat, fish, fowl, cheese, butter, eggs and non-starchy vegetables. Conversely, we should reduce or, preferably, eliminate bread and other baked goods, potatoes, yams, rice, pasta, cereal grains, corn, sugar (both sucrose and high fructose corn syrup) ice cream, candy, soft drinks, fruit juices, bananas and other tropical fruits, and beer. Excluding carbohydrates from the diet, he said, derails the insulin peak/dip roller coaster, so one is never voraciously hungry, making weight loss and healthy-weight maintenance easy. “When you eat this way, the fat just melts off,” he said after his speech – and Taubes is indeed a lean fellow. While Dr. Weil agrees with most of Taubes’ research, he draws the line at the writer’s specific dietary recommendations: “I don’t agree that the way to respond to this information is to eat a diet that is mostly meat and no carbohydrate.” He said instead that people should eat animal protein two to three times per week – mostly as fatty, cold-water fish to reap the benefits of omega-3 fatty acids – and otherwise eat carbohydrate foods that rank low on the glycemic load scale. “All carbohydrates are not the same, nor do all people react to them in the same way,” he said. “That needs to be taken into account.” But overall, Dr. Weil, like the other assembled health-care professionals, came away impressed. “I invited Gary to speak, and I’ve been recommending the book to my medical colleagues and students. It’s important to get this information out to the medical community, because a lot of the ways that we try to prevent and treat obesity are based on assumptions that have no scientific evidence.”