The odd couple

Identical twins have fascinated people throughout history. In many cultures they were long regarded as beings that were not quite human and presaged either a blessing or a curse. Thanks to the natural sciences, we know that there’s nothing magical about them. Nonetheless, for a long time they presented geneticists with a riddle: If the rules of heredity are valid, how can it be that one identical twin develops a hereditary illness such as diabetes while the other one can eat muffins without a qualm, even though both of them have identical genetic information?

Famines provided the initial answers. A few years ago, epidemiological studies showed that the grandchildren of men who had experienced famine as children were much less likely to suffer from diabetes or heart disease than the grandchildren of men who had never starved. The findings indicated that the environmental impacts that have been experienced could have an influence on genetic information.

Another example of the huge effects that environmental impacts have on individual development comes from honeybees. All honeybee larvae have the genetic potential to develop into a queen bee, but only the larva that is fed with royal jelly grows up to be the queen. So there must be a mechanism that turns genes on or off, depending on the specific nutrition received. The branch of biology that searches for these mechanisms was named epigenetics—a combination of the word “genetics” and the Greek syllable “epi” (“besides” or “over”). This concept refers to research focusing on hereditary changes in genetic activity that do not change the sequence of bases in the genetic material.

The main focus of this young discipline is currently on two epigenetic mechanisms. One of them is methylation. In this process, a methyl group consisting of one carbon atom and three hydrogen atoms overlays sites along a strand of DNA. As a result, the genes cannot be read. The second switch is histone acetylation. When a strand of human DNA is completely unfolded, it is about two meters long. In order to fit inside our cells, it is packed in what is known as a histone complex. When information has to be read, the strand is not fully unfolded. Instead, the histone packages are opened only at the required site. Both of these mechanisms are reversible.

In the case of identical twins, research has shown that there are hardly any differences between their epigenetic markings while the twins are young. However, as the twins grow older they become more and more dissimilar epigenetically. In other words, life leaves traces in the molecular biology of our cell nuclei and influences which genes are switched on and which are switched off. If we want to understand the development of an organism, we therefore have to observe not only its genome but also its epigenome—that is, the totality of all its epigenetic structures.

Valuable knowledge is hidden in the epi genomes of human beings and animals. It can be assumed that, thanks to epigenetic applications, in the future it will be possible to identify many diseases at an early stage, accelerate healing processes, and simply switch off genetic diseases. That’s why epigenetics could be a game changer for the field of medicine.

It’s a good thing that Creavis, which has research teams in Germany and Singapore, is already active in the field of epigenetics. The goal of the teams is to make relevant epigenetic information readable quickly and affordably. The Foresight team will also be sounding out the future of epigenetics. Who knows? Maybe this is exactly the hiding place of the right switch that will finally banish the terror of Alzheimer’s disease or diabetes.