Woodland: Epigenetics: More control of our destiny than we thought | SummitDaily.com

Woodland: Epigenetics: More control of our destiny than we thought

David L. “Woody” Woodland
Special to the Daily

I remember well my early schooldays when I first learned about genetics and the theory of evolution. The idea that our genes were a blueprint and that beneficial genes would be selected through generations of breeding was very compelling to me. I also remember learning about a competing theory proposed by Jean-Baptiste Lamarck. Lamarck’s theory held that characteristics acquired during a lifetime would be passed on to the next generation. For example, a farmer who developed strong muscles would pass a strong musculature on to his son. In my mind, and in the minds of many scientists, this alternative idea was clearly wrong in light of the beautiful theory of genetic inheritance. Yet it is now turning out that at least some aspects of Lamarck’s ideas may be right. We are now in the era of epigenetics.

Epigenetics is a field of study referring to changes in gene activity not caused by changes in the genetic code itself, but which can nevertheless be passed on from one individual to another. How can this be? The answer lies in the fact that in order for genes to control an organism’s development and structure, they must be switched on and off at precise moments. For example, genes that control eye color must be switched off in cells that are developing into heart muscles and switched on in cells that are developing into the nascent eye structure. It is these “epigenetic” changes in gene activity that scientists are now realizing can be inherited. Perhaps the clearest example of this is the phenomenon of “imprinting.” We all carry two copies of most of our chromosomes, which means that we all have two copies of each gene, one from our father and one from our mother. However, for approximately 1 percent of our genes, one of the copies has been inactivated, such that gene expression occurs exclusively from the other copy. A good example of this is an insulin-like growth factor which is only expressed from the father’s copy of the gene (the mother’s copy of the gene is inactivated). Inappropriate loss of the imprint, such as activation of the maternal gene, can result in over-expression of the insulin-like growth factor gene and the development of cancer. Imprinting can also result in the inheritance of disease if one copy of the gene is defective and the normal copy of the gene is inactivated. Prader-Willi syndrome and Angelman syndromes are both examples of this phenomenon whereby inactivation of one of the two copies of the gene can lead to the disease.

Epigenetic changes can also occur later in life. An excellent example of this is the agouti gene, present in both mice and people. When the gene is active in mice, it results in a yellow coat color, obesity and propensity to develop diabetes and cancer. When the gene is inactivated in mice, it results in a brown coat color and low disease risk. Yet the two types of mice, yellow and brown, are genetically identical; it’s just the pattern of gene expression that has changed. The interesting thing is that these expression patterns can be controlled by diet. A female yellow mouse that is fed a diet rich in methyl groups will produce offspring with a brown coat color and low risk of disease. Moreover, the grandchildren of the original mouse will retain these characteristics, indicating that these “epigenetic” modifications are passed between generations. In other words, some traits developed during an individual’s life can be transferred to their children with no change in genetic sequences — this is essentially a version of Lamarckism.

How can these epigenetic changes occur? We now know that small chemical tags can be added or removed from DNA molecules that control the ability of a gene to be accessed and translated into protein. In the case of the yellow mice, the methyl-rich diet results in the chemical tagging of certain stretches of DNA with methyl groups, thereby blocking expression of the gene. The patterns of methyl group tags, and other chemical modifications, can be maintained across generations, resulting in inherited patterns of gene expression. The more we learn about the complexities of the control of gene expression, the more it becomes apparent that there are opportunities for early disease diagnosis and the possibility that we may be able to prevent the development of some diseases in certain individuals. As we recover from this holiday season, we can derive comfort (or horror) that certain habits, especially related to diet, might be inherited in a Lamarckian fashion by our kids and grandkids.

The more we learn about the complexities of the control of gene expression, the more it becomes apparent that there are opportunities for early disease diagnosis and the possibility that we may be able to prevent the development of some diseases in certain individuals.

David L. “Woody” Woodland, Ph.D. is the Chief Scientific Officer of Silverthorne-based Keystone Symposia on Molecular and Cellular Biology, a nonprofit dedicated to accelerating life science discovery by convening internationally renowned research conferences in Summit County and worldwide. Woody can be reached at 970-262-1230 ext. 131 or woody@keystonesymposia.org.


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