scholarly journals Empirical evidence for epigenetic inheritance driving evolutionary adaptation

Author(s):  
Dragan Stajic ◽  
Lars E. T. Jansen

The cellular machinery that regulates gene expression can be self-propagated across cell division cycles and even generations. This renders gene expression states and their associated phenotypes heritable, independently of genetic changes. These phenotypic states, in turn, can be subject to selection and may influence evolutionary adaptation. In this review, we will discuss the molecular basis of epigenetic inheritance, the extent of its transmission and mechanisms of evolutionary adaptation. The current work shows that heritable gene expression can facilitate the process of adaptation through the increase of survival in a novel environment and by enlarging the size of beneficial mutational targets. Moreover, epigenetic control of gene expression enables stochastic switching between different phenotypes in populations that can potentially facilitate adaptation in rapidly fluctuating environments. Ecological studies of the variation of epigenetic markers (e.g. DNA methylation patterns) in wild populations show a potential contribution of this mode of inheritance to local adaptation in nature. However, the extent of the adaptive contribution of the naturally occurring variation in epi-alleles compared to genetic variation remains unclear.This article is part of the theme issue ‘How does epigenetics influence the course of evolution?’

2021 ◽  
Author(s):  
Jincheng Long ◽  
James Walker ◽  
Wenjing She ◽  
Billy Aldridge ◽  
Hongbo Gao ◽  
...  

AbstractThe plant male germline undergoes DNA methylation reprogramming, which methylates genes de novo and thereby alters gene expression and facilitates meiosis. Why reprogramming is limited to the germline and how specific genes are chosen is unknown. Here, we demonstrate that genic methylation in the male germline, from meiocytes to sperm, is established by germline-specific siRNAs transcribed from transposons with imperfect sequence homology. These siRNAs are synthesized by meiocyte nurse cells (tapetum) via activity of the tapetum-specific chromatin remodeler CLASSY3. Remarkably, tapetal siRNAs govern germline methylation throughout the genome, including the inherited methylation patterns in sperm. Finally, we demonstrate that these nurse cell-derived siRNAs (niRNAs) silence germline transposons, thereby safeguarding genome integrity. Our results reveal that tapetal niRNAs are sufficient to reconstitute germline methylation patterns and drive extensive, functional methylation reprogramming analogous to piRNA-mediated reprogramming in animal germlines.


2018 ◽  
Author(s):  
Taliesin J. Kinser ◽  
Ronald D. Smith ◽  
Amelia H. Lawrence ◽  
Arielle M. Cooley ◽  
Mario Vallejo-Marin ◽  
...  

ABSTRACTAngiosperm endosperm requires genomic and epigenomic interactions between maternal and paternal genomes for proper seed development. Genomic imprinting, an epigenetic phenomenon where the expression of certain genes is predominantly contributed by one parent, is an essential part of this process and unique to endosperm. Perturbation of imprinting can be fatal to developing seeds, and can be caused by interspecific or interploidy hybridization. However, underlying mechanisms driving these endosperm-based hybridization barriers are not well understood or described. Here we investigate the consequences of genomic imprinting in a naturally occurring interploidy and interspecies hybrid between the diploid, Mimulus guttatus, and the allotetraploid (with two subgenomes), M. luteus (Phrymaceae). We find that the two parental species differ in patterns of DNA methylation, gene expression, and imprinting. Hybrid crosses in both directions, which suffer from endosperm abnormalities and decreased germination rates, display altered methylation patterns compared to parent endosperm. Furthermore, imprinting and expression patterns appear perturbed in hybrid endosperm, where we observe global expression dominance of each of the two M. luteus subgenomes, which share similar expression patterns, over the M. guttatus genome, regardless of crossing direction. We suggest that epigenetic repatterning within the hybrid may drive global shifts in expression patterns and be the result of diverged epigenetic/regulatory landscapes between parental genomes. This may either establish or exacerbate dosage-based epistatic incompatibilities between the specific imprinting patterns that have diverged between parental species, thus driving potentially rapid endosperm-based hybridization barriers.


Agronomy ◽  
2020 ◽  
Vol 10 (10) ◽  
pp. 1484
Author(s):  
Clémentine Mercé ◽  
Philipp E. Bayer ◽  
Cassandria Tay Fernandez ◽  
Jacqueline Batley ◽  
David Edwards

The methylation of gene promoters is an epigenetic process that can have a major impact on plant phenotypes through its control of gene expression. This phenomenon can be observed as a response to stress, such as drought, cold/heat stress or pathogen infection. The transgenerational heritability of DNA methylation marks could enable breeders to fix beneficial methylation patterns in crops over successive generations. These properties of DNA methylation, its impact on the phenotype and its heritability, could be used to support the accelerated breeding of improved crop varieties. Induced DNA methylation has the potential to complement the existing plant breeding process, supporting the introduction of desirable characteristics in crops within a single generation that persist in its progeny. Therefore, it is important to understand the underlying mechanisms involved in the regulation of gene expression through DNA methylation and to develop methods for precisely modulating methylation patterns for crop improvement. Here we describe the currently available epigenetic editing tools and their advantages and limitations in the domain of crop breeding. Finally, we discuss the biological and legislative limitations currently restricting the development of epigenetic modification as a crop improvement tool.


2013 ◽  
Vol 5 ◽  
pp. GEG.S12897 ◽  
Author(s):  
Amanda K. Wyatt ◽  
Monika Zavodna ◽  
Jean L. Viljoen ◽  
Jo-Ann L. Stanton ◽  
Neil J. Gemmell ◽  
...  

The initiation of mammalian puberty is underpinned by an increase in Kisspeptin (Kiss1) signaling via its receptor (Kiss1r/GPR54) on gonadotropin-releasing hormone (GnRH) neurons. Animals and humans with loss-of-function mutations in Kiss1 or Kiss1r fail to go through puberty. The timing of puberty is dependent on environmental factors, and malleability in puberty timing suggests a mechanism that can translate environmental signals into patterns of Kiss1/Kiss1r gene expression. Epigenetics is a powerful mechanism that can control gene expression in an environment-dependent manner. We investigated whether epigenetic DNA methylation is associated with gene expression changes at puberty. We used bisulfite-PCR-pyrosequencing to define the methylation in the promoters of Kiss1 and Kiss1r before and after puberty in female rats. Both Kiss1 and Kiss1r showed highly significant puberty-specific differential promoter methylation patterns. By identifying key differentially methylated residues associated with puberty, these findings will be important for further studies investigating the control of gene expression across the pubertal transition.


Classical genetics has revealed the mechanisms for the transmission of genes from generation to generation, but the strategy of the genes in unfolding the developmental programme remains obscure. Epigenetics comprises the study of the mechanisms that impart temporal and spatial control on the activities of all those genes required for the development of a complex organism from the zygote to the adult. Epigenetic changes in gene activity can be studied in relation to DNA methylation in cultured mammalian cells and it is also possible to isolate and characterize mutants with altered DNA methylase activity. Although this experimental system is quite far removed from the epigenetic controls acting during development it does provide the means to clarify the rules governing the silencing of genes by specific DNA methylation and their reactivation by demethylation. This in turn will facilitate studies on the control of gene expression in somatic cells of the developing organism or the adult. The general principles of epigenetic mechanisms can be defined. There are extreme contrasts between instability or switches in gene expression, such as those in stem-line cells, and the stable heritability of a specialized pattern of gene activities. In some situations cell lineages are known to be important, whereas in others coordinated changes in groups of cells have been demonstrated. Control of numbers of cell divisions and the size of organisms, or parts of organisms, is also essential. The epigenetic determination of gene expression can be reversed or reprogrammed in the germ line. The extent to which methylation or demethylation of specific DNA sequences can help explain these basic epigenetic mechanisms is briefly reviewed.


Science ◽  
2021 ◽  
Vol 373 (6550) ◽  
pp. eabh0556 ◽  
Author(s):  
Jincheng Long ◽  
James Walker ◽  
Wenjing She ◽  
Billy Aldridge ◽  
Hongbo Gao ◽  
...  

The plant male germline undergoes DNA methylation reprogramming, which methylates genes de novo and thereby alters gene expression and regulates meiosis. Here, we reveal the molecular mechanism underlying this reprogramming. We demonstrate that genic methylation in the male germline, from meiocytes to sperm, is established by 24-nucleotide small interfering RNAs (siRNAs) transcribed from transposons with imperfect sequence homology. These siRNAs are synthesized by meiocyte nurse cells (tapetum) through activity of CLSY3, a chromatin remodeler absent in other anther cells. Tapetal siRNAs govern germline methylation throughout the genome, including the inherited methylation patterns in sperm. Tapetum-derived siRNAs also silence germline transposons, safeguarding genome integrity. Our results reveal that tapetal siRNAs are sufficient to reconstitute germline methylation patterns and drive functional methylation reprogramming throughout the male germline.


Blood ◽  
2012 ◽  
Vol 120 (21) ◽  
pp. SCI-4-SCI-4
Author(s):  
Peter A. Jones

Abstract Abstract SCI-4 Epigenetic processes are reinforced by interactions between covalent chromatin marks such as DNA methylation, histone modifications, and variants thereof. These marks ultimately specify the locations of nucleosomes, particularly with respect to transcriptional start sites and other regulatory regions. Understanding how the epigenome functions, therefore, requires a coordinated approach in order to reveal the mechanisms by which the chemical modifications interact with nucleosomal remodeling machines to ensure epigenetic inheritance and control of gene expression. We have developed a new methodology to simultaneously map nucleosomal positioning and DNA methylation on individual molecules of DNA. We used this nucleosomal mapping technology to ascertain alterations in nucleosomal positioning during the abnormal silencing of genes by promoter hypermethylation. These experiments show that the methylation of CpG islands at the transcriptional start sites of key tumor-suppressor genes results in the stable placement of nucleosomes at the transcription start site. Treatment with 5-azanucleoside results in an immediate inhibition of DNA methylation and a sequence of downstream events that ultimately result in the eviction of the nucleosomes from the transcription start site and the activation of gene expression. Disclosures: Jones: Eli Lilly: Consultancy.


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