Non Nuclear Inheritance

8 Key excerpts on "Non Nuclear Inheritance"

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  eBook - ePub

  Epigenetic Gene Expression and Regulation

  • Suming Huang, Michael D. Litt, C. Ann Blakey, Michael D Litt(Authors)
  • 2015(Publication Date)
  • Academic Press

    (Publisher)

  5. Epigenetic inheritance via histone modifications  191

  6. Epigenetic inheritance through noncoding RNA  193

  6.1 sRNA  193

  6.1.1 MicroRNA  193

  6.1.2 Small interfering RNA  195

  6.1.3 Piwi-interacting RNA  196

  6.2 Long noncoding RNA  200

  7. Prions  201

  8. Unknown mechanism studies  201

  8.1 Dutch Hunger Winter  202

  8.2 Paramutation  202

  9. Conclusions  203

  Acknowledgments  204

  References  204

  1. Introduction

  Ever since the discovery that all cells within an organism have the same DNA content despite their vastly different phenotypes, scientists have been trying to understand how this array of phenotypes arises. This question is at the core of the field of epigenetics, which is concerned with the study of mitotically and/or meiotically heritable changes in phenotypes that occur in the absence of DNA sequence changes [131] . Decades of research into epigenetic phenomena such as X-chromosome inactivation, parental imprinting, posttranscriptional gene silencing, RNA interference (RNAi), and others, revealed many of the molecular pathways responsible. These pathways include DNA methylation, histone modifications, chromatin structure, and an ever expanding array of noncoding RNAs. Their study over the last half century has revealed how multiple cellular phenotypes arise from a single genotype.

  As evident from the definition given above, inheritance is required for a phenomenon or mechanism to be considered within the realm of epigenetics. Two types of epigenetic inheritance can be distinguished: inheritance from cell to cell through mitosis and inheritance from parent to offspring through meiosis. Cell-to-cell epigenetic inheritance is typically concerned with maintaining a specific collection of epigenetic marks, i.e., an epigenetic state [1] . The epigenetic state determines a cell’s identity; while all cells of an individual possess the same genetic information, they differ in their epigenetic marks [2] . Epigenetic marks are thus cell type-specific, and passing on the epigenetic state of the parent cell to daughter cells means that the daughter cells will maintain the same cellular identity as the parent cell. While epigenetic states mostly are maintained during mitosis, epigenetic information does change as cell differentiation occurs and can change in response to environmental factors [2 ,3]

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  Prenatal Diagnosis

  Cases and Clinical Challenges

  • Miriam S. DiMaio, Joyce E. Fox, Maurice J. Mahoney(Authors)
  • 2011(Publication Date)
  • Wiley-Blackwell

    (Publisher)

  Chapter 3 Non-Mendelian Inheritance Introduction to Non-Mendelian Inheritance

  Non-Mendelian disorders have patterns of inheritance which do not conform to Mendel's Law of Segregation where each ovum or sperm receives only one copy of a pair of genes. Important examples include mitochondrial inheritance, genetic imprinting, and multifactorial inheritance.

  Mitochondrial disorders can be caused by abnormalities in either nuclear genes or in mitochondrial DNA. Mitochondrial disorders caused by abnormalities of nuclear genes are inherited in a Mendelian fashion. Mutations in mitochondrial DNA (mtDNA) cause disorders which have mitochondrial inheritance. An important feature of disorders with mitochondrial inheritance is heteroplasmy, i.e., varying amounts of mutant and normal mtDNA in each cell. Mitochondrial DNA is almost exclusively maternally transmitted; hence, mitochondrial disorders do not follow Mendel's Law of Segregation as all children of an affected mother will inherit abnormal mtDNA. The manifestations of disorders with mitochondrial inheritance may vary widely among affected offspring because different amounts of normal and mutant mtDNA are present in each ovum.

  Genetic imprinting is responsible for another class of non-Mendelian disorders. Several imprinted genes are normally expressed or silenced depending on whether they have been paternally or maternally transmitted. Chemical modifications to the gene structure but not the gene sequence lead to this phenomenon. Risk of recurrence of an imprinted disorder depends on the specific genetic mechanism leading to aberrant gene imprinting and the parent of origin.

  Disorders with multifactorial inheritance are caused by the effects and complex interactions of multiple susceptibility genes, each usually with a relatively small effect, and environmental and epigenetic factors. Multifactorial conditions constitute a significant fraction of common birth defects such as congenital heart disease, neural tube defects, facial clefting, and common medical problems such as diabetes, autoimmune disease, cancer, and most cases of autistic spectrum disorder. This class of non-Mendelian disorders is the most etiologically complex and poorly understood. While multiple members of the same family are sometimes affected, multifactorial disorders are not associated with Mendelian patterns of inheritance.

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  Organisms, Agency, and Evolution

  • D. M. Walsh(Author)
  • 2015(Publication Date)
  • Cambridge University Press

    (Publisher)

  Epigenetic inheritance: The transmission and imprinting of epigenetic methylation ‘markers’ discussed above, looks to be a distinctly nongenetic mechanism for the passing on of crucial developmental resources. This appears to be a separate mechanism that operates independently of the replication of DNA. Heritable epigenetic variation is decoupled from genetic variation by definition. Hence, there are selectable epigenetic variations that are independent of DNA variations, and evolutionary change on the epigenetic axis is inevitable. The only question is whether these variations are persistent and common enough to lead to interesting evolutionary effects. (Jablonka and Lamb 2002: 93) In addition, cellular structures reoccur generation on generation without the mediation of replicated genes. ‘Cortical inheritance’, for example, has been demonstrated in paramecia. Errors and alterations in the cuticle of paramecia are passed on to daughter cells during cell division (Beisson 2011). Jablonka and Raz (2009) have documented more than 100 instances of epigenetic inheritance in 42 different species (Jablonka and Lamb 2010). It is no mere fringe phenomenon. 10 8 I take the term ‘inheritance pluralism’ and its alternate ‘inheritance holism’ from Mameli (2005), although my conception of holism departs significantly from Mameli’ s. 9 The idea of ‘causal spread’ comes from Clark and Chalmers (1998). 10 Gilbert and Epel (2009) have produced an impressive list of documented instances of epigenetic inheritance in animals. See their Appendix D. 100 Beyond replicator biology Behavioural inheritance: Behavioural inheritance systems involve those in which offspring learn behaviours from parents or others. A classic example is to be found in the spread of the ability of great tits (Parus major) in Britain to extract the cream from milk bottles left on the doorsteps of houses. Further examples include dietary preferences that are transmitted to mammalian foe- tuses though the placenta.

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  Quantum Leaps in Biochemistry

  • L.A. Stocken, M.G. Ord(Authors)
  • 1996(Publication Date)
  • Elsevier Science

    (Publisher)

  Chapter 4

  Extranuclear DNA

  Anil Day and Joanna Poulton

  Non-Mendelian Inheritance 59 The Search for Extranuclear DNA: Early Studies on Organelle Genomes 61 Detailed Characterization of Organelle DNA 65 Origins of Mitochondria and Plastids 66 Mitochondrial DNA 67 Plant Mitochondrial Genomes 73 Organization and Expression of Plastid DNA 75 Relocation of Organelle Genes to the Nucleus 77 Regulatory Interactions between Nucleus and Organelle 78 Vegetative Segregation, Recombination, and Homoplasmy 80 Organelle DNA Is a Useful Molecular Clock 81 Phenotypes Associated with Abnormal Mitochondrial DNA 81 Senescence 87 New Methods for Studying Organelle Genomes 88 Organelle Inheritance 89 Is Extranuclear DNA Located Outside Mitochondria and Plastids? 90 Acknowledgments 91 References 91

  Non-Mendelian Inheritance

  In the mid-nineteenth century Gregor Mendel’s work on garden peas established rules that governed the inheritance of visible differences between parent plants. Mendel’s work lay dormant for 40 years until it was rediscovered independently by Carl Correns, Hugo de Vries, and Erich Tschermark von Seysenegg in 1900. Mendel’s rules stimulated much research on inheritance in the early twentieth century. This work established Mendel’s laws on the segregation of alleles and the independent assortment of genes as the foundation of classical genetics. Work on meiosis, notably by Sutton in 1903, implicated chromosomes located in the nucleus as the agents responsible for Mendelian segregation.

  While Mendel’s legacy was being firmly established in the early part of the twentieth century there was little room for other models of inheritance. Apart from linkage, exceptions to Mendelism were largely overlooked. The influential American School of Geneticists, including Thomas Hunt Morgan and co-workers, concentrated on mapping chromosomes. Carl Correns studied the inheritance of white and pale green sectors on the leaves of variegated Mirabilis jalapa or four o’clock plants (1909). The white patches (chlorophyll-deficient areas) were only inherited by the progeny if they were present in the maternal parent. The male parent did not transmit the variegated phenotype. In other words, egg cells but not pollen transmitted the white trait. This maternal inheritance pattern was transmitted over many generations. This observation clearly contravened Mendelian inheritance where both parents transmit genes to their progeny. Erwin Baur (1909) studied the inheritance of variegation in Pelargonium

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  Inheritance Systems and the Extended Evolutionary Synthesis

  • Eva Jablonka, Marion J. Lamb(Authors)
  • 2020(Publication Date)
  • Cambridge University Press

    (Publisher)

  Similarly, with imitation, many patterns of behaviour, whatever their functional effects, can be imitated; usually, how- ever, the process of imitation is not entirely blind, and patterns of behaviour that have functional significance for the individual are more readily imitated than others. Together, what the two Tables tell us is that the dynamics of inheritance and of evolutionary changes that are based on the various inheritance systems are likely to differ. Models intended to describe these dynamics have to recognize this. They will depend on whether information is modular or holistic, whether variation is blind or targeted, how faithfully it is transmitted, whether it can remain latent, and whether and to what extent transmission is vertical or horizontal. 37 The Extended Evolutionary Synthesis 3 The Evolutionary Implications of Non-Genetic Inheritance If there is more to heredity than DNA, then evolution can no longer be defined in terms of changes in gene frequencies. The DNA-variation-independent effects of non-genetic heritable variations have to be incorporated into evolutionary analyses. When selection is driving evolutionary change, we cannot assume that the process involves only the selection of genes, because selection of epigenetic and cultural variations, and their interactions with the genetic system, may also be involved. So, too, may be selection that is based on non-replicative processes of differential stabilization. 3.1 Arguments against the Importance of Epigenetic Inheritance in Evolution Some passionate adherents of the MS, especially population geneticists, argue that the role of epigenetic inheritance in evolution is trivial at best.

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  Extended Heredity

  A New Understanding of Inheritance and Evolution

  • Russell Bonduriansky, Troy Day(Authors)
  • 2018(Publication Date)
  • Princeton University Press

    (Publisher)

  5 The Nongenetic Inheritance Spectrum The more we learn about the world, and the deeper our learning, the more conscious, specific and articulate will be our knowledge of what we do not know, our knowledge of our ignorance.

  —Karl Popper, Conjectures and Refutations, 1969

  In the excitement surrounding epigenetic discoveries, it’s easy to forget that epigenetic inheritance in the narrow sense comprises only a few among many mechanisms of nongenetic inheritance. Epigenetic inheritance is fascinating, widespread, and important, but the scope of nongenetic inheritance is much greater. Moreover, while narrow-sense epigenetics is a relatively young research field, the scientific literature on nongenetic inheritance actually stretches back a century, and many interesting studies are now all but forgotten. Although some of the phenomena described in this literature may turn out to be examples of transgenerational epigenetic inheritance, it’s clear that many examples of nongenetic inheritance involve other mechanisms of transmission. Many of these examples are encompassed by the broad category of phenomena known as maternal and paternal effects (or, collectively, parental effects). Although parental effects have been recognized for many years and are known to have important functions in many species, they have seldom been incorporated into evolutionary models, and their general role in evolution remains poorly understood.153 We believe that these diverse effects can be understood as instances of nongenetic inheritance and can be included, along with epigenetic inheritance, within the scope of extended heredity.

  In this chapter, we will outline a range of examples of nongenetic inheritance that appear to fall outside the bounds of transgenerational epigenetic inheritance in the strict sense154

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  Transgenerational Epigenetics

  • (Author)
  • 2019(Publication Date)
  • Academic Press

    (Publisher)

  At the time, the tools by which it would become possible to understand these phenomena were in their infancy; thus, few attempts were made to ascertain the molecular mechanism by which parental phenotype dictated offspring phenotype, irrespective of offspring genotype. For example, although genes were considered to be the units of heredity, the language of genes and the regulation of gene expression was still largely a mystery. It was not until 1953 when Watson and Crick described the structure of DNA that the intricacies of gene expression could really be explored. Over the years, many more examples of non-Mendelian inheritance were uncovered in diverse fields of biology, bolstering the need for explanation. It was not until the late 20th century when epigenetics evolved to become a formidable field of study that a theoretical framework was available by which to revisit soft inheritance and secure the importance of its role in evolution and heredity. As discussed in detail later in this chapter, “soft inheritance” of traits largely can be explained by a number of epigenetic processes that are ancestral or environmentally acquired by the parental generation, and that can be meiotically inherited by future generations through the germ line, or that can influence phenotype of future generations without germ line transmission (i.e., prions, mother's milk, parental behavior) [ 53, 54 ], all of which contribute to the study of transgenerational epigenetics. The origins of epigenetics At the time when embryologists such as Karl Ernst von Baer and Ernst Haeckel strived to establish the principles of embryology, the fields of embryology and genetics were studied largely in parallel. Genetics and embryology did not formally intersect until the 1940s when Conrad H. Waddington introduced the concept of epigenetics to explain how a multitude of phenotypes can arise from a single genotype during the development of an organism

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  Social Information Transmission and Human Biology

  • Jonathan CK Wells, Simon Strickland, Kevin Laland(Authors)
  • 2006(Publication Date)
  • CRC Press

    (Publisher)

  We propose 108 Social Information Transmission and Human Biology that the organism can be considered as an entity that can selectively direct its resources toward both genetic and nongenetic fitness by transmitting both genetic and nongenetic information over time. When genes are transmitted over time, two important effects occur. First, each individual passes on only half her or his genes to each member of the next generation. The human genome project has estimated the number of genes in humans at around 40,000. After about 16 generations, the direct descendants of a human may contain not a single one of that ancestor’s genes by direct inheritance. Second, each time an offspring is produced the parental genes are mixed up. The consequence of these effects is that even where genes are successfully transmitted over many generations, they never meet the same selection of genes in any new gene-team. The process of sexual reproduction continually dismantles individual gene-teams. There is no process of sexual reproduction in the replication of nongenetic infor-mation, so it need not necessarily break down over time. The name of any individual is as valid a label denoting that person today as it was millennia ago. The significance of this for evolutionary theory is that genes and nongenetic information may offer different potential returns for a given investment. For any nonhuman species, this approach may be less relevant because the pertinent nongenetic information is sym-bolic and only viable through self-consciousness and learning. But for our species, the replication of symbolic information is more successful than that of our genes at preserving our uniqueness, our individuality. With the evolution of consciousness came both the awareness of death and the urge to overcome it through immortality (Bauman, 1992). Human literature dating from the Epic of Gilgamesh to the present day is testimony of our powerful desire to overcome death.

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