1. what is the difference between genetics and epigenetics

Mycobacterium tuberculosis causes tuberculosis. Colorectal cancers have increased methylation at the SEPT9 gene. When used with other diagnostic screening tests, these epigenetic based tests can help find cancer early 5 6.

People whose mothers were pregnant with them during the famine were more likely to develop certain diseases such as heart disease, schizophrenia, and type 2 diabetes 7. Around 60 years after the famine, researchers looked at methylation levels in people whose mothers were pregnant with them during the famine.

These people had increased methylation at some genes and decreased methylation at other genes compared with their siblings who were not exposed to famine before their birth 8 9 These differences in methylation could help explain why these people had an increased likelihood for certain diseases later in life 7 10 11 Skip directly to site content Skip directly to page options Skip directly to A-Z link.

Section Navigation. Facebook Twitter LinkedIn Syndicate. What is Epigenetics? Minus Related Pages. How Can Your Epigenetics Change? Epigenetics and Development Epigenetic changes begin before you are born. All your cells have the same genes but look and act differently. As you grow and develop, epigenetics helps determine which function a cell will have, for example, whether it will become a heart cell, nerve cell, or skin cell.

Example: Nerve cell vs. Muscle cell. Epigenetics and Age Your epigenetics change throughout your life. Your epigenetics at birth is not the same as your epigenetics during childhood or adulthood. Example: Study of newborn vs. Epigenetics and Reversibility Not all epigenetic changes are permanent. Some epigenetic changes can be added or removed in response to changes in behavior or environment.

Example: Smokers vs. Epigenetics and Health Epigenetic changes can affect your health in different ways:. Youngson, and E. Maggert and G. View at: Google Scholar K. Gehring, J. Huh, T. Hsieh et al. Wolff, I. Weinhofer, J. Seguin et al. Luo, J. Taylor, A. Spriggs et al. Kaykov and B. Vengrova and J. Arico, D. Katz, J. Maggert and K. View at: Google Scholar V. Lloyd, D.

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Dobo, M. Vibranovski, and A. Vibranovski, L. Koerich, and A. Paredes and K. Schneeberger and C. Paredes, A. Branco, D. Hartl, K. Maggert, and B. Lyckegaard and A. Long and I. About letters-worth of DNA or base-pairs is wrapped around each nucleosome, and this helps package the 3 billion base pairs of genetic code into each of our cells. Diagram 2. The familiar DNA double helix blue is wrapped around nucleosomes grey cylinders in cells.

The string of nucleosomes can be coiled into a thicker filament, called the 30 nm fibre and this can be further coiled into a still thicker chromatin fibre. When genes are switched on their nucleosomes are more uncoiled like the 10nm fibre.

Like the methyl tags on DNA, small chemical tags can also be added to these histone tails see Diagram 3. Two of the chemical tags that are added to these tails are acetyl groups and methyl groups. Methyl, acetyl and a few other types of tags can be added to the tails in a large number of combinations and this effects whether an underlying gene is switched on or off. In fact genes can be switched right off this is called silencing , full on, or somewhere in between by DNA methyl tags and histone tail tags.

The combination of DNA and histone tags can also effect how easily a gene is turned on or off. Diagram 3. Grey cylinder, nucleosome; curved black lines, histone tails; green circles, methyl tags; red triangles, acetyl tags; mauve hexagons, other types of tag. When cells divide, the entire DNA sequence from the original cell 3 billion base pairs contained in 23 pairs of chromosomes in a human cell is duplicated so that both daughter cells receive an exact copy.

What, you might ask, happens to all those epigenetic tags? We have known for some time that the DNA-methyl tags are copied too, so that both daughter cells have the same pattern of DNA methylation. We now know that the pattern of histone tags is also mostly duplicated as cells divide, although this is currently less well understood. Nevertheless, cell division is also a time when epigenetic tags can most easily be changed. Right at the beginning we came across the story of the long-lived microscopic worms thatpassed on their longevity to their offspring even if the individual offspring did not inherit the variant gene mutation that originally caused the extended lifespan.

We are now in a position to explain this apparently strange result. In most cases genes contain the information to make a protein molecule, and the protein molecules might be enzymes that carry out chemical reactions in the cell, or parts of the structure of the cell itself.

It turns out that the genes that were mutated in the worm study make proteins that work together to add a methyl tag to nucleosomes. This tag is an on-switch. When one or more of the genes were mutated this tag was absent and several genes that should be on, including some involved in ageing, were switched off and the worms had a longer lifespan.

But this result and other research that shows that this is not always the case and that sometimes, the pattern of epigenetic tags are passed on. But what is it about royal jelly that leads a larva that would otherwise grow up to be a worker, to become a queen?

The answer lies in understanding that the individual chemical tags that are added to the histone tails of nucleosomes are constantly being revised by the cell. Acetyl tags are added by enzymes called histone acetyl transferases and they are removed or erased by a second group of enzymes called histone deacetylases HDACs. Both of these enzymes are present in most cells and this allows genes to be switched on or off over time. Recently, researchers set out to identify compounds in royal jelly that could alter this process, and what they found was something known as an HDAC inhibitor.

This was a relatively simple chemical compound that is present in royal jelly and that stops the action of HDAC enzymes that normally remove acetyl tags from histones. This results in a build-up of acetyl tags in the cells of the bee embryos, and like the reduction in DNA-methyl groups described previously, this is thought to switch on key genes required for development of a queen.

HDAC inhibitors are not only important to queen bees, but are also part of a small but growing number of medically useful drugs that target epigenetic tags and which are useful in treating some kinds of cancer.

Furthermore HDACs also have a role in the way our brains form memories, and novel drugs that affect histone acetylation may have a role in the future in treating memory impairment in elderly patients. We have seen how the difference between a queen and worker bee is determined by exposure to a chemical that directly alters epigenetic tags such as acetyl groups; but are there examples where nutrition or other aspects of the environment affect human populations in a way that can be explained by epigenetics?

One such example is what is known as the Dutch Hunger Winter. In the last year of the Second World War in Europe, a food embargo imposed by occupying German forces on the civilian population of the Netherlands resulted in a severe famine, coinciding with a particularly harsh winter. About 20, people died from starvation as rations dropped to below kilocalories per day.

Despite the chaos of war, medical care and records remained intact allowing scientists to subsequently study the effect of famine on human health. What they found was that children who were in the womb during the famine experienced a life-long increase in their chances of developing various health problems compared to children conceived after the famine.

The most sensitive period for this effect was the first few months of pregnancy. Thus, something appears to happen early in development in the womb that can affect the individual for the rest of their lives.

Even more surprisingly, some data seems to suggest that grandchildren of women who were pregnant during the Hunger Winter experience some of these effects. From what we have already discussed, this strongly suggests an epigenetic mechanism. In fact, research with the Dutch Hunger Winter families continues, and a recent study looking at a gene galled IGF2 found lower levels of the methyl tag in the DNA of this gene in individuals exposed to the famine before birth.

Although IGF2 may not itself be involved in the increased risk of poor health in these people, it shows that epigenetic effects i. Studies in animals have also found that the diet of the mother can have effects on her offspring. For example, feeding sheep a diet lacking the types of food required to make methyl groups leads to offspring with altered patterns of DNA methylation and which have higher than expected rates of certain health problems.

Epigenetics and imprinting, why genes from Mum and Dad are not always equivalent. We all have 23 pairs of chromosomes in our cells. For each pair, one came from mother and one from father. Thus, we inherit one copy of each gene from each parent and we generally assume that the function of the gene does not to depend on which parent it came from.