By: JulieF,
on 10/9/2015
Epigenetics has been a buzzword in biology for the past several years, as scientific understanding has grown about how genes are expressed.
The post The rise of epigenetics and the demise of nature vs nurture appeared first on OUPblog.
By: Shannon Hazard,
on 6/11/2015
Environmental Epigenetics is a new, international, peer-reviewed, fully open access journal, which publishes research in any area of science and medicine related to the field of epigenetics, with particular interest on environmental relevance. With the first issue scheduled to launch this summer, we found this to be the perfect time to speak with Dr. Michael K. […]
The post A Q&A with the Editor of Environmental Epigenetics appeared first on OUPblog.
By: Nicola,
on 3/28/2012
Epidemiology, a well established cornerstone of medical research, is a group level discipline that aims to decipher the distribution and causes of diseases in populations. Epigenetics, perceived by many as the most fashionable research arena in which to be involved, is a mechanism of gene regulation. What brings these perhaps unlikely partners together?
Epigenetic processes are key features in gene regulation. Epigenetic patterns are laid down in early development and are moulded through in utero and early postnatal life and continue to show some degree of plasticity across the lifecourse. Many environmental, behavioural, nutritional and lifestyle factors are believed to influence epigenetic patterns and in some case the evidence base is substantial. What is less clear is the role of this environmentally modifiable ‘epigenome’ on disease risk in populations. This is where epidemiology can help. A good starting point for an epidemiological engagement with epigenetics is clearly identified by Nessa Carey, in her recent popular science book The Epigenetics Revolution:
“The majority of non-infectious diseases that afflict most people take a long time to develop, and then remain as a problem for many years if there is no cure available. The stimuli from the environment could theoretically be acting on the genes all the time in the cells that are acting abnormally, leading to disease. But this seems unlikely, especially because most of the chronic diseases probably involve the interaction of multiple stimuli with multiple genes. It’s hard to imagine that all these stimuli would be present for decades at a time. The alternative is that there is a mechanism that keeps the disease-associated cells in an abnormal state, i.e. expressing genes inappropriately. In the absence of any substantial evidence for a role for somatic mutation, epigenetics seems like a strong candidate for this mechanism”.
Recent literature points to a role for epigenetic variation in a range of diseases including neurological disease, cardiovascular disease, osteoarthritis and obesity but in most instances these are correlations without robust evidence of causality. Indeed, epigenetics is often proffered as the answer to many unresolved causes of disease. The enthusiasm for establishing whether epigenetic mechanisms link the environment with disease development must be tempered by the knowledge that the epigenome is dynamic and has as much potential to respond to disease as respond to the environment. Therefore it is very difficult to disentangle cause from consequence when studying epigenetic variation and disease.
This is just one of the many challenges that face researchers interested in understanding the role of epigenetics in common complex disease. Other challenges include the differences in interpretation of the term ‘epigenetics’ itself – in a field that attracts cell, developmental and evolutionary biologists, epidemiologists and bioinformaticians, amongst others, it is unsurprising that epigenetics means different things to different people and discussions of its relevance to disease can sometimes suffer misinterpretation.
The methods at our disposal to accurately measure epigenetic variation and in turn assess the impact this has upon disease risk are still being developed and there is much to do in this arena with respect to when, where and how to look at the epigenome. The complexity and interplay of multiple factors in determining d
By: Kirsty,
on 11/26/2010
What links a queen honeybee to a particular group of four atoms (one carbon and three hydrogen atoms, to be precise)? The answer lies in the burgeoning field of epigenetics, which has revolutionized our understanding of how biological information is transmitted from one generation to the next.
The genetic information stored in our genome – the set of chromosomes that we inherit from our parents – directs the way in which we develop and behave. (We call the attributes and behaviours exhibited by an organism its ‘phenotype’.) Traditionally, the genetic information was thought to be encoded solely in the sequence of the four different chemical building blocks from which our DNA is constructed (that is, our genome sequence). If a DNA sequence changes, so the resulting phenotype changes too. (This is why identical twins, with genomes whose DNA sequences are identical, look the same, but other individuals, whose genomes comprise different DNA sequences, do not.) However, the field of epigenetics opens up a strong challenge to this traditional view of our DNA sequence being the sole dictator of phenotype.
So what actually is epigenetics? In broad terms, epigenetics refers to the way that the information carried in our genome – and the phenotype that results when this information is ‘deciphered’– can be modified not by changes in DNA sequence, but by chemical modifications either to the DNA itself, or to the special group of proteins called histones that associate with DNA in the cell. (It’s a bit like taking a book, with a story told in the author’s words, and adding notes on the page that alter how the story is interpreted by the next person to read it.)
But what has epigenetics to do with the group of four atoms, the one carbon and three hydrogen atoms mentioned at the start of this blog post? These four atoms can combine to form a methyl group – a central carbon atom, with three hydrogen atoms attached; the addition of methyl groups to both DNA and histone proteins in a process called methylation is a primary way in which epigenetic modification occurs. For example, the addition of a methyl group to one of the four chemical building blocks of DNA (called cytosine, C) either when it appears in the sequence CG (where G is the building block called guanine) or the sequence CNG (where N represents any of the four chemical building blocks of DNA) appears to result in that stretch of DNA being ‘switched off’. Consequently, the information stored in that stretch of DNA is not actively used by the cell; that stretch of DNA falls silent.
But what of our queen honeybee? Where does she fit into our story? A queen honeybee has an identical DNA sequence to her workers. Yet she bears some striking differences to them in terms of physical appearance and behavior (amongst other attributes). These differences are more than just skin-deep, however: the pattern of methylation between queen and worker larvae differs. Their genomes may be the same at the level of DNA sequence, but their different patterns of methylation direct different fates: the queen honeybee and her workers develop into quite distinct organisms.
Things take an interesting turn when we consider the cause of these different methylation patterns: the diets that the queen and workers experience during their development. The queen is fed on large quantities of royal jelly into adulthood, while worker larvae face a more meager feast, being switched to a diet of pollen and nectar early on. It is these diets that influence the way in which the queen and worker bees’ genes are switched on and off.
It is not just the queen honeybee whose genome is affected by the environment (in her case, diet). Mice exposed to certain chemicals during pregnancy have be
