Type 1 diabetes, rheumatoid arthritis, and cancer are just some of the disorders associated with specific genes not “turning on” and “turning off” as they should. By using new CRISPR/Cas9 genome editing technology, in a recent paper in Nature Communications, McGill University researchers have described a new technique that scientists across the world can potentially use to explore novel ways of treating diseases associated with dysregulation in DNA methylation.
By Cynthia Lee
Newsroom
Chronic pain may reprogram the way genes work in the immune system, according to a new study by McGill University researchers published in the journal Scientific Reports.
Until now scientists have believed that the variations in traits such as our height, skin colour, tendency to gain weight or not, intelligence, tendency to develop certain diseases, etc., all of them traits that exist along a continuum, were a result of both genetic and environmental factors. But they didn’t know how exactly these things worked together. By studying ants, McGill researchers have identified a key mechanism by which environmental (or epigenetic) factors influence the expression of all of these traits, (along with many more).
Early life experience results in a broad change in the way our DNA is “epigenetically” chemically marked in the brain by a coat of small chemicals called methyl groups, according to researchers at McGill University. A group of researchers led by Prof. Moshe Szyf, a professor of Pharmacology and Therapeutics in the Faculty of Medicine, and research scientists at the Douglas Institute have discovered a remarkable similarity in the way the DNA in human brains and the DNA in animal brains respond to early life adversity. The finding suggests an evolutionary conserved mechanism of response to early life adversity affecting a large number of genes in the genome.