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The epigenome is a collection of physical “amendments” to DNA—things like proteins around which the double helix is wrapped like thread on a spool and chemical tags on the DNA of specific genes that can make them hard to access. This collection of epigenetic factors works together to help give each cell in the body its specific identity by regulating which genes are expressed—it’s a big reason why skin cells don’t get confused with blood cells and why bone cells are full of calcium instead of fat. The epigenome guides differentiation, the process by which embryonic stem cells (ESCs) go from being pluripotent—having the ability to turn into almost any cell type in the body—to taking on one specific identity. But in order for differentiation to happen, the products of a handful of pluripotency genes, which work to maintain the pre-differentiated state of a cell, must be overcome.

For the past seven years, software engineering manager Tom Green has guided the development and maintenance of software tools that support the Genetic Perturbation Platform at the ӳý, where he can be found working with a team of software engineers or consulting with scientists conducting experimental screens. Two decades ago, however, Green was living without electricity or running water in the jungles of Nicaragua, a houseguest of locals in the remote village of Karawala on the Caribbean coast, doing a very different kind of research.

In published online last week in Nature Genetics, a team led by ӳý visiting scientist Paul de Bakker of University Medical Center Utrecht fine mapped the major histocompatibility complex (MHC) – a linked set of genetic loci known to influence the development of celiac disease. The team’s approach turned up five new associated genetic variants that together account for roughly 18% of the genetic risk for the disease. Combined with previously identified risk factors, these genetic loci can now explain up to 48% of celiac disease heritability.