Looking at the Aging Genes Under New Light

A team of scientists at Salk Institute (California, USA) has recently published their research highlighting that the genetic mutations underlying Werner syndrome, a disorder that leads to premature aging and death, results in the deterioration of bundles of DNA known as heterochromatin. Specifically, deletion of the WRN gene was found to lead to heterochromatin disorganization, suggesting an important role for the WRN protein in maintaining heterochromatin. The researchers further showed that the protein interacts directly with molecular structures known to stabilize heterochromatin.   The study authors submit that: “Our observations uncover a role for [the RecQ helicase-like gene] in maintaining heterochromatin stability and highlight heterochromatin disorganization as a potential determinant of human aging.”

Werner Syndrome is a genetic disorder of premature aging, characterized by genetic mutations thought to be caused by the RecQ helicase-like gene (also known as the WRN gene), which generates the WRN protein. Previous studies suggest that the normal form of the protein is an enzyme that maintains the structure and integrity of a person's DNA. When the protein is mutated in Werner syndrome it disrupts the replication and repair of DNA and the expression of genes, but scientists did not understand how the mutated WRN protein disrupted these critical cellular processes.

Now it’s a question of finding out why WRN protein mutation happens and how to stop it, cracking this code can mean a revolutionary advance in understanding and stopping aging processes.