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December 17, 2005

Discovery of Remarkable Developmental Pathway

Discovery of Remarkable Developmental Pathway Image: Courtesy of Bruno Reversade and Edward De Robertis/HHMI at UCLA
Howard Hughes Medical Institute scientists have discovered an important regulatory pathway that enables frog embryos to develop normally even after being split in half - as happens in the development of identical twins.

The scientists said their findings suggest that efforts to apply embryonic stem cells therapeutically to regenerate damaged or diseased tissue may have to overcome similar self-regulatory mechanisms present in stem cells. Such mechanisms might otherwise drive stem cells to attempt to differentiate into embryos with a number of cell types, rather than restricting themselves to a desired single type of tissue.

The researchers, graduate student Bruno Reversade and HHMI investigator Edward M. De Robertis, both at the University of California at Los Angeles, published their findings in the The experiments were conceived in an attempt to learn more about the mechanisms underlying the establishment of a morphogenetic field. This field consists of a gradient of regulatory proteins that aids in organizing the differentiation of embryonic cells and gives an organism its overall shape. Eventhough scientists had known that morphogenetic fields were responsible for the embryo's remarkable resiliency, very little was understood about how they function at the molecular level, said De Robertis.

For their studies, Reversade and De Robertis used early embryos of the African toad Xenopus. Widely used in embryological studies, Xenopus embryos are easy to grow and can be manipulated by tissue transplantation techniques. The scientists studied Xenopus embryos in the blastula stage, which resembles a hollow sphere of a few thousand cells.

The researchers were seeking to understand more about the regulatory role of a family of proteins called bone morphogenetic proteins (BMPs). Certain BMPs are known to be key regulators of the dorsoventral (back-to-belly) patterning of embryos. In such patterning, dorsal cells differentiate into neural cells and ventral cells become epidermal cells.........

Sue      Permalink


December 17, 2005

How Chlamydia Escapes Defenses

How Chlamydia Escapes Defenses
Duke University Medical Center microbiologists have discovered that the parasitic bacteria Chlamydia escapes cellular detection and destruction by cloaking itself in droplets of fat within the cell. The scientists said that their findings represent the first example of a bacterial pathogen "mimicking" such a structure, or organelle, within a cell.

Not only do the findings suggest a novel mechanism of bacterial infection, but the new insights into Chlamydia's actions within infected cells provide rational targets for potential drugs to halt the spread of the bacteria, said the researchers. Chlamydia has been implicated in sexually transmitted infections, atherosclerosis and some forms of pneumonia.

Chlamydia is an obligate intracellular parasite that prospers within a host cell by hijacking the cell's internal machinery to survive and replicate. The bacterium lives within the cell in a protective capsule known as an inclusion. To date, it has not been clearly understood how Chlamydia has evolved to evade the cell's internal intruder alert system.

"In our experiments, we found that Chlamydia recruits lipid droplets from within the cell and stimulates the production of new droplets, which cover the surface of the inclusion," explained Yadunanda Kumar, Ph.D., a post-doctoral fellow in Duke's Department of Molecular Genetics and Microbiology. "This action of surrounding itself with lipid droplets may represent an example of organelle mimicry, where the chlamydial inclusion is protected from the cell's defenses by being perceived by the cell as just another lipid droplet."

Kumar presented the results of the Duke research Dec. 11, 2005, at the 45th annual meeting of the American Society for Cell Biology in San Francisco. The research was supported by National Institutes of Health, the Pew Foundation and the Whitehead Foundation.........

Mark      Permalink


December 17, 2005

Gene Mutation In Bardet-beidl Syndrome (BBS)

Gene Mutation In Bardet-beidl Syndrome (BBS)
Johns Hopkins researchers studying a rare inherited syndrome marked by eye and kidney problems, learning disabilities and obesity have discovered a genetic mutation that makes the syndrome more severe but that alone doesn't cause it. Their report appears in the advance online edition of Nature (Dec. 4).

The new discovery about Bardet-Beidl syndrome (BBS) came from a panoply of studies -- starting with comparative genomics and experiments with yeast, and moving to experiments with zebrafish and genetic analysis of families with the syndrome -- and mirrors what experts expect for the genetically complex common diseases that kill most Americans, like diabetes, heart disease and cancer.

"Researchers are going to have to think very hard before they discount genetic variation that appears not to directly cause a disease," says the study's leader, Nicholas Katsanis, Ph.D., associate professor in the McKusick-Nathans Institute of Genetic Medicine at Johns Hopkins. "The onus is on us to figure out how to dissect the effects of what appear to be silent genetic variants. I have a greatly renewed respect for the complexity of the genome, for the subtle ways that genes and gene products interact with each other".

Conventional wisdom says that a collection of subtle genetic variations contribute to a person's risk of common diseases, but hunting for such subtle effects is daunting. As a result, most gene hunts have targeted relatively rare diseases that appear from their pattern in families to be fairly simple genetically.

Katsanis and colleagues have recognized for years that BBS, eventhough rare, is more similar to the genetic complexity of common diseases, in part because patients with this condition have extremely variable severity, even within families. The newly identified mutation, in a gene called MGC1203, is the first to affect only the severity of the syndrome. Mutations in eight other genes, all dubbed BBS genes, are known to cause the disease, often in combination with each other.........

Sue      Permalink


December 17, 2005

What Can Change in the Brain?

What Can Change in the Brain?
The brain's ability to reorganize itself - strengthening or weakening connections between neurons or adding or subtracting those connections - allows it to form memories, make transitions between sleep and waking, and focus attention on objects of interest.

This phenomenon is a form of neural plasticity. Chemical synapses, junctions where neurons communicate using chemical substances, have long been implicated in plasticity. Now, for the first time, Brown University researchers have demonstrated that electrical synapses are also subject to long-term changes in the brains of mammals. Their work appears in the journal Science.

"The fact that you can change the function of electrical synapses, and change them for longer than a few seconds, means that they may play a role in certain kinds of plasticity," said Barry Connors, a Brown professor of neuroscience and co-author of the paper.

"But plasticity governs a number of critical brain functions. Since electrical synapses help synchronize the activity of brain cells, these junctions probably help regulate specific brain rhythms that occur while you are awake or sleeping. So this work helps us better understand, in a basic sense, how the brain regulates behavioral states".

Carole Landisman, currently a neurobiology researcher at Harvard Medical School, is the lead author of the paper. Landisman was an investigator in Connors' lab at Brown, where the experiments were conducted.

To better understand how electrical synapses function, Landisman and Connors recorded activity from rat neurons that were connected by electrical synapses and stimulated other brain cells using brief bursts of electricity to see how the neurons would respond. They also treated neurons with two different drugs. All three techniques either activated or blocked metabotropic glutamate receptors or mGluRs, a type of neural trigger that responds to the amino acid glutamate, a transmitter molecule in the brain. The result: a long-lasting 20- to 30-percent reduction in electrical synapse strength.........

Daniel      Permalink


December 17, 2005

gene for debilitating vitamin B12 disease identified

gene for debilitating vitamin B12 disease identified
Researchers at the MUHC and McGill University have identified a gene responsible for a disease that impairs the body's ability to handle vitamin B12 and that may contribute to heart disease, stroke and dementia. The details of the CIHR and March of Dimes funded research are published in this week's issue of Nature Genetics. The research, which began more than 20 years ago, will allow doctors to perform earlier diagnosis, assess 'carriers' of the disease-Combined Methylmalonic aciduria (MMA) and Homocystinuria-and open the door to new and improved therapys for this debilitating disease.

"Eventhough this disease sometimes starts in adolescence or adulthood, we commonly diagnose this rare inability to process vitamin B12 in the first few months of life," says Dr. David Rosenblatt, Chairman of Human Genetics at McGill, Director of Medical Genetics in Medicine at the MUHC, Chief of Medical Genetics at the Jewish General Hospital and lead researcher of the new study. "Babies may have breathing, feeding, visual and developmental difficulties, older patients may develop sudden neurological disease."

Vitamin B12, which is found in all animal products-including dairy, eggs, meat, poultry, and fish-but not in plants, is vital for synthesis of red blood cells and maintenance of the nervous system. Vitamin B12 also helps control homocysteine levels in the human body. Homocysteine control is important because in excess this compound can increase the risk of heart disease, stroke, and dementia.

17 year-old Michael-a typical MMA and Homocystinuria patient-was diagnosed at 6-months of age, and has battled numerous medical challenges as a result of his condition. Michael is developmentally delayed, visually impaired and does not talk; he has suffered seizures since he was three years old, had a stroke by the age of seven and has since developed rheumatoid arthritis and scoliosis. Michael's diagnosis, which led the way to therapy involving injections of vitamin B12, was conducted at Dr. Rosenblatt's laboratory at the MUHC-one of only two centres in the world that perform these tests.........

JoAnn      Permalink


December 16, 2005

Cell-based Nano Machine

Cell-based Nano Machine Image courtesy of Whitehead Institute
Scientists have known for some time that a long, fibrous coil grown by a single-cell protozoan is, gram for gram, more powerful than a car engine. Now, scientists at Whitehead Institute-together with colleagues at MIT, Marine Biological Laboratory in Woods Hole, MA, and University of Illinois, Chicago-have found that this coil is far stronger than previously thought. In addition, the scientists have discovered clues into the mechanism behind this microscopic powerhouse.

"These findings are twofold," says Danielle France, a graduate student in the lab of Whitehead Member Paul Matsudaira, and, along with Matsudaira, a member of MIT's Division of Biological Engineering. "First, they give us an idea of how a cell can manage to generate such enormous force; and second, they provide clues for how engineers might reconstruct these mechanisms for nano-scale devices."

France will present her findings Sunday, December 11, at the 45th Annual Meeting of the American Society for Cell Biology in San Francisco.

Researchers have known about this nano-spring for roughly 300 years, ever since Anton van Leeuwenhoek first observed the protozoan, Vorticella convallaria, through a hand-made microscope. The spring in the unicellular Vorticella is a contractile fiber bundle, called the spasmoneme, which runs the length of the stalk. At rest, the stalk is elongated like a stretched telephone cord. When it contracts, the spasmoneme winds back in a flash, forming a tight coil. To find out how strongly Vorticella recoils, France and his colleagues used a unique microscope to apply an extra load to the spring. The microscope, developed by Shinya Inoue and his colleagues at the Marine Biological Laboratory in Woods Hole, MA, uses a spinning platform to increase the centrifugal force exerted against the protozoan.........

Scott      Permalink


December 16, 2005

Tongue Sensors Taste Fat

Tongue Sensors Taste Fat
As you stand at buffet tables during holiday parties this year, it might cheer you up to know most people don't gain as much weight over the holidays as once was thought. Instead of five or 10 pounds, most of us actually gain only a pound or two. But it might depress you to know that weight gain happens one pound at a time and in the long run, it may be hard to avoid - particularly for some of us, because some of the taste buds in our tongues are programmed to make us crave fatty food - and fat is everywhere in our diets.

French scientists recently reported that mice have a receptor in their tongues that can sense fat, and the presence of that receptor seems to drive the mice to crave fat in their diets. The work was based on research from Nada A. Abumrad, Ph.D., the Dr. Robert C. Atkins Professor of Medicine and Obesity Research at Washington University School of Medicine in St. Louis. She previously had identified a protein receptor for fat and documented its function in recognizing and using fatty food. This led the French scientists from the Taste Institute in Dijon, France, to wonder whether the protein also may have a role in actually tasting fat.

"Fat sensing has been very controversial," Abumrad says. "It once was thought that we could sense five different tastes: sweet, salty, sour, bitter and what researchers refer to as umami, which is the taste of a protein like monosodium glutamate. There was some indirect evidence that the tongue might be able to identify fat, too, but a number of researchers thought that involved sensation of texture more than the actual taste of fat."

Abumrad adds that several researchers had proposed people might not only sense the texture of fat, but also might have fatty acid receptors that lead them to prefer foods containing fat. She studies the molecular mechanisms regulating utilization of fatty acids, and she was the first to identify a protein called CD36 that facilitates the uptake of fatty acids. The CD36 receptor protein is located on the surface of cells and distributed in a number of tissues, including fat cells, the digestive tract, heart tissue, skeletal muscle tissue and, as it happens, the tongue.........

Daniel      Permalink


December 16, 2005

Strategy To Knock Out Cancer

Strategy To Knock Out Cancer These images of cell nuclei treated with damaging radiation show that in the absence of MDC1, repair proteins (bright green areas) are inhibited from gathering at the sites of DNA damage.
To remain healthy, all cells must quickly mend any breaks that arise in their DNA strands. But cancer cells are especially dependent on a process called homologous recombination to repair DNA and stay alive.

Now scientists at Washington University School of Medicine in St. Louis have found that a protein known as MDC1 has a role in homologous recombination. This discovery could be exploited in a two-pronged therapy strategy to eliminate cancer cells' ability to repair DNA.

"Frequently cancer cells are more efficient at DNA repair than normal cells," says Simon Powell, M.D., Ph.D., head of the Department of Radiation Oncology and a researcher with the Siteman Cancer Center at Washington University School of Medicine and Barnes-Jewish Hospital. "That's what makes them resistant to drugs or radiation therapys that physicians use in an effort to damage cancer cells' DNA and destroy them."

But in light of their findings, Powell and colleagues believe MDC1 - along with other proteins involved this repair pathway - may be good targets for dual-drug chemotherapeutic approaches that can completely knock out tumor cells' ability to cope with DNA damage. Their study appears in the recent issue of Nature Structural and Molecular Biology.

The research group discovered that MDC1, a protein previously recognized only for its function in sensing DNA damage and signaling its presence, also transports DNA-repair proteins to the site of DNA strand breaks. Without MDC1 to pave the way, repair happens slowly because the fix-it proteins have a hard time reaching damaged areas, which are buried in the tightly packed chromosomal material of the cell's nucleus.

"MDC1 can bind to chromatin, the complex mixture of DNA and proteins that holds the genetic material," Powell says. "Because of chromatin's properties, getting into it to reach the DNA strand requires the right 'passwords.' MDC1 provides the DNA-repair proteins with this privileged access, and efficiently transports them to the site of damage so they can do their jobs."........

Daniel      Permalink


December 16, 2005

antioxidant linked to Alzheimer's and Parkinson's

antioxidant linked to Alzheimer's and Parkinson's Raymond Swanson, MD
A study conducted at the San Francisco VA Medical Center has identified a protein found in both mice and humans that appears to play a key role in protecting neurons from oxidative stress, a toxic process linked to neurodegenerative illnesses including Alzheimer's and Parkinson's diseases.

The study, led by Raymond Swanson, MD, chief of neurology and rehabilitation services at SFVAMC, identified the protein - known as EAAC1 in mice and as EAAT3 in humans - as the main mechanism through which the amino acid cysteine is transported into neurons. Cysteine is an essential component of glutathione, which Swanson terms "the most important antioxidant in the brain".

It had been thought previously that the main function of the protein was to remove excess glutamate, a neurotransmitter, from brain cells.

"It's known that neurons don't take up cysteine directly, and it's never been clear exactly how it gets there," says Swanson, who is also professor and vice chair of neurology at the University of California, San Francisco. "This study provides the first evidence that EAAC1 is the mechanism by which cysteine gets into neurons - and that transporting cysteine is probably its chief function".

Study findings are currently available in the Advance Online Publication section of Nature Neuroscience.

Antioxidants such as glutathione provide protection from oxidative stress, which kills cells through the "uncontrolled reaction of lipids in the cells with oxygen-basically, burning them out," says Swanson. Since the brain uses a lot of oxygen and is "chock full of lipids," it is especially vulnerable to oxidative stress, he notes.

In the first part of the study, Swanson and his co-authors observed a colony of mice deficient in the gene responsible for the production of EAAC1 and compared their behavior with that of a colony of normal, or "wild type," mice. They noticed that around the age of 11 months - old age for a mouse - the gene-deficient mice began to act listlessly, not groom themselves properly, and exhibit other signs of senility. In contrast, the wild type mice "looked and acted totally normal," according to Swanson.........

Daniel      Permalink


December 15, 2005

E. Coli Bacterium Generates Simplicity From Complexity

E. Coli Bacterium Generates Simplicity From Complexity
The ubiquitous and commonly harmless E. coli bacterium, which has one-seventh the number of genes as a human, has more than 1,000 of them involved in metabolism and metabolic regulation. Activation of random combinations of these genes would theoretically be capable of generating a huge variety of internal states; however, scientists at UCSD will report in the Dec. 27 issue of Proceedings of the National Academy of Sciences (PNAS) that Escherichia coli doesn't gamble with its metabolism. In a surprise about E. coli that may offer clues about how human cells operate, the PNAS paper reports that only a handful of dominant metabolic states are found in E. coli when it is "grown" in 15,580 different environments in computer simulations.

"When it comes to genomes, a great deal of complexity boils down to just a few simple themes," said Bernhard Palsson, a professor of bioengineering at UCSD's Jacobs School of Engineering and co-author of the study, which was made available online Dec. 15. "Scientists have confirmed the complexity of individual parts of biochemical networks in E. coli and other model organisms, but our large-scale reconstruction of regulatory and metabolic networks involving hundreds of these parts has shown that all this genetic complexity yields surprisingly few physiological functions. This is possibly a general principal in a number of, if not all, species."

Palsson and colleagues at UCSD, postdoctoral fellows Christian L. Barrett and Christopher D. Herring, and Ph.D. candidate Jennifer L. Reed, created a computer model of an E. coli cell based on the experimental results of thousands of prior experiments, some of which were completed decades ago. "The goal of this study was to comprehensively simulate all the possible molecular interactions in a well studied strain of E. coli to gain a global view of the range of functional network states," said Barrett. "Complex cellular networks can potentially generate lots of different behaviors, but we find that cells utilize only a few of them."........

Mark      Permalink



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Did you know?
Scientists at Yale have brought to light a mechanism that regulates the way an internal organelle, the Golgi apparatus, duplicates as cells prepare to divide, according to a report in Science Express.Graham Warren, professor of cell biology, and colleagues at Yale study Trypanosoma brucei, the parasite that causes Sleeping Sickness. Like a number of parasites, it is exceptionally streamlined and has only one of each internal organelle, making it ideal for studying processes of more complex organisms that have a number of copies in each cell.

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