Epigenetics
Introduction
The ‘story’ of molecular biology is being re-written. The traditional view of genetics claims that genes are the ultimate (and only) blue print for life – that DNA sequences ‘code for’ RNA, which makes proteins, which are responsible for every facet of our biology (from hair color to predisposition for cancer).
Over the last decade there has been a growing realization among scientists that this traditional, mendelian model is an inadequate description of molecular genetics. The accumulating evidence of ‘exceptions’ to mendelian genetics has focused research on a previously neglected field – epigenetics.
Epigenetics is the study of stable, persistent (and sometimes heritable) changes in gene function that are unrelated to changes in DNA sequence. The mechanisms of epigenetics include (but are not limited to) DNA methylation, histone modification, chromatin organization, impringing, and general RNA-regulation of gene expression.
Interestingly, research indicates that epigenetic mechanisms are influenced by many environmental factors. Some believe that they may even constitute an organisms ability to integrate environmental information into its genetic function. (Maybe Lamarck wasn’t SO wrong after all ;-] )
The classic example of epigenetic inheritance is the <second generation effects> of the <Dutch famine of 1944>. Babies who were in the first and second trimester of development during the famine were born with lower than average birth weights. Low birth weight has been strongly correlated with higher incidence of heart disease and other chronic illnesses. As you would expect, the babies of the famine suffered significantly higher rates of heart disease than their peers who were just a year younger or older. Even more interestingly, longitudinal epidimiology studies have found that the children of the famine babies, also suffered from higher rates of heart disease than their peers (Lumey 1992). This phenomena has been reproduced in animal studies (Martin 2002). The first generation effect is easily explained by womb conditions (generally termed <maternal effects>), the second geneartion effect can only be explained as an epigenetic phenomena.
Implications
The discovery of epigenetics, requires a whole-sale re-envisioning of molecular biology. The <central dogma of molecular biology> needs to be scrapped. Scientists need to complete the transition to the postgenomics era – shift the focus from ‘what each gene does’ towards understanding what genes do in the context of the proteins and genes around it (or its envirnoment).
Epigenetics throws up a major roadblock for the development of next generation genetic technologies such as <gene therapy>. Because of the importance of epigenetic mechanisms in gene expression, gene therapy is a more daunting than merely introducing the desired gene into a cell. This explains a decade of frustration and largely unrealized expectations in gene therapy.
However, ‘epigenetic therapy’ might be an easier, more viable alternative. Harnessing epigenetic mechanisms to turn off, or ‘silence’ harmful genes, and increase activation of beneficial genes, shows great potential. Already, several inhibitors of enzymes controlling epigenetic modifications, specifically DNA methyltransferases and histone deacetylases, have shown promising anti-tumorigenic effects for some malignancies.
Epigenetics opens a whole new can of worms for both human genetics and health care. Epigenetics goes a long way towards explaining the lack of progress in finding the ‘gene responsible for’ many complex diseases. I think that to unlock the genetic basis for the most complex diseases, we need to look beyond the <genome-wide association testing>, to epigenetic epidemiology. <Psychiatric genetics> in particular could be revitalized by a focus on epigenetics.
POSTS – chronological order
Scientists call for international Human Epigenome Project
Epigenetis-based Breast Cancer Test
Chronic Disease and Epigenetics in History
Far Sighted 
[…] male fitness. Consequently, mitochondrial-based variation in sperm traits is likely to persist, even in the face of intense sperm competition. Indeed, mitochondrial nucleotide substitutions, deletions and insertions are now known to be a primary cause of low sperm count and poor sperm motility in humans. Paradoxically, in the field of sexual selection, female-limited response to selection has been largely overlooked. Similarly, the contribution of epigenetics (e.g., DNA methylation, histone modifications and non-coding RNAs) to heritable variation in male fitness has received little attention from evolutionary theorists. Unlike DNA sequence based variation, epigenetic variation can be strongly influenced by environmental and stochastic effects experienced during the lifetime of an individual. Remarkably, in some cases, acquired epigenetic changes can be stably transmitted to offspring. A recent study indicates that sperm exhibit particularly high levels of epigenetic variation both within and between individuals. We suggest that such epigenetic variation may have important implications for post-copulatory sexual selection and may account for recent findings linking sperm competitive ability to offspring fitness. Far Sighted […]
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[…] what we are caused by all this factors at once, and that they influence each other in complex ways (Epigenetic research shows that what we do actually influences which of our genes are turned on and off) many […]