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    News
    Thursday, 30 January 2014 17:20

    A digital test for toxic genes

    Genomic DNALike little factories, cells metabolize raw materials and convert them into chemical compounds. Biotechnologists take advantage of this ability, using microorganisms to produce pharmaceuticals and biofuels. To boost output to an industrial scale and create new types of chemicals, biotechnologists manipulate the microorganisms' natural metabolism, often by "overexpressing" certain genes in the cell. But such metabolic engineering is hampered by the fact that many genes become toxic to the cell when overexpressed.

    Now, Allon Wagner, Uri Gophna, and Eytan Ruppin of Tel Aviv University's Blavatnik School of Computer Science and Department of Molecular Microbiology and Biotechnology, along with researchers at the Weizmann Institute of Science, have developed a computer algorithm that predicts which metabolic genes are lethal to cells when overexpressed. The findings, published in Proceedings of the National Academy of Sciences, could help guide metabolic engineering to produce new chemicals in more cost-effective ways.

    "In the lab, biotechnologists often determine which genes can be overexpressed using trial and error," said Wagner. "We can save them a lot of time and money by ruling out certain possibilities and highlighting other, more promising ones."

    Gaining an EDGE

    When metabolic genes are expressed, the genetic information they contain is converted into proteins, which catalyze the chemical reactions necessary for life. Overexpression means that greater-than-normal amounts of proteins are produced. Biotechnologists typically overexpress native genes of an industrial microorganism to boost a certain metabolic pathway in the cell, thus increasing the production of desired compounds. Sometimes they overexpress foreign genes—genes transferred from other organisms—in an industrial microbe to build new metabolic pathways and allow it to synthesize new compounds. But they often find that their efforts are hindered by the toxicity of the genes that they wish to overexpress.

    Prof. Ruppin's laboratory builds large-scale software models of cellular metabolism, one of the most fundamental aspects of life. These models convert physical, chemical, and biological information into a set of mathematical equations, allowing scientists to learn how cells work and explore what happens if they are tweaked in certain ways. The newly developed algorithm, Expression Dependent Gene Effects, or EDGE, predicts what happens if scientists manipulate cells to overexpress certain genes. EDGE allows biotechnologists to foresee cases in which the overexpressed genes become toxic and then direct their efforts toward other genes.

    To validate their method, TAU researchers used genetic manipulation tools to overexpress 26 different genes in E. coli bacterial cells. Comparing the results of their computer simulations with the actual growth of the overexpressed strains that was measured in the lab, they saw that EDGE was able to predict which of the overexpressed genes turned out to be lethal to E. coli. EDGE was also successful in identifying cases of foreign genes that were toxic to E. coli, as the researchers learned from comparing the simulations' results with data collected by their collaborators at the Weizmann Institute of Science.

    Beyond bacteria

    EDGE's applications appear to extend beyond bacteria. The researchers conducted tests showing that the genes EDGE predicted to be toxic when overexpressed are expressed at low levels not only in microorganisms like bacteria, but also in multicellular organisms, including humans. The researchers say these results reflect the vital evolutionary need to keep the expression of potentially deleterious genes in check.

    "Although EDGE's current focus is biotechnology, gene overexpression also plays a central part in many human diseases, particularly in cancer. We hope that future work will apply EDGE to those directions," Wagner said.

    Wednesday, 29 January 2014 13:58

    Amino acid acts as a substitute for aspirin

    Amino-acid-beauty-therapy-facialsMany people take prophylactic aspirin for fear that it may get blood clots and thus lead to a stroke or heart attack. Acetylsalicylic acid, however, can cause unpleasant symptoms in digestive tract. According to some specialists substance arginine can easily replace it. However, they recognize that further studies.

    Narrowed blood vessels, high blood pressure and problems with blood flow in the heart sick . It is as a pump, which in this case is a system overload. Atherosclerosis begins with small deposits on the inner walls of blood vessels. Thus, the so-called endothelium of the arteries deteriorate functional change that occurs well before the appearance of the typical plate and before the diagnosis of atherosclerosis have been possible. When the plate reaches a certain density, leading to problems with blood supply - there may be pain when walking, problems with concentration, dizziness and tightness in the chest . In the worst case, forming clots that clog a court. The consequence is a stroke or heart attack.

    Dangerous of atherosclerosis is that it occurs silently and imperceptibly. No pain, and symptoms occur when it is already too late. To prevent this process, many people take preparations to thin the blood. Acetylsalicylic acid is the most popular of them. There are a lot of scientific evidence that it prevents clumping of cells in the blood, improves circulation and is therefore considered as the prevention of heart attacks.

    Taking aspirin also has minuses - many people with sensitive stomachs do not tolerate it. Other side effects include heartburn, nausea, vomiting, stomach pain and diarrhea.

    Scientists now have the first data that the amino acid arginine can be used as a substitute of acetylsalicylic acid in the dilution of the blood. It is found in some natural products such as red meat, wheat germ, soybeans, shrimp and nuts. It is found as a dietary supplement. Arginine has a positive effect on the cardiovascular system, it is considered a natural aphrodisiac.

    Substance degree before important for body nitrogen monoxide (NO). It dilates blood vessels, improves blood flow, thus contributing to the decline in blood pressure. Nitrogen monoxide normalized functional disturbances in the inner wall of the arteries, as in atherosclerosis it is not formed in a sufficient amount in the vessel wall.

    Arginine enhances not only the viscosity of the blood. Survey Prof. A. Saleh from Cairo University found that this amino acid can prevent clotting and the formation of plaque on the inner walls of the arteries as well as acetylsalicylic acid. The title, however, is the first study of its kind and its results can not yet be used for general reference.

    Wednesday, 22 January 2014 15:34

    Body's own antibodies can cause leukemia

    rabbit-anti-elisa-targattAcute lymphoblastic leukemia is the most common form of blood cancer. Patients with leukemia in the body produced abnormal red blood cells. A research group from the UK to establish why some children do not respond to treatment of blood cancer .

    The immune system produces millions of different antibodies, but only has a limited amount of DNA that contain "instructions" for this. To generate huge variety of antibodies to protect the body, the DNA is mixed and the excess particles are removed . Particle removal genome likely is the cause resistance to treatment.

    Tools used to strengthen the body's resistance to infection, are also one of the reasons for the most common form of childhood leukemia, scientists say. Equipment for the production of millions of antibodies in the immune system can misfire, making the cells more susceptible to becoming cancerous. The findings are published in the journal Nature Genetics. Scientists at the Sanger Institute in Cambridgeshire and the Institute of Cancer Research in London mechanism used DNA shuffling to make antibodies capable of reducing the risk of developing cancer.

    In a study conducted on 57 children in E, the scientists compared the DNA of the healthy tissue of each child and the DNA of cancer of white blood cells. These data indicate that there are two phases of the disease. The first change occurred before birth, but the kids did not get ill from leukemia at once, and at the age of four to ten years there were further genetic changes caused by the same principle that immune cells use to produce antibodies. This knowledge leads to the fundamental understanding of the disease, but is unlikely to lead to new therapies.

    Experts say that the current therapies debilitating, many patients suffer relapses of cancer. The latest discovery really allow progress in understanding the actual biology, leading to blood cancer and its various forms. The resulting knowledge will develop in the future a more precise treatment, and increase the predictability of the results of the disease. Now nine out of ten sick children have good prospects of long-term survival, said Matt Kaiser, head of research at the children's charity the treatment of leukemia and lymphoma.

    1-trickyprotei

    This illustration shows how the envelope proteins covering the surface of an HIV virion (1, 2) bind to a host cell (3, 4). The trimeric MPER region of gp41 is shown in red and can be disabled by antibodies, shown in light blue

    Duke scientists have taken aim at what may be an Achilles' heel of the HIV virus.
    Combining expertise in biochemistry, immunology and advanced computation, researchers at Duke University have determined the structure of a key part of the HIV envelope protein, the gp41 membrane proximal external region (MPER), which previously eluded detailed structural description.
    The research will help focus HIV vaccine development efforts, which have tried for decades to slow the spread of a virus that currently infects more than 33 million people and has killed 30 million more. The team reported the findings online in the Jan. 13 early edition of Proceedings of the National Academy of Sciences.
    "One reason vaccine development is such a difficult problem is that HIV is exceptionally good at evading the immune system," said Bruce Donald, an author and professor in Duke's computer science and biochemistry departments. "The virus has all these devious strategies to hide from the immune system."
    One of those strategies is a dramatic structural transformation that the virus undergoes when it fuses to a host cell. The envelope protein complex is a structure that protrudes from HIV's membrane and carries out the infection of healthy host cells. Scientists have long targeted this complex for vaccine development, specifically its three copies of a protein called gp41 and closely associated partner protein gp120.
    The authors said they think about a particular region of gp41, called MPER, as an Achilles' heel of vulnerability.
    "The attractiveness of this region is that, number one, it is relatively conserved," said Leonard Spicer, senior author and a professor of biochemistry and radiology. In a virus as genetically variable as HIV, a successful vaccine must act on a region that will be conserved, or similar across subtypes of the virus.
    "Second, this region has two particular sequences of amino acids that code for the binding of important broadly neutralizing antibodies," said Spicer. The HIV envelope region near the virus membrane is the spot where some of the most effective antibodies found in HIV patients bind and disable the virus.

    trickyproteiWhen the virus fuses to a host cell, the HIV envelope protein transitions through at least three separate stages. Its pre- and post-fusion states are stable and have been well studied, but the intermediate step—when the protein actually makes contact with the host cell—is dynamic. The instability of this interaction has made it very difficult to visualize using traditional structure determination techniques, such as x-ray crystallography and nuclear magnetic resonance (NMR) spectroscopy.
    That's where Duke's interdisciplinary team stepped in, solving the structure using protein engineering, sophisticated NMR and software specifically designed to run on limited data.
    First author Patrick Reardon spent years engineering a protein that incorporated the HIV MPER, associated with a membrane and behaved just like gp41 in the tricky intermediate step, but was stable enough to study. Reardon, then a PhD student under Spicer, is now a Wiley postdoctoral fellow at the Environmental Molecular Sciences Laboratory, a scientific facility in the Department of Energy's Pacific Northwest National Laboratory.
    The result captured the shape of the three-parted MPER in its near-native state, but the protein needed to be more than structurally accurate—it had to bind the broadly neutralizing antibodies.
    "One of the most important aspects of the project was ensuring that this construct interacted with the desirable antibodies, and indeed, it did so strongly," Reardon said.
    The team validated the initial structure using an independent method of data analysis developed by Donald's lab, which showed alternate structures were not consistent with the data.
    "The software took advantage of sparse data in a clever way that gave us confidence about the computed structure," Donald said. It used advanced geometric algorithms to determine the structure of large, symmetric, or membrane-bound proteins—varieties that are very difficult to reconstruct from NMR data.
    Donald's lab has been perfecting the method for a nearly decade, and Donald said its application in this paper represents a culmination of that work, demonstrating how the two-pronged approach can illuminate the structure of complex protein systems.
    The next steps of this research have already begun. In December, Duke received a grant of up to $2.9 million from the Bill & Melinda Gates Foundation to fund the development of an HIV vaccine that will build on these findings.

    cervical-smear-test1Researchers have to develop a test with the aid of which will be able to determine the presence of cancer in the body, regardless of the type. Initially, the scientific team of Anderson Cancer Center at the University of Texas working on a quest to discover genetic mutation, which can be confirmed pancreatic cancer without the need for biopsy. The researchers found that cancer cells, like other healthy individual specific small particles known as exosomes, 1983, having "footprint" of the respective tumor.

    Exosomes are small bubbles that form in the cytoplasm and secreted by cells into the extracellular environment. They can be found in a study of various body fluids, such as blood plasma, cerebrospinal fluid, urine, saliva, breast milk even. Their size is in the range of the virus, they are larger than the low density lipoprotein (bad cholesterol molecule), but smaller than the red blood cells. Their diameter is between 30 and 100 nanometers.

    Exosomes carrying the proteins, RNA and lipids. Participate in the regulation of immune responses and are an important component of intercellular communication. Relatively recently it was found that the transferred microRNA and mRNA to specific target cells and in particular, that provide for horizontal transport of mRNA between the cells, i.e. they are carried out by means of differentiation of the cell recipient. It is believed that the nucleic acids are transferred, are involved in the epigenetic inheritance. There is evidence that protein exosomes to create favorable changes in tumor growth cell-around environment.

    Researchers from the University of Texas believes it can develop a test that decipher coded in the excuzemes. This can not only determine the presence of cancerous processes in the body, but he caught at the beginning of tumorigenesis, which will be of immense value in medical practice for early detection, diagnosis and treatment of patients.

    At this stage there is no such medical text with the help of which you can find out whether a person suffers from some kind of tumor. Medicine use multiple tests "recognize" one or another gene mutation, pointing respectively to one or another type of tumor and whether it is malignant or benign.

    To be diagnosed with a tumor disease, it is first necessary to determine if it exists, to reach it, if it is available, and finally there are always risks and costs of surgical interventions, said Dr. Raghu Kaluri team .

    According to him, the genetic analysis of exosomes will help to determine not only the presence of a tumor process in the organism, but also its identification without biopsy. Different types of cancer produce different chromosomal mutations explains it with the test will be possible to know whether the cancer, pancreatic or brain, for example.

    Such a tool will undoubtedly enhance the ability of physicians to detect cancer in its early stages and effectively treating oncological diseases are written in the Journal of Biological Chemistry. Still a lot of work on the development of the test, which is not an easy task, given that the very exosomes is still studied by science.

    Cholera bacteria 605Canadian and Australian researchers were able to identify the strain of cholera bacteria responsible for the pandemic that killed millions of people in the 19th century.

    Scientists have succeeded for the first time sequenced the genome of this pathogen . They were working on a well-preserved stretch of the gut of one of the victims of cholera and penetrated the secrets of bacteria that goes " killing " people today in the poorest countries on the planet . The discovery was considered significant because never before scientists were able to identify the first strains of the bacterium vibrio clolerae - pathogen that develops in the water.

    The bacterium responsible for cholera was long a mystery to scientists because they failed to analyze ancient samples noted Thursday. This pathogen is "hiding" in the intestines of the victims and never reaches the bones or teeth, which means that almost no remnants of the DNA of the bacteria.

    For the study, the researchers had access to a collection of human tissues that have been well preserved in the Museum of the History of Medicine in Philadelphia, founded in 1858, where a few years ago there was a cholera epidemic. DNA of bacteria was extracted from the intestine of a man who died of cholera in 1849

    Scientists have been able to establish that this strain of bacteria called classic, and the second, called El Tor have coexisted in people and in the water of estuaries for many centuries, potentially even for thousands of years before the advent of pandemics in the 19th century.

    The analysis helped the researchers to conclude that the first of the two types of strains was most likely responsible for five of the seven most deadly epidemics in the 19th century. Almost all hailing from the Bay of Bengal . The World Health Organisation considers that there are between 3 and 5 million new cases of cholera per year in the world , that is between 100 000 and 120 000 victims of the disease.

    Cholera causes severe diarrhea leading to severe dehydration and rapid death if not treated quickly. Discovery will help scientists new methods of treatment and even prevention of the disease.

    360w-molecular-marker-could-predict-tumor-progression--mouse-dr4-stem-cell-differentiation-neural-stem-cells-rat-models-gene-targeting-rosa26The U.S. Food and Drug Administration-approved drugs, gefitinib (Iressa) and erlotinib (Tarceva), are prescribed for lung and pancreatic cancer patients but only a few who have mutations in the EGFR gene usually benefit with a prolonged reduction of tumor size. The two drugs block the gene's ramped-up protein production, but patients' response to the drug varies widely -- from no survival benefit to several years. The average is several months.
    "Clinicians have had no reliable method for distinguishing patients who are not likely to respond to EGFR inhibitors and those who will respond very well," says David Sidransky, M.D., professor of otolaryngology, oncology, pathology, urology, and genetics at Johns Hopkins. Looking at the precise level of protein production from the EGFR gene alone in specific patients was not proven to be a good indicator of patients' response to EGFR-blocking drugs, but the presence or absence of Mig 6 might be, he adds.
    In a preliminary study, described July 31 in the online journal, PLoS ONE, the Johns Hopkins scientists found the genetic marker in a series of experiments that began with laboratory-derived lung and head and neck cancer cell lines resistant to EGFR-inhibitor drugs. In the cell lines, the team found very high levels of protein production from the Mig 6 gene -- up to three times the level in sensitive cell lines. Mig 6 is one of the molecules that controls the activity of the EGFR protein.
    "In the first set of experiments, we found that higher levels of Mig 6 occur often in cells that don't respond to EGFR inhibitors," says Sidransky. "Most tumors are known to have high Mig 6 levels and are not expected to respond to EGFR inhibitors."
    Next, the research team studied Mig 6 levels in a variety of tumors that were directly engrafted into mice, a research model known as a xenograft, and treated with an EGFR inhibitor. These new models contain a more complete sampling of the tumor that includes "stromal" cells, which surround and interact with the cancer cells. "These tumors are implanted along with their own microenvironment, into the mice, and we believe this model may be more predictive of what happens in human patients," says Sidransky.
    In the xenografts of tumors without EGFR mutations, as Mig 6 levels increased, so did the resistance to EGFR inhibitors, suggesting a correlation between high Mig 6 and lack of response to the drugs. To confirm the correlation, the scientists tested tissue samples of 65 lung cancer patients treated with EGFR inhibitors to compare their Mig 6 levels with outcomes.
    Of 18 patients with low Mig 6 levels, five of them survived more than a year without progression of their cancer; four survived more than two years progression-free. Among 16 patients with higher Mig 6 levels, two survived more than one year and none survived, progression-free, beyond two years.
    "The beauty of this finding is that it's simple. We're looking for tumors with low levels of Mig 6 to predict clinical benefit, and there aren't many of them," says Sidransky.
    Sidransky's team expects to license the Mig 6 marker to a biotechnology or pharmaceutical company and conduct further tests in larger groups of patients.

    Scientists have obtained the first detailed molecular structure of a member of the Tet family of enzymes.
    The finding is important for the field of epigenetics because Tet enzymes chemically modify DNA, changing signposts that tell the cell's machinery "this gene is shut off" into other signs that say "ready for a change."
    Tet enzymes' roles have come to light only in the last five years; they are needed for stem cells to maintain their multipotent state, and are involved in early embryonic and brain development and in cancer.
    The results, which could help scientists understand how Tet enzymes are regulated and look for drugs that manipulate them, are scheduled for publication in Nature.
    Researchers led by Xiaodong Cheng, PhD, determined the structure of a Tet family member from Naegleria gruberi by X-ray crystallography. The structure shows how the enzyme interacts with its target DNA, bending the double helix and flipping out the base that is to be modified.

    Epigenetics enigma resolved First structure of enzyme that removes methylation

    This is the structure of the Tet enzyme with DNA. Note the purple ball at the active site, close to which one DNA base is flipped out of the double helix. Also note the degree to which the double helix is bent. Credit: Xiaodong Cheng, Emory University

     

    "This base flipping mechanism is also used by other enzymes that modify and repair DNA, but we can see from the structure that the Tet family enzymes interact with the DNA in a distinct way," Cheng says.
    Cheng is professor of biochemistry at Emory University School of Medicine and a Georgia Research Alliance Eminent Scholar. The first author of the paper is research associate Hideharu Hashimoto, PhD. A team led by Yu Zheng, PhD, a senior research scientist at New England Biolabs, contributed to the paper by analyzing the enzymatic activity of Tet using liquid chromatography–mass spectrometry.
    Using oxygen, Tet enzymes change 5-methylcytosine into 5-hydroxymethylcytosine and other oxidized forms of methylcytosine. 5-methylcytosine (5-mC) and 5-hydroxymethylcytosine (5-hmC) are both epigenetic modifications of DNA, which change how DNA is regulated without altering the letters of the genetic code itself.
    5-mC is generally found on genes that are turned off or on repetitive regions of the genome. 5-mC helps shut off genes that aren't supposed to be turned on (depending on the cell type) and changes in 5-mC's distribution underpin a healthy cell's transformation into a cancer cell.
    In contrast to 5-mC, 5-hmC appears to be enriched on active genes, especially in brain cells. Having a Tet enzyme form 5-hmC seems to be a way for cells to erase or at least modify the "off" signal provided by 5-mC, although the functions of 5-hmC are an active topic of investigation, Cheng says.
    Alterations of the Tet enzymes have been found in forms of leukemia, so having information on the enzymes' molecular structure could help scientists design drugs that interfere with them.
    N. gruberi is a single-celled organism found in soil or fresh water that can take the form of an amoeba or a flagellate; its close relative N. fowleri can cause deadly brain infections. Cheng says his team chose to study the enzyme from Naegleria because it was smaller and simpler and thus easier to crystallize than mammalian forms of the enzyme, yet still resembles mammalian forms in protein sequence.
    Mammalian Tet enzymes appear to have an additional regulatory domain that the Naegleria forms do not; understanding how that domain works will be a new puzzle opened up by having the Naegleria structure, Cheng says.

    sugar beet and field

    A study published in Nature today describes the sugar beet reference genome sequence generated by researchers both from the Centre for Genomic Regulation (CRG), the Max Planck Institute for Molecular Genetics and the University of Bielefeld, in cooperation with other centres and plant breeders.
    Sugar beet accounts for nearly 30% of the world's annual sugar production, according to FAO, and provides a source for bioethanol and animal feed.
    The sugar beet genome sequence provides insights into how the genome has been shaped by artificial selection along time.
    What do foodstuff like muffins, bread or tomato sauce have in common? They all contain different amounts of white refined sugar. But, what perhaps may result amazing is that this sugar is probably sourced from a plant very similar to spinach or chard, but much sweeter: the sugar beet. In fact, this plant accounts for nearly 30% of the world's annual sugar production, according to the Food and Agriculture Organization for the United Nations (FAO). Not in vain for the last 200 years, has it been a crop plant in cultivation all around the world because of its powerful sweetener property.
    Now, a team of researchers from the Centre for Genomic Regulation (CRG) and the Max Planck Institute for Molecular Genetics (Berlin, Germany), lead by Heinz Himmelbauer, head of the Genomics Unit at the CRG in Barcelona, together with researchers from Bielefeld and further partners from academia and the private sector, have been able to sequence and analyse for the first time the sweet genes of beetroot. The results of the study, that will be published today in Nature, shed light on how the genome has been shaped by artificial selection.
    "Information held in the genome sequence will be useful for further characterization of genes involved in sugar production and identification of targets for breeding efforts. These data are key to improvements of the sugar beet crop with respect to yield and quality and towards its application as a sustainable energy crop," the authors suggest.
    Sugar beet is the first representative of a group of flowering plants called Caryophyllales, comprising 11,500 species, which has its genome sequenced. This group encompasses other plants of economic importance, like spinach or quinoa, as well as plants with an interesting biology, for instance carnivorous plants or desert plants.
    27,421 protein-coding genes were discovered within the genome of the beet, more than are encoded within the human genome. "Sugar beet has a lower number of genes encoding transcription factors than any flowering plant with already known genome," adds Bernd Weisshaar, a principle investigator from Bielefeld University who was involved in the study. The researchers speculate that beets may harbor so far unknown genes involved in transcriptional control, and gene interaction networks may have evolved differently in sugar beet compared to other species. The researchers also studied disease resistance genes (the equivalent to the immune system in animals) which can be identified based on protein-domains. These genes turned out as particularly plastic, with beet-specific gene family expansions and gene losses.
    Many sequencing projects nowadays targeted at the analysis of novel genomes also address the description of genetic variation within the species of interest. Commonly, "this is achieved by generating sequencing reads obtained from high-throughput sequencing technologies, followed by alignment of these reads against the reference genome to identify differences," explains Heinz Himmelbauer, a principle investigator of this study.
    The current work went one step further and generated genome assemblies from four additional sugar beet lines. This allowed the researchers to obtain a much better picture of intraspecific variation in sugar beet than would have been possible otherwise. In summary, 7 million variants were discovered throughout the genome. However, variation was not uniformly distributed: The authors found regions of high, but also of very low variation, "reflecting both the small population size from which the crop was established, as well as the human selection, which has shaped the plants' genomes. Additionally, gene numbers varied between different sugar beet cultivars, which contained up to 271 genes not shared with any of the other lines", as Juliane Dohm and André Minoche, two scientists involved in the study commented.
    The researchers also performed an evolutionary analysis of each sugar beet gene in order to put them into context with already known genes of other plants. This analysis allowed them to identify gene families that are expanded in sugar beet compared to other plants, but also families that are absent. Notably such gene families were most commonly associated with stress response or with disease resistance, added Toni Gabaldon, group leader in the CRG Bioinformatics and Genomics programme and ICREA research professor.
    Finally, the work also provides a first genome sequence of spinach, which is a close relative of sugar beet.
    Thanks to the sugar beet genome sequence made by the researchers and the associated resources generated, future studies on the molecular dissection of natural and artificial selection, gene regulation and gene-environment interaction, as well as biotechnological approaches to customize the crop to different uses in the production of sugar and other natural products, are expected to be held.
    "Sugar beet will be an important cornerstone of future genomic studies involving plants, due to its taxonomic position", the authors claim.

    131208133646-elisa-kits-assay-kitsHematology researchers at The Children's Hospital of Philadelphia have manipulated key biological events in adult blood cells to produce a form of hemoglobin normally absent after the newborn period. Because this fetal hemoglobin is unaffected by the genetic defect in sickle cell disease (SCD), the cell culture findings may open the door to a new therapy for the debilitating blood disorder.
    "Our study shows the power of a technique called forced chromatin looping in reprogramming gene expression in blood-forming cells," said hematology researcher Jeremy W. Rupon, M.D., Ph.D., of The Children's Hospital of Philadelphia. "If we can translate this approach to humans, we may enable new treatment options for patients."
    Rupon presented the team's findings today at a press conference during the annual meeting of the American Society of Hematology (ASH) in New Orleans. Rupon worked in collaboration with a former postdoctoral fellow, Wulan Deng, Ph.D., in the laboratory of Gerd Blobel, M.D., Ph.D.
    Hematologists have long sought to reactivate fetal hemoglobin as a treatment for children and adults with SCD, the painful, sometimes life-threatening genetic disorder that deforms red blood cells and disrupts normal circulation.
    In the normal course of development, a biological switch flips during the production of hemoglobin, the oxygen-carrying component of red blood cells. Regulatory elements in DNA shift the body from producing the fetal form of hemoglobin to producing the adult form instead. This transition occurs shortly after birth. When patients with SCD undergo this transition, their inherited gene mutation distorts adult hemoglobin, forcing red blood cells to assume a sickled shape.
    In the current study, Rupon and Blobel reprogrammed gene expression to reverse the biological switch, causing cells to resume producing fetal hemoglobin, which is not affected by the SCD mutation, and produces normally shaped red blood cells.
    The scientists built on previous work by Blobel's team showing that chromatin looping, a tightly regulated interaction between widely separated DNA sequences, drives gene transcription -- the conversion of DNA code into RNA messages to carry out biological processes.
    In the current study, the researchers used a specialized tool, a genetically engineered zinc finger (ZF) protein, which they custom-designed to latch onto a specific DNA site carrying the code for fetal hemoglobin. They attached the ZF to another protein that forced a chromatin loop to form. The loop then activated gene expression that produced embryonic hemoglobin in blood-forming cells from adult mice. The team obtained similar results in human adult red blood cells, forcing the cells to produce fetal hemoglobin.
    Rupon and Blobel will continue investigations aimed at moving their research toward clinical application. Rupon added that the approach may also prove useful in treating other diseases of hemoglobin, such as thalassemia.