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Archive - Apr 25, 2013 - Story


New Findings Challenge Traditional View of Transcription

Like musicians in an orchestra who have the same musical score but start and finish playing at different intervals, cells with the same genes start and finish transcribing them at different points in the genome. For the first time, researchers at the European Molecular Biology Laboratory (EMBL) have described the striking diversity of messenger RNAs (mRNAs) that such start and end variation produces, even from the simple genome of yeast cells. Their findings, published online on April 24, 2013 in Nature, shed new light on the importance of mRNA boundaries in determining the functional potential of genes. Hundreds of thousands of unique mRNA transcripts are generated from a genome of only about 8,000 genes, even with the same genome sequence and environmental condition. “We knew that transcription could lead to a certain amount of diversity, but we were not expecting it to be so vast,” explains Dr. Lars Steinmetz, who led the project. “Based on this diversity, we would expect that no yeast cell has the same set of messenger RNA molecules as its neighbor.” The traditional understanding of transcription was that mRNA boundaries were relatively fixed. While it has long been known that certain parts of mRNAs can be selectively “spliced” out, this phenomenon is very rare in baker's yeast, meaning that the textbook one gene - one mRNA transcript relationship should hold. Recent studies have suggested that things aren't quite that simple, inspiring the EMBL scientists to create a new technique to capture both the start and end points of single mRNA molecules. They have now discovered that each gene can be transcribed into dozens or even hundreds of unique mRNA molecules, each with different boundaries. This suggests that not only transcript abundance, but also transcript boundaries, should be considered when assessing gene function.

International Study Finds 14 New Genetic Links to Juvenile Arthritis

Researchers report in Nature Genetics that they have increased the number of confirmed genes linked to juvenile idiopathic arthritis (JIA) from 3 to 17 – a finding that will clarify how JIA fits into the spectrum of autoimmune disorders and help identify potential treatment targets. Published online on April 21, 2013, the study involves an international research team that analyzed 2,816 JIA cases recruited from more than 40 pediatric rheumatology clinics. It was the largest collaborative patient population of JIA to date, including patient DNA samples from across the United States, Germany, and the United Kingdom, according to Susan Thompson, Ph.D., a researcher in the Division of Rheumatology at Cincinnati Children's Hospital Medical Center who was a leader for the study. "These findings will help us understand how the long suspected genetic contributions to JIA are driving the disease process, with the ultimate goal being earlier and improved diagnosis and treatment," Dr. Thompson said. JIA is the most common rheumatic disease of childhood that involves several different but related forms. Affecting some 50,000 children in the US, the actual cause of the disease remains unknown. JIA is considered an autoimmune disorder, in which the body's immune system mounts an attack against its own healthy tissues. JIA can be treated with medications and physical therapy, but the disease can persist for many patients into adulthood. Prior to the current study only three genes were associated with known JIA risk, although scientists have suspected the likelihood that more genes are involved. The research team used what is known as the Immunochip array to measure variation in the genes (DNA) coding for components of the immune system for 2,816 JIA patients in the study.