May 9, 2013, New York, NY and San Diego, CA A large, multi-institutional research team involved in the NIH Epigenome Roadmap Project has published a sweeping analysis in the current issue of the journal Cell of how genes are turned on and off to direct early human development. Led by Bing Ren of the Ludwig Institute for Cancer Research, Joseph Ecker of The Salk Institute for Biological Studies and James Thomson of the Morgridge Institute for Research, the scientists also describe novel genetic phenomena likely to play a pivotal role not only in the genesis of the embryo, but that of cancer as well. Their publicly available data, the result of more than four years of experimentation and analysis, will contribute significantly to virtually every subfield of the biomedical sciences.
After an egg has been fertilized, it divides repeatedly to give rise to every cell in the human bodyfrom the patrolling immune cell to the pulsing neuron. Each functionally distinct generation of cells subsequently differentiates itself from its predecessors in the developing embryo by expressing only a selection of its full complement of genes, while actively suppressing others. "By applying large-scale genomics technologies," explains Bing Ren, PhD, Ludwig Institute member and a professor in the Department of Cellular and Molecular Medicine at the UC San Diego School of Medicine, "we could explore how genes across the genome are turned on and off as embryonic cells and their descendant lineages choose their fates, determining which parts of the body they would generate."
One way cells regulate their genes is by DNA methylation, in which a molecule known as a methyl group is tacked onto cytosineone of the four DNA bases that write the genetic code. Another is through scores of unique chemical modifications to proteins known as histones, which form the scaffolding around which DNA winds in the nucleus of the cell. One such silencing modification, called H3K2
|Contact: Rachel Steinhardt|
Ludwig Institute for Cancer Research