Epigenetics and Human Reproduction (Epigenetics and Human Health)

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John Huntriss: Epigenetics, imprinting and assisted reproduction

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Epigenetics and Reproductive Medicine

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Williams, R. Flavonoids: antioxidants or signalling molecules? Witcher, M. Cell 34, — Epigenetic influence over gene expression possibly originated as a defence against Transposons, parasitic DNA that jumps around in the genome and can disrupt genes by inserting into the middle of them Slotkin and Martienssen, A possible mechanism of defence can be achieved via methylation of DNA, as illustrated in Fig.

Eventually this process evolved into a method of promoting and repressing host genes Feinberg, that could not only be acquired throughout the lifetime of an individual, but also passed onto its offspring Jones, This mechanism of gene silencing may have also allowed for the development of multicellular organisms by allowing a single genome to tailor its expressed genes in each individual cell within the larger organism Badyaev, Methylation as a defence against Transposons.

The figure illustrates how methylation can help an organism defend itself from Transposons. While epigenetics is a relatively new understanding of the systems involved in gene control and expression it also represents something very important, a fundamental revaluation of the theory of evolution. Acquired traits, while not alterations of the genome, can be inherited Jones, This review will examine the implications this has for the concept of human evolution and highlight interesting examples and case studies in which these effects are notable. The study of epigenetics has revealed an interesting facet of this method of gene expression control.

The methylation of DNA and other epigenetic marks do not alter the genes that they influence at a sequence level but nonetheless alter the expression of these genes. Furthermore these marks can be acquired throughout the lifetime of the individual and, if carried in their gametes, these marks are inheritable. In this section, the focus will be on the ways in which these marks can be inherited. The semi-conserved nature of mitosis results in two sets of daughter chromatids, one in each set carrying the Epigenetic marks from the original chromosome Feinberg, , as illustrated in Fig.

This allows the transfer of epigenetic marks from mother cells to daughter cells in somatic tissue. This explains how these marks can be maintained in an individual, but not how they are spread to the next generation of offspring.

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As can be seen in A the original chromosome contains epigenetic marks on both chromatids, and in B both daughter chromosomes contain some of the epigenetic marks of the mother chromosome due to the semi-conserved nature of mitosis. These marks can also be conserved in their daughter chromatid during meiosis, resulting in all gametes carrying the epigenetic marks of the individual of origin. However, many of these marks are removed during the process of gamete formation. Methylation marks can be inherited from either the maternal Giuliani et al.

Through the father, the offspring can inherit a wide array of methylation marks, with the majority of these marks in some way affecting the digestive systems of the child Soubry, For an example of this deleterious nature of hypomethylation one can look at the Dutch Winter of Hunger, a well-documented example of famine in the modern world that occurred from to due to a blockage preventing the movement of fuel and food in the Netherlands.

This starvation resulted in the hypomethylation of the IGF-2 gene, the gene responsible for the formation of insulin-like growth factor 2. The ability of parental malnutrition to affect the epigenome of the offspring in an overtly negative and harmful way will be examined more closely later in the review. This was very useful and advantageous for nomadic peoples and a case study of this can be seen in the comparison of the Oromo peoples and the Amhara peoples of Ethiopia Alkorta-Aranburu et al.

In this case it appears that epigenetic marks actual favour immunological variation within the newly arrived population.

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This will be examined in more depth as part of the Case studies section later in the review. This will eventually result in a population that is genetically similar to the original settlers but will be more adapted to their surrounding environment. To understand the impact epigenetics has had on our development into modern humans we have to compare the areas of gene methylation seen in our species and our closest living relatives. Many of the regions in the human genome that are methylated are not genes that are unique to humans, with the biggest differences in methylation occurring in regions of DNA involved with Transcription Factors or TFs and gene control Hernando-Herraez et al.

This is because TFs have a wide-reaching influence on the expressed phenotype of an individual due to these factors functioning as a form of gene expression regulation, therefore promoting or suppressing other genes in the genome. Even small differences in the epigenome surrounding TFs can result in widely varying phenotypes between individuals of the same species due to their wide-reaching influences Heyn et al. So it can only be assumed just how important these phenotypic changes are in the variation that separates us from our ancestor species.

HARs are regions of DNA that have undergone rapid changes since the emergence of the human species far and above the normal rate of mutation. These regions stand out due to the extremely accelerated rate of mutations they have undergone and are widely understood to be responsible for the speedy divergence of humans from other species Hubisz and Pollard, The exact nature of the role played by epigenetic changes in HARs is not clear but the importance of their role is undoubtable, with epigenetic changes possibly predating sequential changes in DNA Badyaev, A suggested theory is that these marks actually promoted the occurrence of mutations in the genes that are responsible for our species existence.

Studying the epigenomes of our related species sheds light on the relatively large divergence that has occurred since our emergence from our distant cousins, a divergence of such stature that it cannot be solely explained by nucleotide changes Hernando-Herraez et al. It has even been speculated that epigenetic changes could be more impactful on the Darwinian evolution of a species than genomic mutations Badyaev, and this area of research only adds more weight to these claims. Modern humans have survived and thrived in a wide array of environments for thousands of years, from the Arctic tundra to Saharan deserts.

The key to this success has always been the uniquely human ability to adapt quickly and epigenetics has played a role in this capacity to adapt. While cultural adaptations to environments, such as changes in clothing or ritualistic behaviour, are the most visual signs of this adaptability, no less important are the more subtle genetic and epigenetic changes that a population undergoes as they live in an area for generations. For example a population that has lived in an arid environment will carry many genetic mutations that make them more suitable to a dry climate.

If a catastrophic climate shift occurs and their ancestral lands suddenly become cold and damp they can adapt to wear thicker clothing Cavalli-Sforza and Feldman, to protect against the cold and may even take on new customs and rituals around hygienic behaviour to protect against new diseases that have taken root in the region Wiesenfeld, This population will however still carry many of the genetic mutations that made them suited to their old environment until selection pressure allows new mutations to compensate for these genetic relics.

An important idea is the way in which to consider each different type of adaptation in comparison to one another. Cultural adaptation is a catch all term that encompasses all artificial adaptations an individual can pick up to become more comfortable in an environment Cavalli-Sforza and Feldman, In comparison genetic changes, such as the prevalence of Sickle Cell Anaemia in regions prone to malaria outbreaks, represent much longer term adaptations.

These changes take longer to gain and cannot as easily be shaken off once their usefulness has run its course, such as an individual simply changing their attire to suit the weather Laland, Odling-Smee, and Myles, What do epigenetic changes represent in this model then? Firstly they exemplify medium-term adaptations, falling between cultural changes and genetic evolution in the time it takes an individual to acquire them Giuliani et al.

In this model of understanding human adaptation epigenetic changes also serve as a time-keeping mechanism, helping to mitigate the negative effects of genetic relics acquired by ancestor populations under different evolutionary pressures Badyaev, By silencing older genes that once served a vital purpose epigenetics also helps to prevent the build-up of complexity in an organism, silencing older, less frequently transcribed genes Badyaev, , much in the same way that DNA methylation combats the damage caused by transposons Slotkin and Martienssen, A good way to examine this model of adaptation is to consider the way each of these changes would affect a hypothetical population that has suddenly become exposed to a harsh, cold climate.

Very quickly, this population will adapt, first by increasing their protection against the elements by wearing thicker clothes. While this is an effective method of staying warm their bodies have not yet adapted to the cold, and so, their genes controlling homoeostasis will still function in the same way as they had in a warmer climate, something that might be considerably wasteful and possibly deleterious.

Where once their perspiration would help keep the heat from damaging their bodies it now wastes water. At this stage, after a considerable number of generations, epigenetic changes will begin to take affect under selective pressure. DNA methylations and histone modifications will accumulate, fine tuning their homoeostatic gene expression to the colder environment.

This results in the silencing of genes that were better suited to the hotter climate and promotes the expression of other genes that confer an advantage in this colder one. Finally, after even more generations new alleles will take hold in the populations that represent novel genes. These novel genes will encode new proteins that in some way will provide a selective advantage that is near permanent in expression, if not in providing an advantage. Another point highlighted by this model is that the longer an adaptation takes to be acquired the less likely it is to ever be lost.

After all, it is much easier to take a jacket off than to spontaneously lose a gene responsible for increasing metabolic activity. Epigenetics comes in yet again at this point as not only does it silence older genes that are no longer required, under the influence of selective pressure, it also introduces more plasticity into the expression of genes Giuliani et al. Through this mechanism epigenetics allows the variability of phenotypes that are required for adaptation and selection Tobi et al. Since genome-wide profiling in some cases does not give a sufficient answer to explain the complex biological processes in autoimmune disorders, epigenetic modifications are retained additional regulators in immune responses Fig.

Epigenetic dysregulation directly influences the development of autoimmunity by regulating immune cell functions [ 2 ]. The recognition of the complexity of the interaction between epigenetic events and the alteration of the immune system in autoimmune disorders is a prominent challenge for the discovery of novel potential therapeutic strategies. Epigenetic mechanisms, such as DNA methylation, chromatin remodeling, and noncoding RNAs, have been identified as crucial regulators in cellular immunity, owing to their mechanisms in modulating gene expression and transcription in targeted cells and tissues [ 3 ].

Extensive evidences indicate that autoimmune diseases are mainly an interplay of genetic and non-genetic factors, although the role of the latter ones often remains unclear. Over the last decade, the influence of epigenetic modifications on innate and adaptive immunity has been intensively investigated, especially in autoimmune disorders. Histone modifications Histone-modifying enzymes have an essential role in modulating chromatin compaction state, nucleosomal processes, and DNA repair [ 16 — 18 ].

Autoimmune diseases are characterized by an immune response to antigenic components of the host itself autoantigens. Two main types of autoimmune diseases can be distinguished: on the one hand, the systemic ones and on the other, the organ-specific ones. In systemic diseases, the immune system attacks in a generalized manner its own antigens in several organs, while in organ-specific diseases the immune response is directed towards a single organ. Table 1 Most relevant autoimmune diseases with known autoantigen targets. Rheumatoid arthritis Joints, lung, heart, etc.

IgG, filaggrin, fibrin etc. Dermal fibroblast antigens, fibrillarin-1, metalloproteinases, etc. Antibody 0. Autoimmunity is defined by the breakdown of self-tolerance that produces a state of abnormal humoral and cell-mediated responses against self-components. Until now, no effective treatments have been identified for SARDs, even though the use of glucocorticoids has been considered as a first-line therapy.

Nowadays, however, antimalarial and immunosuppressive drugs are most commonly used due to their limited long-term side effects. Such autoimmune disorders are often associated with an autoimmune dysregulation which determines morbidity and, in most cases, premature mortality [ 35 , 36 ]. In particular, most of these conditions happen when the immune system produces autoantibodies ANA directed against intracellular antigens. Understanding the molecular mechanisms of SARDs appears to be extremely important to achieve beneficial outcomes in these chronic conditions.

Characterization of epigenetic modifications that occur across these autoimmune diseases may yield valuable insights into their pathogenesis and treatment. Thus, in an attempt to determine the most important epigenetic changes in SARDs, researchers investigated the role of epigenetic processes in regulating autoimmunity. Up to now, blockers of the immune response produced a greater success in the clinical use than treatments exploiting natural immune regulation.

In fact, blocking the immune response is crucial in autoimmunity, even though immunosuppression leads to various side effects, including the reactivation of latent infections and the reduction of immunosurveillance. Thus, antigen-specific immune therapeutical options, instead of rather unspecific therapies targeting the immune system, are an important goal to reach towards the treatment of autoimmune disorders. Importantly, the discovery of an epigenetic therapy to treat such autoimmune disorders may unearth potential biomarkers for disease diagnosis and prediction. Table 4 Effects of Epi-drugs on autoimmune disorders discussed in this review.

Acknowledgments Not applicable. Availability of data and materials Not applicable. Ethics approval and consent to participate Not applicable. Consent for publication Not applicable. Competing interests The authors declare that they have no competing interests. References Bird A. Perceptions of epigenetics. Role of epigenetics in biology and human diseases.

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Epigenetics in autoimmunity - DNA methylation in systemic lupus erythematosus and beyond.

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Epigenetics and autoimmunity. The epigenetics of autoimmunity. Cell Mol Immunol. Epigenome profiling reveals significant DNA demethylation of interferon signature genes in lupus neutrophils. Primer: epigenetics of autoimmunity. Nat Clin Pract Rheumatol. Mechanism of drug-induced lupus. Cloned Th2 cells modified with DNA methylation inhibitors in vitro cause autoimmunity in vivo.

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