In New Zealand, researchers at the fruit science company HortResearch and the biotech company Genesis Research & Development Corporation Ltd. announced the public release of the world’s most extensive collection of kiwi fruit DNA sequences. The release comprises over 130,000 kiwi fruit gene sequences – referred to by scientists as expressed sequence tags (ESTs). These are DNA sequences from active genes in the plant – genes that govern such characteristics as flavour, colour, shape, vitamin content and aspects of fruit development such as ripening and shelf life.

HortResearch scientist Dr. William Laing says the kiwi fruit ESTs will be used by the company’s breeders to speed up development of new kiwi fruit varieties through Marker Assisted Selection (MAS) technique. In a MAS breeding programme, breeders use traditional crossing techniques to breed new varieties – which are then assessed for their commercial potential by searching their DNA for markers that indicate the presence of genes linked to desirable fruit traits, and ESTs are essential to identify the specific genes. Dr. Laing says it will help in breeding new commercial varieties that include some of the numerous health, flavour and colour characteristics found in wild kiwi fruit.

Source: www.sciencedaily.com

In Canada, Dr. Lawrence Rosenberg from the McGill University Health Centre together with Dr. Bernard Massie from the Centre hospitalier de l’Université de Montréal have shown in vitro that insulin-producing â-cells can return to a more primitive developmental state called stem-like cells. This process, known as “dedifferentiation”, highlights the plasticity of this cell type. This same result has also been validated for the three additional types of cells that, along with â-cells, make up the islets of Langerhans. These islet cells together produce insulin and the other hormones in the pancreas.

“At this stage, we can’t confirm whether the cells’ ability to turn into stem-like cells occurs naturally in a healthy pancreas, but the results are very encouraging for the development of regenerative therapies to fight diabetes,” Dr. Rosenberg said. The cells’ in-vitro plasticity opens up totally new paths of investigation into the underlying causes of diabetes, and will validate the development of innovative treatments.

This study is the latest in an extensive regenerative therapies research programme based on a peptide called Islet Neogenesis Associated Protein or INGAP. Dr. Rosenberg and his colleagues had demonstrated INGAP’s potential to induce new islet formation in the pancreas. Clinical trials with INGAP have already showed that it is possible to regrow new functional insulin-producing cells in diabetic patients. “We know that the peptide works, but we are still lacking certain theoretical bases to explain its mechanism,” said Dr. Rosenberg. “This finding will allow us to move ahead on firmer ground.”

Source: www.sciencedaily.com

Scientists are collecting vast amounts of diverse genomic data with ever-increasing speed, but effective ways to visualize these data in an integrated manner have lagged behind the ability to generate them. To address this growing need, researchers at the Broad Institute, the United Sates, have developed the Integrative Genomics Viewer (IGV), a freely available visualization tool that helps users simultaneously integrate and analyse different types of genomic data, and gives them the flexibility to zoom in on a specific genomic region of interest or to pan out for a broad, whole-genome view.

“This new tool offers a Google Maps-like view of integrative genomic data,” said Ms. Jill Mesirov, Chief Informatics Officer and Director of Computational Biology and Bioinformatics at the Broad Institute. With IGV, researchers can choose a Google Maps-like “street view” of the As, Cs, Ts and Gs that make up the genome, but they can also simultaneously visualize additional layers of complex information about gene expression as well as sequence alterations, or mutations, in the genetic code. Other genomic details, such as copy number variation, chromatin immunoprecipitation data, and epigenetic modifications, can also be viewed in IGV.

Moreover, all these data types can be overlaid or superimposed to determine how changes at one level will affect another. Users can choose from a variety of display options, viewing their data as a heat map, histogram, scatter plot, or other formats of their choice. IGV is free and available to researchers via the Web. It promises to increase the flow of discovery in many areas of biomedical research.

Source: www.physorg.com

In Germany, scientists at the Helmholtz Zentrum München (HZM), together with colleagues from the Department of Dermatology and Allergy and the Centre for Allergy and Environment of the Technische Universität München (TUM), have pinpointed a major gene for allergic diseases. The gene was localized using cutting edge technologies for examining the whole human genome at HZM.

The newly discovered FCER1A gene encodes the alpha chain of high-affinity IgE receptor, which plays a major role in controlling allergic responses. The team of scientists led by Dr. Stephan Weidinger from TUM and Dr. Thomas Illig from HZM found that certain variations of the FCER1A gene decisively influence the production of immunoglobulin E (IgE) antibodies. IgE antibodies are normally used to protect against parasites, but in some environments elevated IgE levels are associated with allergic disorders.

In genetically susceptible individuals, the immune system becomes biased and produces IgE antibodies against harmless agents such as pollen, dust mites or animal hair. These IgE antibodies then work in conjunction with certain cells to get rid of the allergens, a process that gives rise to the symptoms of allergy such as allergic rhinitis (hay fever), atopic dermatitis or asthma. The researchers examined the genomes of more than 10,000 adults and children from across Germany to detect the genetic factors. Although research is in its early stages, the new knowledge on the regulation of IgE production does have the potential to guide the development of new drugs.

Source: www.eurekalert.org

Researchers from the United States, Italy and Belgium have found a gene that causes most inherited forms of neuroblastoma, a rare and deadly form of childhood cancer, and say the discovery points to new treatments. Mutations in a gene called ALK were strongly linked to neuroblastoma, the researchers reported. The disease causes 15 per cent of childhood cancer deaths, with just a 40 per cent survival rate.

“This discovery enables us to offer the first genetic tests to families affected by the inherited form of this disease,” said Dr. Yael Mosse of The Children’s Hospital of Philadelphia, who worked on the study. “Furthermore, because there already are drugs in development that target the same gene in adult cancers, we can soon begin testing those drugs in children with neuroblastoma.”

The researchers studied 20 families with children having neuroblastoma. They found mutations in the ALK gene that cause it to be constantly active in helping cells proliferate. After finding the ALK mutations in familial neuroblastoma, they looked at sporadic cases – those not occurring in families with a history of the disease. They found ALK mutations in 12 per cent of 194 tumour cases of children with the aggressive, high-risk form of the disease.

                     
Source: www.reuters.com

Scientists from the Structural Genomics Consortium (SGC), a non-profit international organization, have determined the 3-D structure of a key protein component, which is involved in enabling the epigenetic code to be copied accurately from cell to cell. Epigenetic code is a series of chemical switches that is added onto the DNA in order to ensure that the body cells can form different tissue types, such as liver and skin tissues, despite having identical DNA genetic code.

The importance of the nuclear protein UHRF1 in the copying of epigenetic code has been earlier established. The scientists believe that when the code is copied, UHRF1 ensures the accuracy of the process, like a proof-reader checks a typeset article before printing. The key element of UHRF1 involved in this “proofreading” process is known as the Set and Ring Associated (SRA) domain, but the exact mechanisms by which the SRA domain accomplishes this task were unclear.

Now, the structure of the key element of UHRF1 that facilitates this process has been revealed, thanks to SGC, by three studies. SGC, in keeping with its policy of making its data immediately and freely available, made the underlying information available in the Protein Data Bank in 2008. The availability of this information allowed the other groups to make more rapid progress in their own work. One of the studies is by a research team led by Professor Masahiro Shirakawa from Kyoto University, Japan, who openly acknowledged that the SGC data was crucial to his team’s study.

Source: www.eurekalert.com

Simultaneous expression of certain versions of KIR3DL1 and HLA-B*57 genes – which has been linked with a reduced risk of HIV progressing to AIDS – also lowers the risk of HIV infection in exposed uninfected individuals, according to a group of researchers from Research Institute of the McGill University Health Centre and University of Montreal Hospital Centre, Canada.

The strongest protection from disease progression in KIR3DL1 homozygotes (3DL1 hmz) is the co-expression of HLA-B*57 and a set of KIR3DL1 genotypes (3DL1*h/*y) lacking low-expressing allotypes on natural killer cells. The scientists evaluated whether this allele combination could also influence resistance to infection. The genetic distribution of 3DL1*h/*y and HLA-B*57 was compared in 41 HIV-exposed uninfected and 186 HIV-infected KIR3DL1 homozygotes. It was found that 12.2 per cent HIV-exposed uninfected people and 4.3 per cent of individuals in the primary infection cohort expressed HLA-B*57. The percentage of 3DL1*h/*y carriers were similar in both cases. The 3DL1*h/*y-HLAB *57 combined genotype was more frequent in exposed uninfected individuals (12.2 per cent) than those with primary infection (2.7 per cent). It was thus concluded that the co-expression of 3DL1*h/*y and HLA-B*57 helps to lower the risk of developing HIV when exposed to the virus.

Source: www.genengnews.com