SAN FRANCISCO April 16, 2011 Scientists at the Gladstone Institutes have identified networks of genes that play an important role in embryonic-heart development, advancing knowledge of how healthy hearts developand offering clues about how to combat a common birth defect known as congenital heart disease.
Congenital heart disease affects nearly 1 out of every 100 babies born worldwide and is the most common cause of death from a birth defect. In the disease, cells in the embryo often fail to get the right instructions while the heart is being formed. Many genes and proteins must be deployed at just the right time and in the right amounts for healthy heart formation to occur. Disruption of the correct dosage of proteins can lead to congenital heart defects.
One way cells control the amount of protein made from genes is through a recently discovered molecule called a microRNA. MicroRNAs are tiny strands of genetic material that do not encode the information to make enzymes and proteins, as most RNAs do. Instead, microRNAs inhibit other RNA molecules from producing protein. In recent years, scientists have discovered that each microRNA inhibits protein production from hundreds of RNAs, regulating almost every process in every cell of the body by fine-tuning the dosage of key proteins.
"MicroRNAs provide an extra layer of regulation that helps ensure that the correct amount of protein is made from a particular gene at the right time," said Isabelle King, a Gladstone scientist and an assistant professor of pediatrics at the University of California, San Francisco. Dr. King is the lead author on the study, the results of which were published in the April 17 issue of Developmental Cell. "In the fetal heart, subtle changes in gene dosage and timing can yield heart defects in children."
While microRNAs are powerful, it has been challenging to identify the hundred or more genes that each microRNA regulates. To overcome t
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| Contact: Mara Brazer mara@brazercommunications.com 415-305-6677 Gladstone Institutes Source:Eurekalert |
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