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Tuesday, September 29, 2015

Benyam Kinde: Gene Expression and Rett Syndrome

From Science News
Vol. 188, No. 7, October 3, 2015, p. 22

By Sarah Schwartz
September 22, 2015

Medical student explores how gene expression molds higher brain function. 

Benyam Kinde, 27
Many people view the brain as the last frontier of human health research, says Benyam Kinde.

“We still don’t know very much about how individual cells in the brain coordinate the activity of higher-level function that defines us as humans,” he says.

This mystery is one that Kinde, an M.D. and Ph.D. student at Harvard Medical School and MIT, aims to solve. He is interested in how chemical modifications of DNA affect brain function, focusing on a protein nicknamed MeCP2. When this protein is damaged or missing, it changes the activity of multiple genes and causes Rett Syndrome, a disorder marked by developmental delays, seizures and autism-like behaviors.


When MeCP2 grabs onto DNA, it can limit the activity of genes to which it attaches. Kinde, along with former postdoctoral researcher Harrison Gabel and colleagues, went looking for common features in genes controlled by MeCP2 and those altered by the protein’s absence.

In June, the researchers reported that MeCP2 prefers to attach to a specific cluster of DNA and chemicals found mainly in the brain. The genes that MeCP2 normally turns down are longer than average, and are most active in brain cells. In Rett Syndrome, when MeCP2 is reduced, these long genes are overactive.

Kinde and his colleagues found that a chemical that disables DNA-winding proteins can quiet such overactive genes. These insights could help researchers design treatments for Rett Syndrome and similar developmental and autism spectrum disorders. The work appeared in Nature and the Proceedings of the National Academy of Sciences.



RETTS REVELATION: Benyam Kinde and his colleague
Harrison Gabel talk about their recent finding about
the role of mutated MeCP2 in Rett Syndrome.

Like his brother Isaac, Kinde says he became fascinated with biology while watching his veterinarian father figure out why a horse or an elephant had died. “I was really interested in the investigative nature of his work,” Kinde says. As a Meyerhoff Scholar at the University of Maryland, Baltimore County, Kinde got his first experience with neuroscience research and became passionate about solving medical mysteries.


He credits excellent mentors, including his research advisers, Gabel and his older brother for his achievements so far. Kinde hopes to tackle neurobiology questions in the clinic and the lab. There’s a still lot to learn about how the brain develops, he says.

Citations

H.W. Gabel et al. Disruption of DNA-methylation-dependent long gene repression in Rett syndrome. Nature.Vol. 522, June 4, 2015. doi: 10.1038/nature14319.

B. Kinde et al. Reading the unique DNA methylation landscape of the brain: Non-CpG methylation, hydroxymethylation, and MeCP2. Proceedings of the National Academy of Sciences. Vol. 122, June 2, 2015. doi: 10.1073/pnas.1411269112.

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