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Cleft Palate in Fetal Mice Prevented by Treating

s unthinkable when he first began his work. "This is a great example of expectations changing as technology evolves," he said.

For this study, co-author and postdoctoral scholar Karen Liu, PhD, used a short amino-acid tag to disrupt the function of a protein called GSK-3 beta. GSK-3 beta function is important in a variety of biological processes, and mice with the tagged protein exhibited many problems in utero, including cleft palates and sternum defects. However, Liu was able to reverse the defects by injecting the pregnant mice with rapamycin-a small molecule that stabilized the tag and restored the protein's function.

In addition to revealing for the first time that GSK-3 beta is important in palate formation, Liu discovered that the technique could be used to identify the specific times during development that the protein's function is required. For example, maternal rapamycin treatment between embryonic days 13.5 and 15 corrected the palate defect, but normal sternal development required functional protein between days 15.5 and 17. It's likely that the same chemical genetic approach could be applied to a variety of proteins and developmental processes to create a series of molecular snapshots of embryogenesis.

"The beauty of the technique is that it nails down the developmental window for various embryonic events," said Longaker. "We don't need to treat the mother long term, but just during the time that the organ or structure is forming."

Although promising, direct human applications of the research will require several key advances: an ability to predict which women are likely to have fetuses with birth defects before the defects occur; knowledge of an effective, small-molecule based therapy that can prevent the defect; and an accurate method of tracking fetal development to allow time-appropriate administration of the therapy.

"Over time, I expect we will have the ability to overcome these obstacle
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