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ARTIFACT 1 – TESTICULAR CANCER INFORMATION Testicular cancer occurs in the testicles (testes), which are located inside the scrotum, a loose bag of skin underneath the penis. The testicles produce male sex hormones and sperm for reproduction. Compared with other types of cancer, testicular cancer is rare. But testicular cancer is the most common cancer in American males between the ages of 15 and 35. Testicular cancer is highly treatable, even when cancer has spread beyond the testicle. Depending on the type and stage of testicular cancer, you may receive one of several treatments, or a combination. Regular testicular self-­‐examinations can help identify growths early, when the chance for successful treatment of testicular cancer is highest. Source: Mayo Clinic http://www.mayoclinic.org/diseases-­‐conditions/testicular-­‐
cancer/basics/definition/con-­‐20043068 Note: Environmental Risk factors for Testicular Cancer are similar to other cancers ARTIFACT 2 – TWIN PREGNANCY INFORMATION Identical twins come from a single egg that has been fertilized by one sperm. For unknown reasons, the fertilized egg splits into two embryos during the first stage of development. In the mother's womb (uterus), most identical twins share the same placenta. (They get oxygen and nutrients from the mother and get rid of wastes through the placenta.) But they usually grow within separate amniotic sacs. In rare cases, identical twins share one amniotic sac. Fraternal twins develop when two eggs are fertilized by two separate sperms. The fetuses have separate placentas and amniotic sacs. Source: Webmd: http://www.webmd.com/baby/twin-­‐pregnancy-­‐types ARTIFACT 3 – CELL SPECILZATION BY TURNING GENES ON AN OFF
Caption: Early in
development, genes are "poised" like runners in the starting blocks, ready to jump to action. In a
differentiated cell, only 10 to 20% of the genes are active. Different sets of active genes make a skin
cell different from a brain cell. Environmental signals such as diet and stress can trigger changes in
gene expression. Epigenetic flexibility is also important for forming new memories.
As a fertilized egg develops into a baby, dozens of signals received over days, weeks, and months cause incremental changes in gene expression patterns. Epigenetic tags record the cell's experiences on the DNA, helping to stabilize gene expression. Each signal shuts down some genes and activates others as it nudges a cell toward its final fate. Different experiences cause the epigenetic profiles of each cell type to grow increasingly different over time. In the end, hundreds of cell types form, each with a distinct identity and a specialized function. Even in differentiated cells, signals fine-­‐tune cell functions through changes in gene expression. A flexible epigenome allows us to adjust to changes in the world around us, and to learn from our experiences. The epigenome changes in response to signals. Signals come from inside the cell, from neighboring cells, or from the outside world (environment). Early in development, most signals come from within cells or from neighboring cells. Mom's nutrition is also important at this stage. The food she brings into her body forms the building blocks for shaping the growing fetus and its developing epigenome. Other types of signals, such as stress hormones, can also travel from mom to fetus. After birth and as life continues, a wider variety of environmental factors start to play a role in shaping the epigenome. Social interactions, physical activity, diet and other inputs generate signals that travel from cell to cell throughout the body. As in early development, signals from within the body continue to be important for many processes, including physical growth and learning. Hormonal signals trigger big changes at puberty. Even into old age, cells continue to listen for signals. Environmental signals trigger changes in the epigenome, allowing cells to respond dynamically to the outside world. Internal signals direct activities that are necessary for body maintenance, such as replenishing blood cells and skin, and repairing damaged tissues and organs. During these processes, just like during embryonic development, the cell's experiences are transferred to the epigenome, where they shut down and activate specific sets of genes. Source: University of Utah http://learn.genetics.utah.edu/content/epigenetics/epi_learns/ ARTIFACT 4 – EPIGENETICS What is Epigenetics?
Epigenetics is the study of other factors besides the DNA sequence that influence whether or not a gene is transcribed into mRNA and then translated (conversion of mRNA sequence into amino acids) into a protein. An individual’s environment, even in the womb, can influence these factors and permanently alter the expression of genes in the adult. Alterations in epigenetic mechanisms lead to development of diseases, such as some forms of cancer, including colorectal cancer and leukemia, neurodevelopmental disorders, obesity, and type 2 diabetes. Source: Haine, D. DNA wrap: Packaging Matters. UNC’s Superfund Research Program Epigenetics vs DNA Code There’s no debate that the DNA blueprint is the starting point—a very important starting point and absolutely necessary, without a doubt. But it isn’t a sufficient explanation for all the sometimes wonderful, sometimes awful complexity of life. If the DNA sequence were all that mattered, identical twins would always be absolutely identical in every way. Babies born to malnourished mothers would gain weight as easily as other babies who had a healthier start in life. And we would all look like big amorphous blobs, because all the cells in our bodies would be completely identical. That’s because epigenetics is the mechanism by which cells with the same genetic code express different parts of it during development, becoming liver, muscle, brain, or any of the hundreds other cell types in the human body. Huge areas of biology are influenced by epigenetic mechanisms, and the revolution in our thinking is spreading further and further into unexpected frontiers of life on our planet. Why can’t we make a baby from two sperm or two eggs, but must have one of each? What makes cloning possible? Why is cloning so difficult? Why do some plants need a period of cold before they can flower? Since queen bees and worker bees are genetically identical, why are they completely different in form and function? Why are virtually all tortoiseshell cats female? Why is it that humans contain trillions of cells in hundreds of complex organs, and microscopic worms contain about a thousand cells and only rudimentary organs, but we and the worm have the same number of genes? Source: Carey, N. (2012) The epigenetics revolution: how modern biology Is rewriting our understanding of genetics, disease, and inheritance. Columbia University Press. Retrieved from: http://www.naturalhistorymag.com/features/142195/beyond-­‐dna-­‐epigenetics ARTIFACT 5A – DNA METHYLATION
Figure 1: This representative DNA helix depicts two methyl groups (M) covalently attached to two cytosine bases in DNA.
A: DNA “methylation” means that a chemical compound called a methyl group attaches to a region of DNA, and serves as a flag. DNA methylation is involved in the normal control of gene expression, flagging certain genes to “turn on” (be expressed) or “turn off” (be silenced). Sometimes, DNA methylation can contribute to cancer or disease, either by silencing genes that that should otherwise be active or by causing the expression of genes that are usually turned off. Methylation suppresses (silences) genes by stopping the transcription of DNA into RNA (see Figure 2). These DNA methylation changes do not involve changes in DNA sequence and are therefore described as ‘epigenetic’ changes, meaning ‘above the genome’, the literal translation of ‘epigenome.’ Epigenetic changes can be maintained and inherited by daughter cells during mitosis and meiosis. Therefore, epigenetic modifications that occur in utero can be passed on to subsequent generations. Source: Haine, D. DNA wrap: Packaging Matters. UNC’s Superfund Research Program Figure 2: This
diagram shows
methylation during
the initial stages of
transcription, as
the DNA double
helix unwinds.
Source:
http://episona.com/s
hort-introductionepigenetics/
ARTIFACT 5B – DNA METHYLATION EXPERIMENT
GFP stands for “Green Fluorescent Protein,” and
it is the protein that causes jellyfish and other
organisms to glow. It is an easy protein to isolate
and thus is used in a lot of scientific studies.
To learn more about epigenetics, researchers
isolated the GFP protein, and transformed
bacterial cells by inserting the GFP gene into
them. The researchers then grew the genetically
modified bacterial cells in culture dishes.
In each culture dish, scientists added different
compounds. They then compared the amount of
GFP that the cells produced before and after they
added the compounds to see whether the compounds
made the GFP gene more or less active.
Figure 3: Results of a typical GFP culture using AdoMet and Valproic A compound called AdoMet, a source of methyl tags,
decreased GFP output. Valproic acid, an anti-epilepsy drug and mood stabilizer,
increased GFP output. The researchers analyzed the GFP genes from these cells and
confirmed that the compounds changed the number of methyl tags attached to the DNA.
Cells like this, along with other biological tools, help researchers understand how signals
from the environment shape the epigenome.
Source: University of Utah http://learn.genetics.utah.edu/content/epigenetics/control/
ARTIFACT 6 – AGOUTI MICE
This artifact contains information about yellow Agouti Mice. The mice in the photo and in the chart below are genetically identical, yet as you can see, they do not appear identical. Agouti mice (yellow) are obese and are more prone to diabetes and cancer. The Pseudo agouti (brown) mice are normal in their weight and are not prone to disease. Note that Bisphenol A is commonly known as BPA (many products are now BPA free) and Folate is commonly known as folic acid, a vitamin found in most multivitamins, especially in prenatal vitamins. Source: Dolinoy, D. Weidman, J., Waterland, R. & Jirtle, R. 2006. Maternal Genistein Alters Coat Color and Protects Avy Mouse offspring from obesity by modifying the fetal epigenome. Environmental Health Perspective. Retrieved from: http://www.learnnc.org/lp/media/uploads/2013/11/ehp_epigenetics_worksheet_oct_2013.pdf. ARTIFACT 7 -­‐ METHYLATION IN TWINS
Figure 2. Differential DNA methylation between two sets of monozygotic twins, one set
at age 3 (left), one set at age 50 (right) using AIMS (amplification of inter- methylated
sites). Different bands, corresponding to sibling-specific changes of DNA methylation,
are indicated with arrows. (Panel A of Figure 2 in Fraga et al., 2005. Epigenetic
differences arise during the lifetime of monozygotic twins. PNAS
Source: 102:10604–10609. Copyright 2005 National Academy of Sciences, USA.
ARTIFACT 8A – DUTCH HUNGER FAMINE: LONG TERM AND
MULTIGENERATIONAL EPIGENETIC EFFECTS
PART A - Epigenetics and the Dutch Hunger Famine
Conditions in the uterus can give rise to life-long changes in genetic material.
People in their sixties who were conceived during the Hunger Winter of 1944-45 in
the Netherlands have been found to have a different molecular setting for a gene
which influences growth.
Epigenetics Search for food in the Hunger Winter
During the Hunger Winter (the Dutch famine of 1944-1945) the west of the
Netherlands suffered from an extreme lack of food. It now appears that the limited
food intake of mothers who were pregnant during this period altered the genetic
material of embryos in the early stages of development. The effects of this can still
be observed some sixty years later. These alterations are not changes in the
genetic code, but a different setting for the code which indicates whether a gene is
on or off. This is known as epigenetics. One of the main processes in epigenetics
is connecting the small molecule methyl to DNA.
Vulnerability The researchers compared the degree of methylation of a piece of DNA, the IGF2
gene, of people who were conceived in the Hunger Winter with that of their
brothers and sisters. They chose this particular gene because it plays an important
role during gestation. People in their sixties who were conceived during the Hunger
Winter have less methyl groups on the IGF2 gene than their siblings. This did not
apply to children of the Hunger Winter who were in later stages of gestation when
the famine occurred. They did have a lower birth weight than their siblings, but the
IGF2 gene was not 'packaged' differently. This indicates that epigenetic information
is particularly vulnerable in the early stages of pregnancy.
Source: http://www.news.leiden.edu/news/dutch-hunger-winter.html
ARTIFACT 8B – DUTCH HUNGER FAMINE: LONG TERM AND
MULTIGENERATIONAL EPIGENETIC EFFECTS
Part B: Long Term/Multigenerational Effects
One of the first aspects they studied was the effect of the famine on the birth weights of children who had been in the womb during that terrible period. If a mother was well fed around the time of conception and malnourished only for the last few months of the pregnancy, her baby was likely to be born small. If, on the other hand, the mother suffered malnutrition only for the first three months of the pregnancy (because the baby was conceived toward the end of the terrible episode), but then was well fed, she was likely to have anormal-­‐size baby. The fetus “caught up” in body weight. That all seems quite straightforward, as we are all used to the idea that fetuses do most of their growing in the last few months of pregnancy. But epi-­‐demiologists were able to study these groups of babies for decades, and what they found was really surprising. The babies who were born small stayed small all their lives, with lower obesity rates than the general popula-­‐tion. For forty or more years, those people had access to as much food as they wanted, and yet their bodies never got over the early period of malnutrition. Why not? How did their early life experiences affect these individuals for decades? Why weren’t they able to go back to normal once their environment reverted to the way it should be? More unexpectedly, the children whose mothers had been malnourished only early in pregnancy had higher obesity rates than normal. Recent reports have shown a greater incidence of other health problems as well, including effects on certain measures of mental health. Even though those individuals had seemed perfectly healthy at birth, something had happened to their devel-­‐opment in the womb that affected them for decades after. And it wasn’t just the fact that something had happened that mattered, it was when it happened. Events that take place in the first three months of gestation, a stage when the fetus is really very small and developing very rapidly, can affect an individual for the rest of his or her life. Even more extraordinarily, some of these effects seem to be present in the children of this group, that is, in the grandchildren of the women who were malnour-­‐ished during the first three months of their pregnancy. So something that happened in one pregnant population affected their children’s children. That raised the really puzzling question of how those effects were passed on to subsequent generations. Source: Carey, N. (2012) The epigenetics revolution: how modern biology Is rewriting our understanding of genetics, disease, and inheritance. Columbia University Press. Retrieved from: http://www.naturalhistorymag.com/features/142195/beyond-­‐dna-­‐epigenetics ARTIFACT 9 – GENETIC INFLUENCES ON TRAITS IN TWINS
Comparing Identical and Fraternal Twins: A higher percentage of disease incidence in both identical
twins is the first indication of a genetic component. Percentages lower than 100% in identical twins
indicates that DNA alone does not determine susceptibility to disease.
Source: http://learn.genetics.utah.edu/content/epigenetics/twins/