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Archive - Mar 21, 2011

Exotic Kingfisher on Verge of Extinction

The Tuamotu kingfisher is a multicolored, tropical bird with bright blue feathers, a dusty orange head, and a bright green back. The entire population of these birds – fewer than 125 – lives on one tiny island in the south Pacific, and without serious intervention, they will soon no longer exist. One University of Missouri researcher is trying to stop the birds' extinction by working with farmers and residents on the island inhabited by the kingfishers. "If we lose these birds, we lose 50,000 years of uniqueness and evolution," said Dr. Dylan Kesler, assistant professor in fisheries and wildlife at the University of Missouri's School of Natural Resources in the College of Agriculture, Food and Natural Resources. "Because it has lived in isolation for a very long time, it's unlike any other bird. There is no other bird like this on the planet." In new studies published in the journal The Auk (published by the American Ornithologists Union) and the Journal of Wildlife Management, Dr. Kesler and his team of researchers have uncovered important information to help ensure the birds' survival and a unique way to attach radio transmitters to the birds to track them. To survive, the kingfishers need several specific habitat characteristics: (1) Hunting Perches about 5 feet off the ground – The birds hunt by "pouncing." They watch their prey and then fall on them from hunting perches about 5 feet high. Without the perches in broadleaf trees at the appropriate height, the birds have no way to hunt. (2) Exposed ground – the birds' food consists mainly of lizards, which are easier to spot where the ground is clear of vegetation. When coconut farmers conduct intermediate burns on their land – which are hot enough to kill brush, but do not lead to widespread fires or kill the lizards – it exposes more ground and the birds can see the lizards.

Jumping Gene Used in New Method to Study Gene Regulation

Scientists at the European Molecular Biology Laboratory (EMBL) in Heidelberg, Germany, have developed a new method for studying gene regulation, by employing a jumping gene as an informant. Described online on March 21, 2011, in Nature Genetics, the new method is called GROMIT. It enables researchers to systematically explore the very large part of our genome that does not code for proteins, and which likely plays a large role in making each of us unique, by controlling when, where, and to what extent genes are expressed. Thanks to GROMIT, scientists can also create mouse models for human diseases such as Down syndrome. "Our findings change how we think about gene regulation, and about how differences between individual genomes could lead to disease," said Dr. François Spitz from EMBL, who led the study. Until now, scientists thought that regulatory elements essentially controlled a specific gene or group of genes. With GROMIT, Spitz and colleagues discovered that the genome is not organized in such a gene-centric manner. Instead, it appears that each regulatory element can potentially control whatever is within its reach. This means that mutations that simply shuffle genetic elements around (without deleting or altering them) can have striking effects, by bringing genes into or out of specific regulators' zones of influence. The EMBL scientists also discovered that many of these regulatory elements act in specific tissues, which suggests that the expression levels of every gene, even those that are active all over the body, are fine-tuned at the tissue level. Jumping genes – or transposons – are sequences of DNA that can move from place to place within a cell's genome. This can have detrimental effects, for example if this extra genetic material is inserted into an important gene, disrupting it. But Dr.

LincRNA Plays Key Role in Determining Cell Identity

If some of your brain cells suddenly decided to become fat cells, it could cloud your decision-making capacity. Fortunately, early in an organism's development, cells make firm and more-or-less permanent decisions about whether they will live their lives as, say, skin cells, brain cells, or fat cells. These decisions essentially boil down to which proteins, among all the possible candidates encoded in a cell's genes, the cell will tend to make under ordinary circumstances. But exactly how a cell chooses its default protein selections from an overwhelmingly diverse genetic menu is somewhat mysterious. A new study from the Stanford University School of Medicine and collaborating institutions may help solve the mystery. The researchers discovered how a particular variety of the biomolecule RNA that had been thought to be largely irrelevant to cellular processes plays a dynamic regulatory role in protein selection. In unraveling this molecular mechanism, the study also offers enticing clues as to how certain cancers may arise. Dr. Howard Chang, associate professor of dermatology at Stanford, is the senior author of the study, published online on March 20, 2011, in Nature. "All the cells in your body have the same genes, but they don't all make the same proteins," said Dr. Chang, who is also a Howard Hughes Medical Institute Early Career Scientist. In this new study, Dr. Chang and his colleagues identified a novel action by a subset of RNA that reinforces cells' decisions about which combinations of their genes are to be active and which must stay silent. RNA, according to older textbooks, mainly functions as a messenger: a copy of a gene, made by a cell's gene-reading machinery, that can float away from the chromosomes where genes reside to other places in the cell where proteins are made.