The epigenetic revolution

The completion of the Human Genome Project in April 2003 was a milestone in science. Ten years on, however, Bill Clinton’s prediction that it would “revolutionise the diagnosis, prevention and treatment of most, if not all, human diseases” is far from the truth. For all the project’s contributions to biology, little of this has translated into promised “personal medicine” treatments.

The relatively new field of epigenetics is beginning to fill in the gaps in understanding left by genome sequencing. Epigenetics – the study of factors which control gene expression, other than the genetic code itself – accounts for why cells in different parts of the body develop differently, despite sharing the same DNA.

Epigenetic markers switch off individual genes, causing them not to be expressed in a cell. More recently, epigenetic markers have been shown to be passed on to children and grandchildren, shaking the belief that disease caused by lifestyle can have no effect on offspring.

Both sperm and egg are specialised cells with their own epigenetic makeup. Until recently, it was believed that when these fused, the epigenetic markers were completely removed in a process called ‘Reprogramming’, allowing the embryo to develop completely from scratch.

New evidence suggests that this may not be the case. Last year, researchers at the Los Angeles Biomedical Research Institute found that injecting pregnant rats with nicotine caused asthma to occur not only in the next generation, but the one following that: the epigenetic changes caused by nicotine, it seems, are inheritable.

In the 1980s, a Swedish scientist called Dr. Lars Olov Bygren studied the lifespans of people living in Norrbotten, the country’s northernmost and least populated county. In the late 19th and early 20th centuries, poor harvests here often led to starvation, though some years were unusually abundant with food.

Dr. Bygren found that grandchildren of people who had plenty of food as a child had much shorter lives than those who did not. Controlling for other factors such as disease and socioeconomic status, the difference in longevity between grandchildren of well-fed and starved Norbotten residents was 32 years. Epigenetic markers passed down through generations seem to be the most probable cause.

The idea of inheritable epigenetic markers has made its way into evolutionary biology, giving a clue as to how invasive species can thrive in new environments. For a species to do well and adapt to its environment, say the laws of natural selection, it must have a lot of variation. However, invasive species often have limited gene pools and some, such as the Japanese knotweed, reproduce asexually, so are genetically identical. This has long been a puzzle for biologists: how do these species manage to survive?

Christina Richards, an evolutionary ecologist at the University of South Florida in Tampa, studied Japanese knotweed and found that individual plants have high variation in their leaf shape and height ­– characteristics controlled by epigenetic factors. Epigenetic variation, Richards believes, is one of the things which gives invasive species their ability to do well in novel environments.

Some scientists are not so convinced. Though the role of epigenetics is largely accepted within medical science, many evolutionary biologists are sceptical about its effect on invasive species, believing their success can be fully explained by current evolutionary theory.

Epigenetic inheritance need not oppose Darwinian evolution, but can integrate with it. The study of epigenetics could lead to new disease treatments and preventative measures, as well as ecological insights. Where the Human Genome Project has failed to keep its promises, epigenetics may deliver.