One Step Closer to Diabetes Cure?
Scientists identified a master regulator gene for embryonic development of the pancreas, putting researchers closer to a possible cure for type1 diabetes. The disease occurs when the immune system attacks insulin producing beta cells in the pancreas, usually destroying them beyond repair before the illness is diagnosed.
Besides having important implications in diabetes research, the study offers new insights into congenital birth defects involving the pancreas and biliary system by demonstrating that both organs share a common cellular ancestry in the early mouse embryo.
The pancreas regulates digestion and blood sugar, and the biliary system is vital for digestion. Failure of the organs to form properly during fetal development can be fatal.
The study reports that one gene, Sox17, which controls which genes are turned on or off in a cell, is the key regulator for instructing cells in early mouse embryos to become either a pancreatic cell or part of the biliary system.
Jason Spence, Ph.D., and James Wells, Ph.D., both of the Division of Developmental Biology at Cincinnati Children’s Hospital Medical Center, authored the paper. “We show that Sox17 acts like a toggle switch that sets off a cascade of genetic events,” Dr. Wells is quoted as saying. “In normal embryonic development, when you have an undecided cell, if Sox17 goes one way the cell becomes part of the biliary system. If it goes the other way, the cell becomes part of the pancreas.”
“With this study showing us that turning one gene on or off in a mouse embryo instructs a cell to become pancreatic or biliary, now we’ll see if that same gene, Sox17, can be used to direct an embryonic stem cell to become a biliary cell instead of a pancreatic cell. This might be used one day to replace a diseased pancreas or bile duct in people,” said Dr. Wells.
Dr. Wells and his colleagues are also using data from the current study to conduct experiments that should reveal what other genes are turned on or off along the molecular cascade set into motion by Sox17. “Although Sox17 is the master switch, it triggers a molecular cascade of switches,” Dr. Wells explained, “and a defect in any of those can cause the whole thing to go wrong, resulting in congenital defects of the pancreas and biliary system.”
SOURCE: Developmental Cell, July 21, 2009