Science Today

In order to create proteins, the protein-coding gene must be transcribed into RNA and in the so-called splicing process shortened to the correct template. Scientists at the Helmholtz Zentrum München and Munich's Technical University have now discovered how the U2AF protein enables this process. The results have been published in the current edition of the journal Nature. Scientists at the Helmholtz Zentrum München and the Technical University of Munich (TUM) along with their colleagues from the European Molecular Biology Laboratory (EMBL) in Heidelberg and the Centre for Genomic Regulation in Barcelona have discovered how the U2AF protein enables the pre-mRNA to be spliced to form the mRNA, which serves as a template for protein synthesis in the body. Splicing requires the cooperation of different proteins, i.e. splicing factors. One such splicing factor, U2AF, was examined by the Munich scientists. It consists of two structural modules and binds to the RNA near the intron-exon ...

A difficult-to-treat form of childhood leukemia relies on changes in the structure of DNA -- so-called epigenetic changes -- to wreak genomic havoc within white blood cells, according to one of two studies conducted by a research team at Children's Hospital Boston and Dana-Farber Cancer Institute. Together with collaborators from a biotechnology company, the same team also showed that a new drug that blocks these changes could deactivate cancer-promoting genes and halt the growth of this cancer. These studies, reported in a pair of papers in the July 11, 2011 issue of Cancer Cell, are the first to therapeutically target a core epigenetic vulnerability in the subgroup of leukemias caused by a "reshuffling" or rearrangement of the mixed lineage leukemia (MLL) gene. "We have known for a while that MLL leukemias arise from widespread alterations not in the genetic code itself, but in the structure of the DNA and the proteins associated with it," according to Scott ...

Using the latest gene sequencing tools to examine so-called epigenetic influences on the DNA makeup of colon cancer, a Johns Hopkins team says its results suggest cancer treatment might eventually be more tolerable and successful if therapies could focus on helping cancer cells get back to normal in addition to strategies for killing them. In a report published June 26 in Nature Genetics, the investigators focused on a particular epigenetic biochemical signature known as methylation, which silences genes. Although not part of a gene's central DNA sequence, it is copied when a cell divides, perpetuating its activity. By comparing the epigenomes of eight human tissue samples -- three from noncancerous colon tissue, three from colon tumors and two from polyps (early-stage colon cancer) -- the team found that in all the colon tumors the defining characteristic was a universally "chaotic" pattern of methylation. In noncancerous tissue, they found methylation occurring in wel...