Who Is Epigenetics Relevant To Animal Production

Our surroundings influences our genome through the so-called epigenetic modifications. For example, with identical genetic heritages, two twins may evolve differently depending on their corresponding environments. There is growing evidence that our genes "heed " to the surroundings in circuitous ways that affect our health and behaviour. The diets, many  iterative diseases, the drugs and the toxins, anxiety and stress, our lifestyle & where we live tin can modify both the host cells and their DNA. Thus, in monozygotic twin pairs, large differences in life trajectory could be found. 1 could develop obesity and the other could remain thin; one could exist sane and the other could develop a mental illness. A few examples from animals and humans highlight the role of epigenetics [1] in the manual of acquired traits.

one. Methylation: the keystone of epigenetics

Information technology is now known that genes can be "turned on" or "off" by several types of chemical modifications that exercise not change the DNA sequence: Deoxyribonucleic acid methylations and histone modifications, those proteins on which Dna is wrapped to class chromatin [2]. All these modifications constitute "epigenetic marks" [3] grouped under the term epigenome (Figures 1 & 2). Epigenetic modifications are induced past the environment in the broad sense: the cell constantly receives all kinds of signals informing it about its environment, so that it specializes during development, or adjusts its activity to the situation (meet Epigenetics, the Genome and its Environment). These signals, including those related to our behaviours (diet, smoking, stress, etc.), can lead to changes in the expression of our genes, without affecting their sequence. The phenomenon may be transient, simply there are permanent epigenetic changes, which persist when the indicate that induced them disappears. Different genetic mutations, which are irreversible, epigenetic "tagging" can change. A simple change of environment tin can change the style the genes nosotros inherit at nativity, and therefore our "phenotype" [iv].

Figure 1. The modifications are materialized by biochemical marks, affixed by specialized enzymes (Dnmt or DNA methyltransferases) on the Dna or on the proteins that construction it, the histones (meet below). The all-time characterized brands are the methyl groups (CH3): one carbon atom and three hydrogen atoms) affixed to the DNA, likewise as various chemical modifications of histones (methylation, acetylation…). These minor "methyl" groups are sufficient to change the spatial organization of Deoxyribonucleic acid and thus forestall the expression of certain genes. The effect is reversible (demethylase action). Familiar nutrients similar folic acid, B vitamins, and SAM-eastward (Southward-Adenosyl methionine, a popular over-the-counter supplement) are key components of this methyl-making pathway. Diets high in these methyl-donating nutrients can speedily alter gene expression, especially during early evolution when the epigenome is first being established.

In addition, at that place is another scale in epigenetic processes since in that location is a gear up of regulatory elements of the epigenetic processes themselves. Either regulatory structures inserted into the DNA sequence, sometimes at slap-up distance from genes, or mobile small molecules called microRNAs (miRNAs) or interfering small RNAs are involved in many processes in eukaryotes (due east.thou. methylation elimination, chromatin assembly, and suppression of protein formation that are activated in immediate stress responses). Much smaller than messenger RNAs, these miRNAs prevent them from conveying their message, by neutralizing or destroying them.

Figure 2. Biochemical modification of histones with alter in chromatin structure due to methylation.

In other words, if the chromosome is the magnetic tape of a cassette and each gene corresponds to a track recorded on the tape, epigenetic modifications are pieces of repositionable adhesive tape that will mask or unmask sure tracks, making them unreadable or readable. Regarding the modifications that mask, nosotros speak about methylating agents, responsible for the methylation of DNA and histones (encounter to a higher place). On the other paw, other molecules have the effect of stimulating gene expression. These are called "acetyl groups" and are referred to as acetylating agents and histone acetylation.

2. What are the consequences for the beast kingdom?

2.1. General information

Some epigenetic marks are likely to pass to offspring. The intergenerational transmission of marks materialized by Dna methylation is well documented in plants. In mammals, the study of the phenomenon is much more circuitous and still controversial. In this paragraph and through some examples taken from animals (the Agouti mice, Drosophila red eyes and cross-adoption experiments in rats), we discover epigenetics equally a field studying the influence of the surround and private history on gene expression.

ii.two. The Agouti mouse model

Figure 3. The colour of the peel depends on the methylation country of a pocket-size sequence in the Avy gene present in the vicinity of the gene responsible for the colour: in the methylated state, the Agouti gene is suppressed, the colour volition exist brownish, but in the demethylated state, the gene volition be agile and the color xanthous. Several versions of this Agouti gene exist, which leads to different glaze colours, by modifying the level and type of pigment in the fur.

Information technology was not until the end of the twenty^th century that a type of mouse was discovered assuasive scientists to highlight the complex connections linking food to epigenetics. Amid the many genes that contribute to glaze color in mice, ane of them is called "Agouti". The most interesting version of the Agouti gene is known as "Agouti viable yellowish" or Avy (Figure 3). If the Avy gene has little or no methylation, it is agile in all cells, and mice are yellowish. These xanthous mice are susceptible to the development of diseases such as obesity, diabetes or sure cancers. But if Avy is hypermethylated, his expression "fades out", which implies that the mouse has a brown color, and has no health problems, fifty-fifty if it has exactly the aforementioned Agouti factor as yellow mice. Between these 2 extremes, Avy can exist methylated to varying degrees, which affects the level of activity of the cistron [v]. The result is a beautiful gradation of spotted mice, in which the activity of the Avy gene even differs from one cell to another. The same genetically identical litter of mice varies in colour according to this spectrum, due to epigenetic variations established in the uterus. In addition, regardless of coat color, it highlights the furnishings of diet on methylation. Randy Jirtle, an American researcher, has had a remarkable experience with these mice conveying the Agouti gene. By feeding them B vitamins, he did not "cure" these genetically ill mice, simply the beneficial effect was felt on the offspring [half dozen]. In other words, the offspring of mice carrying the Agouti cistron fed with B vitamins are no longer ill or even beige (the Agouti cistron is yet in that location, but it is no longer expressed), while the offspring of those who have not received B vitamins remain sick from generation to generation!

2.3. Drosophila and red eyes

Figure 4. Portrait of JB Lamarck (1744 –1829)

Drosophila are insects ordinarily used in the laboratory. Their genome is relatively simple to sympathise and as a result, they are the "stars" of genetic research… In April 2009, Dr Renato Paro, from the University of Basel, appear a wonderful new discovery concerning them: if a fruit fly egg is heated to 37° degrees before hatching, the fly has red eyes. Otherwise, her eyes are white….. Better! The "red eye" character has been passed down from generation to generation. It is therefore a characteristic acquired through the influence of an external factor (temperature) that becomes hereditary [7]. These animal studies, like the post-obit studies, seem to back up the scientific theory represented by Lamarckism. According to his famous publication – "The Influence of Circumstances" – published in 1809-1810 [viii], Lamarck supports the idea that physical changes acquired during an individual'south lifetime could be transmitted to his descendants [9]. However, in humans we have no testify of the persistence of these epigenetic effects beyond a few generations. These results do not therefore really phone call into question the Darwinian conception of the long-term evolution of species through the action of natural choice on accidental hereditary variations (run across Theory of development: misunderstandings and resistance & Adaptation: responding to environmental challenges).

two.4. Mouse mothering: beyond the uterus

Do simple caresses also have the power to influence genes? In rats, licking fulfils the same office equally caressing in humans. However, studies show that babe rats often licked by their mothers are calmer. But at Mc Gill University in Montreal (Canada), Professor Michael Meaney's team went much further by revealing footprints of this maternal care into the brains of immature rats, at the hippocampus level [10].

In fact, information technology is the "licking" that influences the action of a factor that protects rats against stress. This gene, called NRC31, produces a protein (glucocorticoid receptor GC) that helps to reduce the concentration of stress hormones (cortisol) in the body [11]. However, a specific portion of this gene must exist activated using the epigenetic switch represented past DNA methylation. Analysis of the brains of rats that did not receive enough amore by licking demonstrated this: the switch linked to the NRC31 gene (gene coding for the glucocorticoid receptor) was defective (gene that had undergone methylation, and therefore inactive) in the neurons of the rats hippocampus (a encephalon area that incorporates ambient stresses). Every bit a upshot, the amount of stress hormones (cortisol) increases in the blood and therefore, fifty-fifty in the absence of disruptive elements, they live in a land of constant stress.

Effigy 5a. Experiment past Weaver et al. demonstrating the behavioural programming of epigenetic status as a function of maternal behaviour.

Figure 5b. Cross-Fostering Experiments: Maternal licking, grooming and breastfeeding behaviour in rats will attune epigenetic regulation of the glucocorticoid receptor locus in young co-ordinate to its intensity. Stable differences in maternal behaviour during the first calendar week of life, which is a critical menstruum for the evolution of the nervous system, volition induce different phenotypes in the immature in terms of response to stress.

3. Touch on of food on our genes

Figure half-dozen. During the Dutch famine, the inhabitants ate an boilerplate of 500 calories per 24-hour interval (about a quarter of the minimum necessary for a human being).

In club to show the link betwixt epigenetics and diet, especially in humans, let's go back to the history of the dramatic "Dutch hunger famine of 1944". It offers scientists a kind of life-size laboratory to test these hypotheses. During the winter of 1944-1945, the due west of the netherlands was starving due to a blockade by Nazi Federal republic of germany [12].

Studies have shown that children of significant women exposed to this famine got pathologies such every bit diabetes, obesity, cardiovascular disease, microalbuminuria (albumin in the urine), etc. In addition, they were smaller than normal. Every bit adults, they then had smaller than average children too! [13].

These data propose that the famine experienced past mothers caused epigenetic changes that were passed on to subsequent generations. Their genetic heritage had kept runway of this event, which supports the theory that an individual's wellness is partly programmed past the environment to which the foetus is exposed in the uterus. We at present know that these effects on size come from changes in the epigenetic markers present on their DNA, linked to deficiencies in certain crucial molecules in the diet of Dutch grandmothers during this period. Indeed, in club to faithfully maintain a good level of methylation during cell divisions, new methyl groups must exist added to the newly copied Dna. However, this constant supply of methyl groups comes directly from our nutrient from amino acids and vitamins (such as methionine, betaine or choline). In addition, we can also manufacture "methyl" groups from chemical precursors such as folic acid.

But in 2008, researchers further elucidated these epigenetic changes [14] : individuals who have experienced famine in utero accept fewer methyl groups attached to the gene that controls the production of a growth gene, IGF-2 (insulin-likegrowth gene-2). Other chemical elements from our food are also needed to transport methyl groups through the trunk and carefully attach them to Dna: zinc, vitamin B12…

iv. What lessons can be learned from this?

While the genome is fixed, the epigenome is much more dynamic. Epigenetic modifications would allow individuals to quickly explore an adaptation to a change in the environment, without "engraving" this adaptive change into the genome. The challenges of epigenetics concern not only medicine and public health (run into Epigenetics, the Genome and its Surroundings) but also evolution (see Theory of evolution: misunderstandings and resistance). Indeed, it casts suspicion on the environment that could modulate the action of some of our genes to modify our traits, or fifty-fifty induce certain diseases potentially transmissible to offspring. Clearly, the Dutch famine of the winter of 1944-1945 shows that permanent changes take occurred in the genetic heritage of the women who were pregnant at this time and then passed on from generation to generation. This would mean that the trauma also affects the germ cells (sperm and eggs), the just biological link betwixt generations.

Information technology is now widely accepted that epigenetic abnormalities contribute to the evolution and progression of human diseases, in item cancers. Epigenetic processes are involved in the regulation of many events such equally jail cell sectionalization, differentiation (specialization of cells in a particular office), survival, mobility… The alteration of these mechanisms promotes the transformation of healthy cells into cancer cells, whatsoever epigenetic aberration tin can be involved in carcinogenesis. Epigenetic abnormalities activating oncogenes (genes which overexpression promotes carcinogenesis) or inhibiting tumor suppressor genes have been identified. Similarly, mutations affecting genes encoding the enzymes responsible for epigenetic markings take been identified in tumour cells. It remains to be seen whether these phenomena are the crusade or consequence of cancer development. All the same, information technology seems that they participate in tumor progression (or cancer progression).

In improver, the role of epigenetics is suspected and extensively studied in the development and progression of complex and multifactorial diseases, such every bit neurodegenerative diseases (Alzheimer'due south, Parkinson's, amyotrophic lateral sclerosis, Huntington…) or metabolic diseases (obesity, type 2 diabetes…). In the same mode that we now know how to obtain the sequence of a consummate genome, it is also possible to know all the epigenetic modifications that narrate it: we speak of an epigenome. It is this blazon of global and unbiased approach that volition brand it possible to improve understand the involvement of epigenetics in human diseases…

What near telomerases?
In improver to the epigenetic processes discussed more than than 50 years agone by the British biologist Conrad Waddington (1905-1975) [xv] and mentioned above, we must mention a phenomenon of crucial importance, and sensitive to our environment. This is a major discovery in molecular biology initiated by Elizabeth Blackburn and Carol Greider, the laureates of the 2009 Medicine & Physiology Nobel Prize: the identification of an enzyme called telomerase. This enzyme regulates the length ofthe " telomers", which are repeated segments of non-coding DNA, located at the end of each chromosome (see focus Slowing down aging: the telomerase rails?). These telomeres tin be represented as the pocket-sized plastic pieces that protect the tips of your shoelaces and are called "aglets". These telomers form small caps at the ends of the chromosomes, preventing the genetic material from "fraying". These are, among other things, the aglets of aging and they tend to shorten over time. Thus, under the influence of telomerase, telomeres can finish shortening and fifty-fifty lengthen. Crumbling is therefore a dynamic process that can be accelerated or slowed down. The piece of work of Elizabeth Blackburn and nutritionist medical doctor Dean Ornish has clearly shown the effects of lifestyle changes on the lengthening of these telomeres (see focus Slowing down aging: the telomerase track?) [xvi].

In conclusion, the importance of the role of the surround in epigenetic heredity is far from being resolved, despite the proclamation effects that have led to a renewed interest in Lamarck's thesis of "the heritability of acquired traits" (come across Lamarck and Darwin: two divergent visions of the living world). The ultimate research is that of the importance of epigenetic processes in Evolution. The scientific customs remains divided and a central question remains: are epigenetic states transmitted over a sufficient number of generations to give rise to natural pick? Practice doctors and sociologists inquire another one, which interests us in the brusk and medium term: Does our lifestyle matter more than our heredity?

---

References and notes

Cover image. These twins have the same genotype, but their epigenotype and phenotype are different because they did not live in the verbal aforementioned environs. [Source : Photo © Peter Voerman photography via Visual Hunt / CC By-NC.]

[ane] Epigenetics: All changes in cistron action that are transmitted over cell divisions or over generations without the utilize of Dna mutations. This "memory of gene activeness" is based on chromatin states, or "epigenetic marks".

[2] Chromatin: A basic substance of chromosomes consisting of the DNA molecule associated with proteins called "histones", around which information technology is wrapped.

[3] Epigenetic marks: Chemic modifications of Dna or associated proteins in chromatin. These modifications (e.g. cytosine methylation or C) contribute to the control of cistron activity without affecting the nucleotide sequence, the "letters" (A, T, C or G) that write the gene bulletin on the DNA.

[4] Jablonka E & Lamb G (2005) Evolution in four dimensions. Cambridge MA. MIT press

[5]  Morgan Hd et al. (1999) Epigenetic Inheritance at the agouti locus in the mouse. Nature genetics 23: 314-318

[vi] Jirtle, RL & Tyson, FL, eds. (2013) Environmental Epigenomics in Wellness and Affliction: Epigenetics and Complex Diseases Origins, Heidelberg: Springer

[7] Thou & R Paro Shit (2009) About Combs, Notches, and Tumors: Epigenetics Meets Signaling. Developmental Cell 17: 440-442

[8] Lamarck JB (1809-1810) Influence des circonstances sur les actions des animaux (5^eastward leçon), Muséum National d'Histoire Naturelle de Paris (in french)

[ix] Evolution according to Charles Darwin (1809-1882): Species evolve every bit a issue of "variations" (character changes) that occur randomly, and are transmitted to descendants. Simply the advantageous ("adaptive") variations are selected by the environment: this is "natural selection". Evolution according to Jean-Baptiste de Lamarck (1744-1829): The surround would dictate a beneficial change for the individual, which would be transmitted to his descendants. This "heredity of caused traits" would govern the evolution of species.

[x] Francis D et al (1999) Nongenomic transmission across generations of Maternal behavior and stress in the rat. Science 1155-1158

[11] Weaver IC et al (2004) Epigenetic programming by maternal behavior. Nature Neuroscience seven: 847-854

[12] Lumey LH et al (2007) Cohort profile: The dutch Hunger Winter Families Study. Int J Epidemiol. 36: 1196-1204

[13] Stein AD et al (2004) Intrauterine famine exposure and body proportions at birth: the Dutch Hunger Winter. Int J Epidemiol 33: 831-836

[14] Heijmans BT et al (2008) Persistent epigenetic differences associated with prenatal exposure to famine in humans. PNAS 17046-17049

[15] Baedke J (2013) The epigenetic landscape in the course of fourth dimension: Conrad Hal Waddington's methodological bear upon on the life sciences. Studies in History and Philosophy of Science Part C: Studies in History and Philosophy of Biological and Biomedical Sciences 44 : 4 Office B 756-773

[16] Ornish D et al. (2008) Increased telomerase activity and comprehensive lifestyle changes: a pilot study. Lancet Oncol. 2008 9(11):1048-57

---

The Encyclopedia of the Surroundings past the Association des Encyclopédies de l'Environnement et de l'Énergie (www.a3e.fr), contractually linked to the University of Grenoble Alpes and Grenoble INP, and sponsored by the French Academy of Sciences.

To cite this article: DROUET Emmanuel (2022), Epigenetics: How the surroundings influences our genes, Encyclopedia of the Surroundings, [online ISSN 2555-0950] url : https://www.encyclopedie-environnement.org/en/health/epigenetics-how-the-environs-influences-our-genes/.

The articles in the Encyclopedia of the Surround are made available under the terms of the Creative Eatables Past-NC-SA license, which authorizes reproduction subject to: citing the source, not making commercial use of them, sharing identical initial conditions, reproducing at each reuse or distribution the mention of this Artistic Commons BY-NC-SA license.

Source: https://www.encyclopedie-environnement.org/en/health/epigenetics-how-the-environment-influences-our-genes/

Posted by: camposbaccomithe.blogspot.com

Share this post