Using data from blood and brain tissue, a team led by researchers at Johns Hopkins Bloomberg School of Public Health found that they could gain insights into mechanisms that might help explain autism by analyzing the interplay between genes and chemical tags that control whether genes are used to make a protein, called epigenetic marks.
The findings, were published Oct. 24 in Nature Communications, could ultimately help lead to new ways of treating and preventing the disorder.
Researchers have long known that chemical modifications, a collection of “marks” on DNA known as the epigenome, play a key role in how cells operate by guiding differences between various tissue types in a given individual’s body, despite the fact that they all carry the same genetic code.
“The reason a brain cell is different from a heart cell is because of the epigenome, which affects which parts of a cell’s DNA are read,” says study lead Dr. M. Daniele Fallin, chair of the Bloomberg School’s Department of Mental Health and director of the School’s Wendy Klag Center for Autism and Developmental Disabilities. “Think of it like an encyclopedia with a bunch of tabs. Cells don’t need to read the entire encyclopedia; they jump to the tabs they need to get things done.”