Nutrigenomics and Beyond Informing the Future: Workshop Summary (2007) / Chapter Skim
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2 Scientific Session II: Epigenetics
2 Scientific Session II: Epigenetics
Pages 17-30
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From page 17... ...
First, epigenetics is "the transmission of information through meiosis or mitosis that is not based on the DNA sequence." That is, during cell division (which accompanies meiosis or mitosis) information encoded in the DNA sequence is passed from one stage of cell division to the next; epigenetics concerns itself with the remainder of that information.
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From page 18... ...
The differences arise from variations in the expression of the agouti gene; and coat color expression can be controlled by varying the mother's diet before, during, and after pregnancy. The agouti allele is normally expressed only in a mouse's skin, creating a yellow fur wherever it is expressed, but in agouti mice the gene is expressed throughout the body.
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From page 19... ...
Methylation can inhibit expression of the agouti gene altogether, resulting in a mouse with brown fur and normal weight. A key point is that the methylation state can be passed from one replicative generation to the next or from parent to offspring, as in the case of the agouti mouse, causing the differences in phenotypic expression.
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From page 20... ...
The development of cancer depends upon a complex series of events. Some of these events are genetic, involving genetic mutations, whereas others are epigenetic, involving changes in DNA methylation or in the chromatin state, such as histone modifications.
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From page 21... ...
Methylation has various effects on the development of tumors, depending on the tissue and the situation. In the thymus and soft tissue, for example, decreasing the level of methylation enhances tumor formation by increasing genome instability, increasing the probability that mutations that repress the expression of tumor suppressor genes will occur.
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From page 22... ...
A series of experiments were conducted in which somatic cell nuclear transfer techniques were used to remove the nuclei from tumor cells and inject them into enucleated eggs. The eggs were then allowed to develop to the blastocyst stage, which were then explanted in culture to derive cloned embryonic stem cells.
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From page 23... ...
. Noticing that coronary heart disease was the most common cause of death among a group of men who had none of the usual risk factors, such as obesity or smoking, he noticed a pattern of low birth weight and suggested that the increased risk for heart disease might have its origins in nutritional deprivation in the womb decades earlier.
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From page 24... ...
The question that arises is how the nutritional environment in utero programs the genome epigenetically and, in particular, how a nutritionally deficient environment results in programming that increases disease risk later in life. "We know that programming is associated with chromatin modification," Stover noted, "whether it be DNA methylation or demethylation, acetylation, ADP ribosylation, or biotinylation of histone proteins.
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From page 25... ...
This change in biochemistry confers both risks and benefits. The decreased methylation rate increases the risk for neural tube defects in the developing fetus, but in adults the increased level of thymidylate synthesis leads to a lower risk of colon cancer.
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From page 26... ...
"So," Stover concluded, "metabolism can influence reversibly imprinted gene expression once the imprint is already established." This may be a property that is exclusive to stem cells. Lastly, Stover offered examples of how folate can induce epigenetic changes to compensate for genetic shortcomings.
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From page 27... ...
Human and animal studies such as these raise three questions that are especially relevant to public health: Are the long-term adverse effects of early prenatal nutrition experiences on chronic disease risk reversible? Do increased risks persist across generations?
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From page 28... ...
The best human data relevant to the first category come from studies of the impact of maternal size on the progeny's birth weight. Maternal stature, not uncommonly, is a good indicator of past nutritional status but is independent of current nutritional status; yet, an infant's birth weight remains significantly dependent on maternal stature.
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From page 29... ...
Data from studies with humans and animals that support links between prenatal and early childhood growth patterns and multiple long-term disease risks underscore the need for promoting physiologic growth in utero and throughout childhood and the need for robust tools to enable those assessments.
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