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Study implicates new epigenetic player in mental retardation and facial birth defects
Date:7/12/2010

the scientific literature, Qi and his collaborators, Madathia Sarkissian and Thomas Roberts at Dana-Farber Cancer Institute, tested the normal enzyme function in zebrafish, a popular model for genetic function.

It is hard to judge cognitive impairment in a small fish, but the dramatic impact on craniofacial development was obvious. Fish without the enzyme developed virtually no jawbone, a condition that could be prevented by providing the functioning enzyme, showing its importance in development. As importantly, providing more of the fish version of the MSX1 gene (whose activity the demethylase enzyme encourages) also partially prevented the biological defects caused by the missing enzyme.

Hope for the reversibility of some aspects of mental retardation arose three years ago in a Scottish mouse study of Rett syndrome, a disorder on the autism spectrum that is also a cause of severe mental retardation in girls. The disease is caused by a molecule, MeCP2, that binds to methylated DNA and may be involved in another form of epigenetic regulation.

"In practical terms, we use gene expression as a read out," says Shi, also a professor of pathology at Harvard Medical School. "Epigenetic states affect the expression of critical genes. These studies suggest that the imbalance of histone methylation dynamics plays a critical role in mental retardation. You can imagine a therapeutic approach to enhance the compromised enzymatic activity or to restore the downstream function."


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Contact: Erin McColgan
erin.mccolgan@childrens.harvard.edu
617-919-3110
Children's Hospital Boston
Source:Eurekalert

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