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Introduction to

Watch 1st YouTube: Epigenetics 9:20 minutes https://youtu.be/kp1bZEUgqVI

Summary points from 1st YouTube: Epigenetics is the study of heritable phenotype changes that do not involve alterations in the DNA sequence. The term “epigenetics” has been used since the 1990s, but significant discoveries in 2007 led to its current usage. So epigenetics, which means “above genetics,” is a brand new science, and deals with the various mechanisms involved in .

Gene expression occurs several ways. Adding a methyl group acts like a light switch, and turns genes on or off. Gene expression is also controlled by , small proteins that work like a light dimmer knob, changing the degree of expression. Histones are spools that DNA winds around. Histones can tighten or loosen the strand. Loose strands allow more DNA to be read, and tight strands cause less DNA to be read.

The DNA is the genome, and may be thought of as the hard drive of our bodies. The epigenome correlates to the computer software, telling the genome what to do. It can change throughout life. Our environment, stress, diet, habits (smoking, alcohol, etc) all can change our epigenome.

Most of the epigenetic information of the parent is stripped off a few days after birth, but some of the the parents’ epigenome stays with the offspring. Epigenetic disease information that did not appear in our primitive ancestors is learned and passed down by the epigenetic information from our parents.

Watch 2nd YouTube: Epigenetic transformation -- you are what your grandparents 21:14 minutes https://youtu.be/Udlz7CMLuLQ

Summary points from 2nd YouTube: These epigenetic changes may last through cell divisions for the duration of the cell's life, and may also last for multiple generations even though they do not involve changes in the underlying DNA sequence of the organism.

One example of an epigenetic change in eukaryotic biology is the process of cellular differentiation. During morphogenesis, totipotent stem cells become the various pluripotent cell lines of the embryo, which in turn become fully differentiated cells. In other words, as a single fertilized egg cell – the zygote – continues to divide, the resulting daughter cells change into all the different cell types in an organism, including neurons, muscle cells, epithelium, endothelium

2 of 9 of blood vessels, etc., by activating some genes while inhibiting the expression of others.

Gene expression can be controlled through the action of repressor proteins that attach to silencer regions of the DNA. These epigenetic changes may last through cell divisions for the duration of the cell's life, and may also last for multiple generations even though they do not involve changes in the underlying DNA sequence of the organism.

Watch 3rd YouTube: Gene Silencing by microRNAs 4.53 minutes https://youtu.be/t5jroSCBBwk

Summary points from 3rd YouTube: MicroRNAs (miRNAs) are members of non-coding RNAs that range in size from 17 to 25 nucleotides. MicroRNAs regulate a large variety of biological functions in plants and animals. As of 2013, about 2000 miRNAs have been discovered in humans (these can be found online in a miRNA database). Each miRNA expressed in a cell may target about 100 to 200 messenger RNAs that it downregulates. Most of the downregulation of mRNAs occurs by causing the decay of the targeted mRNA, while some downregulation occurs at the level of translation into protein.

You can inherit from your parents and their parents. Cancer: a variety of epigenetic mechanisms cause different types of cancer.

Diabetic wound healing: epigenetic modifications have given insight into the understanding of the pathophysiology of different disease conditions like wound healing in diabetic patients.

Stress: is passed on to the next generations by epigenetic tags from parents.

Addiction: is a disorder of the brain's reward system which arises through transcriptional and neuroepigenetic mechanisms.

Anxiety: is the transgenerational epigenetic inheritance of anxiety-related phenotypes and has been reported in preclinical studies. The transmission of paternal stress- induced traits across generations involved small non-coding RNA signals transmitted via the male germline.

Depression: epigenetic inheritance of depression-related phenotypes has also been reported in a preclinical study.

Fear conditioning: studies on mice have shown that certain conditional fears can be inherited from either parent.

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Other non-coding RNAs sRNAs are small (50–250 nucleotides), highly structured, non-coding RNA fragments found in bacteria. They control gene expression including virulence genes in pathogens and are viewed as new targets in the fight against drug- resistant bacteria.They play an important role in many biological processes, binding to mRNA and protein targets in prokaryotes.

(Ted Talks) What you can do to prevent Alzheimer's | Lisa Genova https://youtu.be/twG4mr6Jov0

What Parkinson’s Taught Me | Emma Lawton | TEDxSquareMile https://youtu.be/Hs-vPqfsO0Q

The protein folding problem: a major conundrum of science: TED https://youtu.be/zm-3kovWpNQ

Genetics and Parkinson's disease | Nervous system diseases | NCLEX-RN | Khan Academy https://youtu.be/FsE3QvWqeqs

Specific epigenetic processes include: paramutation, bookmarking, imprinting, gene silencing, X chromosome inactivation, position effect, DNA methylation reprogramming, transvection, maternal effects, the progress of carcinogenesis, many effects of teratogens, regulation of modifications and heterochromatin, and technical limitations affecting parthenogenesis and cloning.

https://youtu.be/i9a-ru2ES6Y https://youtu.be/UMFUQkN0ecU In epigenetics, a paramutation is an interaction between two alleles at a single locus, whereby one allele induces a heritable change in the other allele.[1] The change may be in the pattern of DNA methylation or histone modifications.[2] The allele inducing the change is said to be paramutagenic, while the allele that has been epigenetically altered is termed paramutable.[1] A paramutable allele may have altered levels of gene expression, which may continue in offspring which inherit that allele, even though the paramutagenic allele may no longer be present.[1] Through proper breeding, paramutation can result in sibling plants that have the same genetic sequence, but with drastically different phenotypes. https://youtu.be/XohX8Ke1maI Bookmarking (also "gene bookmarking" or "mitotic bookmarking") refers to a potential mechanism of transmission of gene expression programs through cell division.

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During mitosis, gene is silenced and most transcription factors are removed from chromatin.[1][2] The term “bookmarking” compares transcription to reading from a book. The pause in transcription during mitosis is like closing the book. "Molecular bookmarks" are the factors that allow transcription to resume in an orderly fashion in newborn cells following mitosis (when the book is re-opened). Bookmarks fulfill the following criteria: • at some point prior to the onset of mitosis, the promoters of genes that exist in a transcription-competent state become "marked" in some way, • this "mark" persists both during and after mitosis, and • the marking transmits gene expression memory by preventing the mitotic compaction of DNA at this locus, or by facilitating reassembly of transcription complexes on the , or both. https://youtu.be/3hBoNGozlCo is an epigenetic phenomenon that causes genes to be expressed in a parent-of-origin-specific manner. Forms of genomic imprinting have been demonstrated in fungi, plants and animals. As of 2014, there are about 150 imprinted genes known in the mouse and about half that in humans. Genomic imprinting is an inheritance process independent of the classical Mendelian inheritance. It is an epigenetic process that involves DNA methylation and histone methylation without altering the genetic sequence. These epigenetic marks are established ("imprinted") in the germline (sperm or egg cells) of the parents and are maintained through mitotic cell divisions in the somatic cells of an organism.[8] Appropriate imprinting of certain genes is important for normal development. Human diseases involving genomic imprinting include Angelman syndrome and Prader–Willi syndrome.

https://youtu.be/J2Y_S4EkLy8 https://youtu.be/5YsTW5i0Xro Gene silencing is the regulation of gene expression in a cell to prevent the expression of a certain gene.[1][2] Gene silencing can occur during either transcription or translation and is often used in research.[1][2] In particular, methods used to silence genes are being increasingly used to produce therapeutics to combat cancer and diseases, such as infectious diseases and neurodegenerative disorders. Gene silencing is often considered the same as gene knockdown.[3][4] When genes are silenced, their expression is reduced.[3][4] In contrast, when genes are knocked out, they are completely erased from the organism's genome and, thus, have no expression.[3][4] Gene silencing is considered a gene knockdown mechanism since the methods used to silence genes, such as RNAi, CRISPR, or siRNA, generally reduce the expression of a gene by at least 70% but do not completely eliminate it. Methods using gene silencing are often considered better than gene knockouts since they allow researchers to study essential genes that are required for the animal models to survive and cannot be removed. In addition, they provide a more complete view on the development of diseases since diseases are generally associated with genes that have a reduced expression.[3]

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https://youtu.be/veB31XmUQm8 X-inactivation (also called lyonization) is a process by which one of the copies of the X chromosome present in female mammals is inactivated. The inactive X chromosome is silenced by its being packaged in such a way that it has a transcriptionally inactive structure called heterochromatin. As nearly all female mammals have two X chromosomes, X-inactivation prevents them from having twice as many X chromosome gene products as males, who only possess a single copy of the X chromosome (see dosage compensation). The choice of which X chromosome will be inactivated is random in placental mammals such as humans, but once an X chromosome is inactivated it will remain inactive throughout the lifetime of the cell and its descendants in the organism. Unlike the random X-inactivation in placental mammals, inactivation in marsupials applies exclusively to the paternally derived X chromosome.

https://youtu.be/oEa4ja9mogE Position effect is the effect on the expression of a gene when its location in a chromosome is changed, often by translocation. This has been well described in Drosophila (fruit fly) with respect to eye color and is known as position effect variegation (PEV).[1] The phenotype is well characterized by unstable expression of a gene that results in the red eye coloration. In the mutant flies the eyes typically have a mottled appearance of white and red sectors. These phenotypes are often due to a chromosomal translocation such that the color gene is now close to a region of heterochromatin. The heterochromatin can spread stochastically and switch off the color gene resulting in the white eye sectors. Position effect is also used to describe the variation of expression exhibited by identical transgenes that insert into different regions of a genome. In this case the difference in expression is often due to enhancers that regulate neighboring genes. These local enhancers can also affect the expression pattern of the transgene. Since each transgenic organism has the transgene in a different location each transgenic organism has the potential for a unique expression pattern.

https://youtu.be/B5DU9lgbsSE https://youtu.be/SrqmuYvk3iQ https://youtu.be/IGOWdrF20iE In biology, reprogramming refers to erasure and remodeling of epigenetic marks, such as DNA methylation, during mammalian development or in cell culture.[1] Such control is also often associated with alternative covalent modifications of histones. DNA methylation patterns are largely erased and then re-established between generations in mammals. Almost all of the methylations from the parents are erased, first during gametogenesis, and again in early embryogenesis, with demethylation and remethylation occurring each time. Demethylation of early embryogenesis occurs in the preimplantation period in two stages – initially in the zygote, then the first few embryonic replication cycles of morula and blastula. A wave of methylation then takes place during

6 of 9 the implantation stage of the embryo, with CpG islands protected from methylation. This results in global repression and allows housekeeping genes to be expressed in all cells. In the post-implantation stage, methylation patterns are stage- and tissue-specific with changes that would define each individual cell type lasting stably over a long time.[2] https://youtu.be/cPA2OQv8qA8 https://youtu.be/noNJjOthtJ8 Transvection is an epigenetic phenomenon that results from an interaction between an allele on one chromosome and the corresponding allele on the homologous chromosome. Transvection can lead to either gene activation or repression. It can also occur between nonallelic regions of the genome as well as regions of the genome that are not transcribed. The first observation of mitotic (i.e. non-meiotic) chromosome pairing was discovered via microscopy in 1908 by Nettie Stevens.[1] Edward B. Lewis at Caltech discovered transvection at the bithorax complex in Drosophila in the 1950s.[2] Since then, transvection has been observed at a number of additional loci in Drosophila, including white, decapentaplegic, eyes absent, vestigial, and yellow.[3][4] [5][6][7] As stated by Ed Lewis, "Operationally, transvection is occurring if the phenotype of a given genotype can be altered solely by disruption of somatic (or meiotic) pairing. Such disruption can generally be accomplished by introduction of a heterozygous rearrangement that disrupts pairing in the relevant region but has no position effect of its own on the phenotype" (cited by Ting Wu and Jim Morris 1999[8]). Recently, pairing-mediated phenomena have been observed in species other than Drosophila, including mice, humans, plants, nematodes, insects, and fungi. In light of these findings, transvection may represent a potent and widespread form of gene regulation.[9][10] Transvection appears to be dependent upon chromosome pairing. In some cases, if one allele is placed on a different chromosome by a translocation, transvection does not occur. Transvection can sometimes be restored in a translocation homozygote, where both alleles may once again be able to pair. Restoration of phenotype has been observed at bithorax, decapentaplegic, eyes absent, and vestigial, and with transgenes of white. In some cases, transvection between two alleles leads to intragenic complementation while disruption of transvection disrupts the complementation. Transvection is believed to occur through a variety of mechanisms. In one mechanism, the enhancers of one allele activate the promoter of a paired second allele. Other mechanisms include pairing-sensitive silencing and enhancer bypass of a chromatin insulator through pairing-mediated changes in gene structure.[11][12]

https://youtu.be/xOut2QT2jsg A maternal effect is a situation where the phenotype of an organism is determined not only by the environment it experiences and its genotype, but also by the environment and genotype of its mother. In genetics, maternal effects occur when an organism shows the phenotype expected from the genotype of the mother, irrespective of its own genotype, often due to the mother supplying messenger RNA or proteins to the egg. Maternal effects can also be caused by the maternal environment independent of genotype, sometimes controlling the size, sex, or behavior of the offspring. These

7 of 9 adaptive maternal effects lead to phenotypes of offspring that increase their fitness. Further, it introduces the concept of phenotypic plasticity, an important evolutionary concept. It has been proposed that maternal effects are important for the evolution of adaptive responses to environmental heterogeneity.

https://youtu.be/TVg57wd9Jvk https://youtu.be/JMT6oRYgkTk https://youtu.be/RZhL7LDPk8w https://youtu.be/NO0eKiIUcBg Carcinogenesis, also called oncogenesis or tumorigenesis, is the formation of a cancer, whereby normal cells are transformed into cancer cells. The process is characterized by changes at the cellular, genetic, and epigenetic levels and abnormal cell division. Cell division is a physiological process that occurs in almost all tissues and under a variety of circumstances. Normally the balance between proliferation and programmed cell death, in the form of apoptosis, is maintained to ensure the integrity of tissues and organs. According to the prevailing accepted theory of carcinogenesis, the somatic mutation theory, mutations in DNA and epimutations that lead to cancer disrupt these orderly processes by disrupting the programming regulating the processes, upsetting the normal balance between proliferation and cell death. This results in uncontrolled cell division and the evolution of those cells by natural selection in the body. Only certain mutations lead to cancer whereas the majority of mutations do not.

In biology, histones are highly alkaline proteins found in eukaryotic cell nuclei that package and order the DNA into structural units called nucleosomes.[1][2] They are the chief protein components of chromatin, acting as spools around which DNA winds, and playing a role in gene regulation. Without histones, the unwound DNA in chromosomes would be very long (a length to width ratio of more than 10 million to 1 in human DNA). For example, each human diploid cell (containing 23 pairs of chromosomes) has about 1.8 meters of DNA; wound on the histones, the diploid cell has about 90 micrometers (0.09 mm) of chromatin. When the diploid cells are duplicated and condensed during mitosis, the result is about 120 micrometers of chromosomes.

Heterochromatin vs Euchromatin https://youtu.be/Ml9kiaRSKps

Heterochromatin is a tightly packed form of DNA or condensed DNA, which comes in multiple varieties. These varieties lie on a continuum between the two extremes of constitutive heterochromatin and facultative heterochromatin. Both play a role in the expression of genes. Because it is tightly packed, it was thought to be inaccessible to polymerases and therefore not transcribed, however according to Volpe et al. (2002),[1] and many other papers since,[2] much of this DNA is in fact transcribed, but it

8 of 9 is continuously turned over via RNA-induced transcriptional silencing (RITS). Recent

studies with electron microscopy and OsO4 staining reveal that the dense packing is not due to the chromatin.[3] Constitutive heterochromatin can affect the genes near itself (e.g. position-effect variegation). It is usually repetitive and forms structural functions such as centromeres or telomeres, in addition to acting as an attractor for other gene-expression or repression signals. Facultative heterochromatin is the result of genes that are silenced through a mechanism such as histone deacetylation or Piwi-interacting RNA (piRNA) through RNAi. It is not repetitive and shares the compact structure of constitutive heterochromatin. However, under specific developmental or environmental signaling cues, it can lose its condensed structure and become transcriptionally active.[4] Heterochromatin has been associated with the di- and tri-methylation of H3K9 in certain portions of the genome

Reproducing Without A Male | Parthenogenesis https://youtu.be/dNoY9ribw4A

Parthenogenesis (/ˌpɑːrθɪnoʊˈdʒɛnɪsɪs, -θɪnə-/;[1][2] from the Greek παρθένος, parthenos, 'virgin' + γένεσις, genesis, 'creation'[3]) is a natural form of asexual reproduction in which growth and development of embryos occur without fertilization. In animals, parthenogenesis means development of an embryo from an unfertilized egg cell. In plants parthenogenesis is a component process of apomixis. Parthenogenesis occurs naturally in some plants, some invertebrate animal species (including water fleas, some scorpions, aphids, some mites, some bees, some Phasmida and parasitic wasps) and a few vertebrates (such as some fish,[4] amphibians, reptiles[5][6] and very rarely birds[7]). This type of reproduction has been induced artificially in a few species including fish and amphibians.[8] Normal egg cells form after meiosis and are haploid, with half as many chromosomes as their mother's body cells. Haploid individuals, however, are usually non-viable, and parthenogenetic offspring usually have the diploid chromosome number. Depending on the mechanism involved in restoring the diploid number of chromosomes, parthenogenetic offspring may have anywhere between all and half of the mother's alleles. The offspring having all of the mother's genetic material are called full clones

9 of 9 and those having only half are called half clones. Full clones are usually formed without meiosis. If meiosis occurs, the offspring will get only a fraction of the mother's alleles since crossing over of DNA takes place during meiosis, creating variation.

Former illuminati insider: There are 2 types of Cloning https://youtu.be/HJRkZd7DO1U

Cloning is the process of producing genetically identical individuals of an organism either naturally or artificially. In nature, many organisms produce clones through asexual reproduction. Cloning in biotechnology refers to the process of creating clones of organisms or copies of cells or DNA fragments (molecular cloning). Beyond biology, the term refers to the production of multiple copies of digital media or software. The term clone, invented by J. B. S. Haldane, is derived from the Ancient Greek word κλών klōn, "twig", referring to the process whereby a new plant can be created from a twig. In botany, the term lusus was traditionally used.[1] In horticulture, the spelling clon was used until the twentieth century; the final e came into use to indicate the vowel is a "long o" instead of a "short o".[2][3] Since the term entered the popular lexicon in a more general context, the spelling clone has been used exclusively.

A 4:59 Summary of Epigenetics

Epigenetics: Methylation, Acetylation, and ncRNA https://youtu.be/CfDWIWykp-k methylation of genes stops gene expression. acetylation of histones relaxes the histones and makes it easier to transcribe genes. Removing acetyl groups on histones tightens the histones and makes it harder to transcribe genes. types of non codingRNA (ncRNA) long non codingRNA (lncRNA) binds proteins like methyl or acetyl transferase, a demethylase or deacetylase telling them where to add or subtract a methyl or acetyl group. short interfering RNA (siRNA) bind to a target mRNA with help of a protein and destroys or blocks mRNA translation.

Piwi interacting RNA (piRNA) can silence genes by binding to certain regions of DNA. This tells the cell to add a methyl group here. micro RNA (miRNA) bind to a target mRNA with help of a protein and destroys or blocks mRNA translation.