scholarly journals When is incomplete epigenetic resetting in germ cells favoured by natural selection?

2015 ◽  
Vol 282 (1811) ◽  
pp. 20150682 ◽  
Author(s):  
Tobias Uller ◽  
Sinead English ◽  
Ido Pen
Keyword(s):  
Dna Methylation ◽  
Germ Cells ◽  
Generation Time ◽  
Epigenetic Inheritance ◽  
Environmental Cues ◽  
Heterogeneous Environments ◽  
Stochastic Noise ◽  
Transgenerational Epigenetic Inheritance ◽  
Early Embryos ◽  
Adaptive Role

Resetting of epigenetic marks, such as DNA methylation, in germ cells or early embryos is not always complete. Epigenetic states may therefore persist, decay or accumulate across generations. In spite of mounting empirical evidence for incomplete resetting, it is currently poorly understood whether it simply reflects stochastic noise or plays an adaptive role in phenotype determination. Here, we use a simple model to show that incomplete resetting can be adaptive in heterogeneous environments. Transmission of acquired epigenetic states prevents mismatched phenotypes when the environment changes infrequently relative to generation time and when maternal and environmental cues are unreliable. We discuss how these results may help to interpret the emerging data on transgenerational epigenetic inheritance in plants and animals.

scholarly journals What Is Lost in the Weismann Barrier?

2020 ◽  
Vol 8 (4) ◽  
pp. 35
Author(s):  
Abigail P. Bline ◽  
Anne Le Goff ◽  
Patrick Allard
Keyword(s):  
Developmental Biology ◽  
Health Status ◽  
Germ Cells ◽  
Scientific Research ◽  
Epigenetic Inheritance ◽  
Environmental Context ◽  
Transgenerational Epigenetic Inheritance ◽  
Basic Tenet ◽  
Weismann Barrier ◽  
Historical Origins

The Weismann barrier has long been regarded as a basic tenet of biology. However, upon close examination of its historical origins and August Weismann’s own writings, questions arise as to whether such a status is warranted. As scientific research has advanced, the persistence of the concept of the barrier has left us with the same dichotomies Weismann contended with over 100 years ago: germ or soma, gene or environment, hard or soft inheritance. These dichotomies distract from the more important questions we need to address going forward. In this review, we will examine the theories that have shaped Weismann’s thinking, how the concept of the Weismann barrier emerged, and the limitations that it carries. We will contrast the principles underlying the barrier with recent and less recent findings in developmental biology and transgenerational epigenetic inheritance that have profoundly eroded the oppositional view of germline vs. soma. Discarding the barrier allows us to examine the interactive processes and their response to environmental context that generate germ cells in the first place, determine the entirety of what is inherited through them, and set the trajectory for the health status of the progeny they bear.

scholarly journals Gametes deficient for Pot1 telomere binding proteins alter levels of telomeric foci for multiple generations

2021 ◽  
Vol 4 (1) ◽  
Author(s):  
Evan H. Lister-Shimauchi ◽  
Michael Dinh ◽  
Paul Maddox ◽  
Shawn Ahmed
Keyword(s):  
Germ Cells ◽  
Binding Proteins ◽  
Epigenetic Inheritance ◽  
Transgenerational Epigenetic Inheritance ◽  
Heterochromatin Formation ◽  
Multiple Generations ◽  
C Elegans ◽  
Protection Of Telomeres 1

AbstractDeficiency for telomerase results in transgenerational shortening of telomeres. However, telomeres have no known role in transgenerational epigenetic inheritance. C. elegans Protection Of Telomeres 1 (Pot1) proteins form foci at the telomeres of germ cells that disappear at fertilization and gradually accumulate during development. We find that gametes from mutants deficient for Pot1 proteins alter levels of telomeric foci for multiple generations. Gametes from pot-2 mutants give rise to progeny with abundant POT-1::mCherry and mNeonGreen::POT-2 foci throughout development, which persists for six generations. In contrast, gametes from pot-1 mutants or pot-1; pot-2 double mutants induce diminished Pot1 foci for several generations. Deficiency for MET-2, SET-25, or SET-32 methyltransferases, which promote heterochromatin formation, results in gametes that induce diminished Pot1 foci for several generations. We propose that C. elegans POT-1 may interact with H3K9 methyltransferases during pot-2 mutant gametogenesis to induce a persistent form of transgenerational epigenetic inheritance that causes constitutively high levels of heterochromatic Pot1 foci.

Transgenerational inheritance of epigenetic traits

2019 ◽  
pp. 213-224
Author(s):  
John C. Lucchesi
Keyword(s):  
Cardiovascular Disease ◽  
Dna Methylation ◽  
Histone Methylation ◽  
Physiological Stress ◽  
Adult Life ◽  
Epigenetic Inheritance ◽  
Transgenerational Inheritance ◽  
Early Postnatal Development ◽  
Transgenerational Epigenetic Inheritance ◽  
Non Coding Rnas

Aberrant nutrition during pregnancy or in early postnatal development can result in obesity, diabetes, cardiovascular disease, defective cognition or psychopathologies in adult life. In some cases, the epigenetic modifications responsible for these effects can be transmitted to descendants who have not been exposed to the same environmental factors as their parents. Examples range from the transgenerational inheritance of conditions caused by physiological stress and exposure to endocrine disruptors, and behavioral and psychiatric effects. Transgenerational inheritance has been correlated with changes in DNA or histone methylation. The transmission of methylated DNA signals faces the problem of reprogramming in the germline. A few of the signals that protect imprinted regions for demethylation have been identified. Small non-coding RNAs such as piwi-interacting RNAs (piRNAs) and fragments of tRNAs are clearly involved at some level in transgenerational epigenetic inheritance. This is particularly the case in organisms such as flies and worms that lack DNA methylation.

How do histone modifications contribute to transgenerational epigenetic inheritance in C. elegans?

2020 ◽  
Vol 48 (3) ◽  
pp. 1019-1034 ◽  
Author(s):  
Rachel M. Woodhouse ◽  
Alyson Ashe
Keyword(s):  
Histone Modifications ◽  
Molecular Mechanisms ◽  
Epigenetic Inheritance ◽  
Nematode Caenorhabditis Elegans ◽  
Histone Methyltransferases ◽  
Transgenerational Epigenetic Inheritance ◽  
C Elegans ◽  
Recent Developments ◽  
Gene Regulatory

Gene regulatory information can be inherited between generations in a phenomenon termed transgenerational epigenetic inheritance (TEI). While examples of TEI in many animals accumulate, the nematode Caenorhabditis elegans has proven particularly useful in investigating the underlying molecular mechanisms of this phenomenon. In C. elegans and other animals, the modification of histone proteins has emerged as a potential carrier and effector of transgenerational epigenetic information. In this review, we explore the contribution of histone modifications to TEI in C. elegans. We describe the role of repressive histone marks, histone methyltransferases, and associated chromatin factors in heritable gene silencing, and discuss recent developments and unanswered questions in how these factors integrate with other known TEI mechanisms. We also review the transgenerational effects of the manipulation of histone modifications on germline health and longevity.

Examination of the dynamics of global DNA methylation pattern establishment during spermatogenesiss

2007 ◽  
Vol 30 (4) ◽  
pp. 90
Author(s):  
Kirsten Niles ◽  
Sophie La Salle ◽  
Christopher Oakes ◽  
Jacquetta Trasler
Keyword(s):  
Dna Methylation ◽  
Germ Cell ◽  
Germ Cells ◽  
Epigenetic Modification ◽  
Methylation Pattern ◽  
Chromosome 9 ◽  
Specific Gene ◽  
Global Methylation ◽  
Dna Methylation Pattern ◽  
Methylation Patterns

Background: DNA methylation is an epigenetic modification involved in gene expression, genome stability, and genomic imprinting. In the male, methylation patterns are initially erased in primordial germ cells (PGCs) as they enter the gonadal ridge; methylation patterns are then acquired on CpG dinucleotides during gametogenesis. Correct pattern establishment is essential for normal spermatogenesis. To date, the characterization and timing of methylation pattern acquisition in PGCs has been described using a limited number of specific gene loci. This study aimed to describe DNA methylation pattern establishment dynamics during male gametogenesis through global methylation profiling techniques in a mouse model. Methods: Using a chromosome based approach, primers were designed for 24 regions spanning chromosome 9; intergenic, non-repeat, non-CpG island sequences were chosen for study based on previous evidence that these types of sequences are targets for testis-specific methylation events. The percent methylation was determined in each region by quantitative analysis of DNA methylation using real-time PCR (qAMP). The germ cell-specific pattern was determined by comparing methylation between spermatozoa and liver. To examine methylation in developing germ cells, spermatogonia from 2 day- and 6 day-old Oct4-GFP (green fluorescent protein) mice were isolated using fluorescence activated cell sorting. Results: As compared to liver, four loci were hypomethylated and five loci were hypermethylated in spermatozoa, supporting previous results indicating a unique methylation pattern in male germ cells. Only one region was hypomethylated and no regions were hypermethylated in day 6 spermatogonia as compared to mature spermatozoa, signifying that the bulk of DNA methylation is established prior to type A spermatogonia. The methylation in day 2 spermatogonia, germ cells that are just commencing mitosis, revealed differences of 15-20% compared to day 6 spermatogonia at five regions indicating that the most crucial phase of DNA methylation acquisition occurs prenatally. Conclusion: Together, these studies provide further evidence that germ cell methylation patterns differ from those in somatic tissues and suggest that much of methylation at intergenic sites is acquired during prenatal germ cell development. (Supported by CIHR)

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