Genetic 'brakes' could halt disease

A team of scientists has identified 'genetic brakes' that could potentially slow or halt diseases such as multiple sclerosis and cancer. Scientists from University of Edinburgh's Roslin Institute found that hundreds of genes interact with each other to control how cells behave in the body, including potentially the cells that are involved in the development of these conditions. The study was published in the journal Nature Genetics.

It was previously believed that gene activity was controlled by a limited selection of 'master' or regulator genes. But this research showed that there are hundreds of these types of genes all interacting in many ways. The scientists believe that variation in these networks may explain why people develop diseases in different ways.

Professor David Hume, who led the research, said: 'This study has effectively shown us where the brakes are which could slow down or stop diseases like cancer and multiple sclerosis. We believe this could lead to treatments and cures for many diseases of the immune system'.

The study is part of a larger investigation called FANTOM4, which is studying the properties and role of particular elements of DNA. Repetitive elements make up between 30 and 50 per cent of mammalian DNA, and whilst most do not appear to have a role in the cell, in some cases they are involved in switching on gene expression. The researchers are particularly interested in the activity of elements called retrotransposons because they are found in a broad range of cells, and when they are inserted incorrectly into genes they can cause mutations that lead to changes in gene expression and subsequent disease.

The scientists examined mice and human tissue to investigate whether the regions of DNA where gene expression starts, transcription start sites (TSS), were located within retrotransposons. To do this the scientists used a technology called Cap Analysis Gene Expression (CAGE), which marks the genome at the locations where transcription begins. They found that 18 per cent of human TSS and 31 per cent of mice TSS were located within retrotransposons. They also found that the expression varied across tissue type.