Perhaps the most baffling observation about our parents’ IGF2 genes is that they have identical DNA sequences, despite one being switched off. Closer inspection has revealed that there are subtle differences beyond the DNA sequences of silent and active genes. They differ in the way that nearby DNA is methylated. This affects which proteins can bind to the DNA and activate genes. Mum’s IGF2 gene (not methylated) is silenced by a repressor protein that binds to DNA. Dad’s chromosome is methylated near the IGF2 gene, which stops the repressor from binding and turning off Dad’s copy. Methyl is a very simple molecule involved in many biological processes. Adrian Bird (University of Edinburgh, UK) and other scientists recognise the importance of this tiny collection of atoms in silencing DNA.

However, silent genes are not a simple matter. There are a variety of means by which the volume knobs of our DNA might be twiddled. Considerable cross-talk occurs between three main players in silencing: DNA methylation, nucleosomes and RNA (see What Neil says). These epigenetic features facilitate a dialogue between the environment and our genetic hard-wiring. The extent to which epigenetic features are heritable is not yet clear, but we are getting a clearer picture of how they are set up. Taking DNA methylation as an example, such décor can result from what your mother ate when she was pregnant.  Experiments with agouti mice have shown that feeding methyl-supplements to pregnant mothers can affect the volume settings of genes in their offspring.

The demonstration that nutrients can directly affect DNA is relatively recent news. Although we don’t yet know how much our environment shapes gene silencing, there is increasing evidence to show that messing up DNA methylation during development can cause a range of health problems from cancer to schizophrenia. Without doubt, the greatest implication of such heritable epigenetic features is the influence your diet might have on the genes of your children and grandchildren.