# How Epigenetics Affects Evolution: Mechanisms and Evidence ## Key Takeaways - Epigenetics, through DNA methylation, histone modification, and non-coding RNAs, generates heritable phenotypic variation without altering DNA sequence, offering a mechanism distinct from genetic mutation. - Epimutation rates, significantly higher (10⁴-10⁵ fold) than genetic mutation rates, provide a substantial substrate for natural selection, potentially accelerating adaptation, particularly in fluctuating environments. - Transgenerational epigenetic inheritance, where epigenetic marks survive developmental reprogramming, is robust in plants but more limited in mammals due to extensive germline and embryonic epigenetic resetting. - Evidence from natural populations, such as *Arabidopsis thaliana* and Darwin's finches, demonstrates that epigenetic variation is associated with environmental adaptation and influences fitness-related traits. - Epigenetic changes are generally reversible and less stable than genetic mutations, suggesting a primary role in rapid, short-term responses to environmental cues, with potential for genetic assimilation to stabilize beneficial states. --- ## Introduction to Epigenetics and Evolution ### What is Epigenetics? Epigenetics refers to heritable changes in gene expression that occur without alterations to the underlying DNA sequence. The term, coined by Conrad Waddington in 1942, originally described "the causal interactions between genes and their products which bring the phenotype into being." Today, epigenetics encompasses three primary molecular mechanisms: DNA methylation, histone modification, and non-coding RNA-mediated regulation. These mechanisms collectively control chromatin structure, transcriptional accessibility, and post-transcriptional gene silencing. The distinction between genetic and epigenetic information is fundamental. Genetic mutations alter the nucleotide sequence of DNA—substitutions, insertions, deletions, or chromosomal rearrangements. Epigenetic modifications, by contrast, chemically modify DNA or its associated proteins without changing the sequence. The most well-studied epigenetic mark is 5-methylcytosine (5mC), formed by the addition of a methyl group to the fifth carbon of cytosine residues, typically within CpG dinucleotides. This modification is catalyzed by DNA methyltransferases (DNMTs), including DNMT1 (maintenance methylation) and DNMT3A/3B (de novo methylation). ### Traditional Evolutionary Mechanisms Classical evolutionary theory, synthesized from Darwinian natural selection and Mendelian genetics, holds that heritable phenotypic variation arises from random genetic mutations. These mutations occur at rates of approximately 10⁻⁸ to 10⁻⁹ per base pair per generation in most organisms. Natural selection then acts on the resulting phenotypic variation, favoring alleles that confer reproductive advantage. This framework—the Modern Synthesis—has been remarkably successful in explaining adaptation and speciation. However, the Modern Synthesis has limitations. It struggles to explain rapid adaptive responses to environmental change, the inheritance of acquired traits, and the observation that phenotypic variation can arise faster than genetic mutation rates would predict. Epigenetics offers a potential resolution: if epigenetic marks can be inherited across generations and influence fitness, they provide an additional substrate for natural selection. This does not replace genetic evolution but supplements it, potentially accelerating adaptation and enabling organisms to respond to environmental cues within a single generation. ## Mechanisms of [Epigenetic Inheritance](/knowledge/molecular-biology/epigenetic-inheritance) ### DNA Methylation DNA methylation is the covalent addition of a methyl group to the C5 position of cytosine, producing 5-methylcytosine. In mammals, this occurs predominantly at CpG dinucleotides, where approximately 70–80% of CpG sites are methylated. CpG islands—regions of high CpG density often found in promoter regions—are typically unmethylated when associated with actively transcribed genes. The enzymatic machinery is well characterized. DNMT3A and DNMT3B establish methylation patterns de novo during embryogenesis, recognizing specific sequence contexts and chromatin states. DNMT1 maintains methylation patterns during DNA replication by recognizing hemimethylated CpG sites—where the parental strand is methylated but the newly synthesized strand is not—and methylating the daughter strand. This maintenance activity is essential for the faithful propagation of methylation patterns across cell divisions. Demethylation occurs through two mechanisms: passive and active. Passive demethylation happens when DNMT1 is inhibited or absent during replication, resulting in progressive dilution of methylation marks. Active demethylation involves the ten-eleven translocation (TET) enzymes, which oxidize 5mC to 5-hydroxymethylcytosine (5hmC), then to 5-formylcytosine (5fC) and 5-carboxylcytosine (5caC), ultimately leading to base excision repair and replacement with unmethylated cytosine. ### Histone Modifications Histones are the protein components of nucleosomes, around which DNA wraps approximately 147 base pairs. Each nucleosome contains an octamer of two copies each of H2A, H2B, H3, and H4. The N-terminal tails of these histones protrude from the nucleosome and are subject to numerous post-translational modifications, including acetylation, methylation, phosphorylation, ubiquitination, and sumoylation. Histone acetylation is catalyzed by histone acetyltransferases (HATs) such as p300/CBP and removed by histone deacetylases (HDACs). Acetylation of lysine residues neutralizes the positive charge of histone tails, weakening their interaction with negatively charged DNA and promoting an open chromatin conformation permissive to transcription. Histone methylation, catalyzed by histone methyltransferases (HMTs) and removed by demethylases (KDMs), has context-dependent effects. For example, trimethylation of histone H3 at lysine 4 (H3K4me3) marks active promoters, while trimethylation at lysine 27 (H3K27me3) is associated with Polycomb-mediated gene silencing. Histone modifications can be inherited through cell division. During DNA replication, parental histones are distributed to both daughter strands and serve as templates for modifying newly deposited histones. The histone code hypothesis proposes that specific combinations of modifications determine chromatin states and gene expression patterns, and this information can be propagated epigenetically. ### Non-coding RNAs Non-coding RNAs (ncRNAs) constitute a third layer of epigenetic regulation. MicroRNAs (miRNAs), approximately 22 nucleotides in length, mediate post-transcriptional gene silencing by base-pairing with complementary sequences in messenger RNAs (mRNAs), leading to mRNA degradation or translational repression. Piwi-interacting RNAs (piRNAs) silence transposable elements in germ cells, protecting genome integrity across generations. Long non-coding RNAs (lncRNAs), exceeding 200 nucleotides, regulate gene expression through diverse mechanisms. The lncRNA Xist is essential for X-chromosome inactivation in female mammals, coating the inactive X chromosome and recruiting chromatin-modifying complexes. Other lncRNAs act as scaffolds, bringing together protein complexes that modify chromatin, or as decoys, sequestering [transcription factors](/knowledge/molecular-biology/transcription-factor) away from their target genes. The heritability of ncRNA-mediated epigenetic states is particularly evident in plants and nematodes, where small RNAs can trigger RNA-directed DNA methylation (RdDM) at homologous genomic loci, establishing heritable silencing. In mammals, the extent of RNA-mediated transgenerational inheritance remains debated, but evidence from mouse models suggests that certain small RNA populations can be transmitted through sperm. ## Transgenerational [Epigenetic Inheritance](/knowledge/molecular-biology/epigenetic-inheritance) ### Reprogramming and Its Exceptions During mammalian development, epigenetic marks undergo two major waves of reprogramming. The first occurs in primordial germ cells (PGCs), where genome-wide demethylation erases most parental methylation marks. The second occurs after fertilization, when the paternal genome is actively demethylated and the maternal genome undergoes passive demethylation. These reprogramming events ensure that most epigenetic marks are reset, allowing the zygote to establish a pluripotent state. However, some genomic regions escape reprogramming. Imprinted genes, for example, maintain parent-of-origin-specific methylation at differentially methylated regions (DMRs), regulated by imprinting control centers. Retrotransposons and other repetitive elements also resist demethylation, partly through the action of the zinc-finger protein ZFP57, which recruits the maintenance methyltransferase machinery to specific sequences. Transgenerational epigenetic inheritance occurs when epigenetic marks survive both waves of reprogramming and are transmitted to offspring. The term "transgenerational" is strictly defined: in mammals, it requires that the effect persists in the F3 generation (great-grandchildren) for a gestating female exposed to an environmental insult, because the F1 embryo contains F2 germ cells, and the F2 embryo contains F3 germ cells. For paternal exposure, F2 is sufficient, as no in utero exposure occurs. ### Examples in Plants and Animals Plants exhibit the most robust transgenerational epigenetic inheritance. The flowering plant *Arabidopsis thaliana* has provided numerous examples. The *FWA* gene, normally silenced by methylation, can be reactivated by ectopic expression of the demethylase ROS1, and this reactivated state is inherited for multiple generations. Similarly, the *SPL* gene and the *BONSAI* locus show heritable methylation variants that affect morphology. In animals, the nematode *Caenorhabditis elegans* demonstrates RNA-mediated transgenerational inheritance. Injection of double-stranded RNA targeting a gene can produce silencing that persists for several generations, mediated by small RNAs and the Argonaute protein HRDE-1. In mammals, the agouti viable yellow (Avy) allele in mice is a classic example. The Avy allele contains an intracisternal A-particle (IAP) retrotransposon inserted upstream of the agouti gene. Methylation of this element varies between individuals, producing a range of coat colors from yellow (unmethylated) to agouti (methylated), and these methylation states are transmitted to offspring. ## Epigenetic Variation and Natural Selection ### Epialleles and Phenotypic Variation An epiallele is a variant form of a gene defined by its epigenetic state rather than its DNA sequence. Epialleles can arise spontaneously or in response to environmental cues, and they can produce heritable phenotypic variation. The Avy allele in mice is a metastable epiallele—its methylation state is established stochastically early in development and then maintained, producing a bimodal distribution of phenotypes. Spontaneous epimutation rates are substantially higher than genetic mutation rates. Studies in *Arabidopsis* have measured epimutation rates at CpG sites of approximately 10⁻⁴ per site per generation, compared to genetic mutation rates of approximately 10⁻⁸ to 10⁻⁹. This four to five orders of magnitude difference means that epigenetic variation can be generated rapidly, potentially allowing populations to respond to environmental challenges faster than genetic mutation alone would permit. Epialleles can also arise from genetic variants that affect nearby methylation patterns. These are termed "obligate" epialleles, as their epigenetic state is determined by the underlying sequence. In contrast, "facultative" epialleles are independent of sequence variation and represent truly epigenetic variation. Distinguishing between these types is crucial for understanding the evolutionary significance of epigenetic variation. ### Selection on Epigenetic States Natural selection can act on epigenetic variation if three conditions are met: the epigenetic state must influence phenotype, the phenotype must affect fitness, and the epigenetic state must be heritable. Numerous studies have demonstrated that epigenetic variation affects traits under selection. In *Arabidopsis*, methylation variants at the *FWA* locus affect flowering time, a trait closely tied to reproductive success. In yeast, epigenetic silencing of the *FLO11* gene affects biofilm formation and invasive growth, traits subject to selection in natural populations. The evolutionary dynamics of epigenetic variation differ from genetic variation in important ways. Epimutations are reversible—a methylated epiallele can revert to unmethylated at a rate much higher than genetic reversion. This reversibility means that selection on epigenetic states can be rapid but also that stable adaptation may require genetic assimilation, where beneficial epigenetic states are eventually fixed by genetic mutations. ## Evidence from Natural Populations ### Plants: Arabidopsis and Beyond Natural populations of *Arabidopsis thaliana* show extensive epigenetic variation. A landmark study of 1,107 wild *Arabidopsis* accessions identified thousands of differentially methylated regions (DMRs) that were not explained by underlying genetic variation. Many of these DMRs were associated with differentially expressed genes, and some correlated with environmental variables at the collection sites, suggesting local adaptation of epigenetic states. The role of DNA methylation in plant adaptation is further supported by studies of stress responses. When *Arabidopsis* plants are exposed to drought, salt, or pathogen attack, they acquire specific methylation changes at stress-responsive genes. Some of these changes persist in progeny, potentially providing a mechanism for transgenerational stress memory. Similar findings have been reported in rice (*Oryza sativa*), where methylation variation at the *OsMIR156* locus affects tillering and yield, and in poplar trees, where methylation differences correlate with latitude and climate at the site of origin. ### Animals: Darwin's Finches and Fish Evidence for epigenetic variation in natural animal populations is accumulating. Studies of Darwin's finches on the Galápagos Islands have examined DNA methylation in relation to beak morphology and diet. Researchers have identified differentially methylated regions between species with different beak shapes, including genes involved in bone morphogenesis and craniofacial development. Whether these methylation differences are causes or consequences of genetic divergence remains an active area of investigation. In fish, epigenetic variation has been linked to [environmental adaptation](/blog/careers/environmental-adaptation-how-organisms-adjust-and-what-it-means-for-careers). Three-spined sticklebacks (*Gasterosteus aculeatus*) that have independently colonized freshwater habitats from marine ancestors show convergent methylation changes at genes involved in osmoregulation and fin morphology. Similarly, Atlantic salmon show methylation differences associated with migration timing and life-history strategies. These studies suggest that epigenetic variation can facilitate rapid adaptation to new environments, potentially preceding genetic changes that later stabilize the adaptive phenotype. ## Methods for Studying Epigenetic Evolution ### Genome-wide Epigenetic Profiling Several techniques enable genome-wide mapping of epigenetic marks. Bisulfite sequencing is the gold standard for DNA methylation analysis. Treatment of DNA with sodium bisulfite converts unmethylated cytosines to uracil while leaving methylated cytosines intact. Subsequent PCR amplification and sequencing reveal the methylation status of individual cytosines. Whole-genome bisulfite sequencing (WGBS) provides single-base resolution across the entire genome, while reduced representation bisulfite sequencing (RRBS) enriches for CpG-dense regions, reducing cost and sequencing depth requirements. Chromatin immunoprecipitation followed by sequencing (ChIP-seq) maps histone modifications and transcription factor binding sites. Chromatin is cross-linked with formaldehyde, sheared by sonication, and immunoprecipitated with antibodies specific to particular histone modifications. The associated DNA is then purified and sequenced, revealing genomic regions enriched for the modification of interest. Typical ChIP-seq protocols use 1% formaldehyde for cross-linking, sonication to fragment chromatin to 200–600 base pairs, and 1–5 μg of antibody per immunoprecipitation. The assay for transposase-accessible chromatin using sequencing (ATAC-seq) identifies regions of open chromatin. The hyperactive Tn5 transposase simultaneously fragments and tags accessible chromatin with sequencing adapters, enabling the identification of regulatory elements. ATAC-seq requires only 50,000–100,000 cells and can be completed in a single day, making it particularly suitable for studies of limited samples from natural populations. ### Common Model Systems *Arabidopsis thaliana* remains the premier model for plant epigenetic research due to its small genome (135 Mb), short generation time, and extensive resources including mutant collections for all known chromatin modifiers. The availability of epigenetic recombinant inbred lines (epiRILs)—populations derived from parents that differ in methylation but not sequence—has enabled mapping of epigenetic quantitative trait loci (epiQTLs). In animals, mice provide the best mammalian model, particularly for transgenerational studies. The agouti and axin-fused alleles offer visually scorable epigenetic phenotypes. However, the long generation time and cost of mouse breeding limit the scale of evolutionary experiments. *C. elegans* and *Drosophila melanogaster* offer faster generation times and powerful genetic tools, though their [epigenetic mechanisms](/knowledge/molecular-biology/epigenetic-mechanisms) differ from mammals in important respects. For example, *C. elegans* lacks canonical DNA methylation but relies heavily on small RNA-mediated inheritance. ## Epigenetics vs. Genetic Mutations in Evolution ### Mutation Rates and Epimutation Rates The rates of genetic and epigenetic change differ dramatically. Genetic mutation rates in nuclear genomes range from 10⁻⁸ to 10⁻⁹ per base pair per generation. In contrast, epimutation rates at CpG sites in *Arabidopsis* have been measured at approximately 10⁻⁴ per site per generation—four to five orders of magnitude higher. This difference has profound implications for evolutionary dynamics. High epimutation rates mean that epigenetic variation is abundant in populations, providing a large substrate for selection. However, high rates also mean that epigenetic states are less stable than genetic alleles. A beneficial epiallele may be lost through reversion before selection can fix it in a population. This trade-off between variation generation and stability is a central consideration in understanding the evolutionary role of epigenetics. The stability of epigenetic marks varies by type and genomic context. CG methylation in plants is highly stable, with rates of spontaneous loss at approximately 10⁻⁴ per generation. Non-CG methylation (CHG and CHH contexts) is less stable and more dynamic. Histone modifications are generally less stable than DNA methylation, with turnover times ranging from minutes to hours for acetylation and days to weeks for methylation. ### Stability Across Generations The transgenerational stability of epigenetic marks is a critical parameter for evolutionary models. In *Arabidopsis*, most CG methylation variants are stably inherited across generations, while CHH methylation variants show more variability. In mammals, the extensive reprogramming during embryogenesis limits transgenerational inheritance, but some loci consistently escape reprogramming. Mathematical models of epigenetic evolution have explored the conditions under which epigenetic inheritance can contribute to adaptation. These models show that epigenetic variation is most beneficial when environments fluctuate on timescales of a few generations, allowing populations to track environmental changes through reversible epigenetic responses. When environments are stable over long periods, genetic assimilation of beneficial epigenetic states is favored, converting transient epigenetic adaptations into permanent genetic changes. ## Common Pitfalls and Misconceptions ### Overstating Inheritance A common error is assuming that all epigenetic changes are heritable across generations. In reality, most epigenetic marks are reset during development, and only a small fraction survive reprogramming. Somatic epigenetic changes—those occurring in body cells rather than germ cells—are not inherited by offspring. Even germline epigenetic changes must survive the two waves of reprogramming to be transmitted transgenerationally. Another frequent mistake is conflating "transgenerational" with "intergenerational." An intergenerational effect is one that persists only in the directly exposed generation or its immediate offspring (F1 for maternal exposure, F2 for paternal exposure). True transgenerational inheritance requires persistence in unexposed generations (F2 or F3 and beyond). Many claimed examples of transgenerational epigenetic inheritance in mammals fail to meet this strict criterion. ### Confusing Epigenetics with Gene Expression Epigenetics is often conflated with gene expression changes in general. Not all changes in gene expression are epigenetic. Epigenetics specifically refers to heritable changes—stable across cell divisions or generations—that occur without DNA sequence alteration. A transient change in transcription factor activity or mRNA stability is not epigenetic unless it results in a self-propagating state. Similarly, it is important to distinguish between [epigenetic mechanisms](/knowledge/molecular-biology/epigenetic-mechanisms) and the phenotypes they produce. DNA methylation, histone modification, and non-coding RNAs are mechanisms; the resulting gene expression patterns are consequences. Demonstrating that a phenotype is epigenetic requires showing that it is heritable and not explained by genetic variation. A related misconception is that epigenetic changes are always beneficial or adaptive. Epimutations, like genetic mutations, are largely neutral or deleterious. Only a small fraction of epigenetic variation is likely to be adaptive, and the same selective filters that act on genetic variation also act on epigenetic variation. ## Summary and Future Directions ### Open Questions Several fundamental questions remain unresolved. First, what is the relative contribution of epigenetic versus genetic variation to adaptation in natural populations? Answering this requires studies that jointly measure genetic and epigenetic variation and their effects on fitness. Second, how common is transgenerational epigenetic inheritance in mammals, and what molecular mechanisms protect certain loci from reprogramming? Third, what are the evolutionary dynamics of epigenetic variation in populations—how do epimutation rates, selection coefficients, and reversion rates interact to determine the fate of epialleles? Technological advances are enabling new approaches to these questions. [Long-read sequencing technologies](/knowledge/bioinformatics/long-read-sequencing-technologies-pacbio-and-oxford-nanopore) can simultaneously detect genetic and epigenetic variation, allowing comprehensive characterization of both types of variation in natural populations. CRISPR-based epigenome editing enables causal manipulation of specific epigenetic marks, testing their functional significance. Finally, experimental evolution studies in organisms with short generation times can directly observe the dynamics of epigenetic variation under controlled selection regimes. The integration of epigenetics into evolutionary biology represents a significant expansion of the Modern Synthesis. It does not challenge the centrality of natural selection or genetic inheritance but enriches our understanding of the mechanisms that generate heritable phenotypic variation. As research progresses, the boundary between genetic and epigenetic inheritance is likely to blur, revealing a more complex and dynamic picture of how organisms evolve. ## Frequently Asked Questions ### Does epigenetics affect evolution? Yes. Epigenetic variation can be heritable, influence phenotype, and be subject to natural selection. Epigenetic changes can generate heritable phenotypic variation faster than genetic mutations, potentially accelerating adaptation. However, epigenetic effects on evolution are generally considered supplementary to genetic mechanisms rather than replacements for them. ### Can epigenetic changes be passed to offspring? Some epigenetic changes can be passed to offspring through transgenerational epigenetic inheritance. This requires that epigenetic marks survive the reprogramming that occurs during gamete formation and early embryonic development. Plants show robust transgenerational epigenetic inheritance, while mammals show more limited inheritance due to extensive reprogramming. Not all epigenetic changes are heritable—somatic changes are never passed to offspring. ### Are epigenetic changes permanent? No. Epigenetic changes are generally reversible. DNA methylation can be removed by passive dilution during cell division or active demethylation by TET enzymes. Histone modifications are dynamically regulated by opposing enzymes. Epimutation rates are typically orders of magnitude higher than genetic mutation rates, meaning epigenetic states can change rapidly within and across generations. ### How do epigenetic changes arise? Epigenetic changes arise through several mechanisms. They can occur spontaneously during DNA replication or repair, when methylation patterns are mis-copied or incompletely maintained. They can be induced by environmental factors, including stress, nutrition, and toxins, which can alter the activity of epigenetic enzymes. They can also be influenced by genetic variation, as sequence differences can affect nearby methylation patterns. ### What is an epiallele? An epiallele is a variant form of a gene defined by its epigenetic state rather than its DNA sequence. For example, the same gene sequence can exist in a methylated (silenced) or unmethylated (active) state, and these states can be inherited. Epialleles can produce heritable phenotypic variation even when the underlying DNA sequence is identical. ### Do epigenetic changes replace genetic mutations in evolution? No. Epigenetic changes do not replace genetic mutations in evolution. Both types of variation contribute to heritable phenotypic diversity. Epigenetic variation is generated faster and is more reversible, making it useful for short-term adaptation to fluctuating environments. Genetic mutations provide more stable, long-term changes. Beneficial epigenetic states may eventually be stabilized by genetic mutations through a process called genetic assimilation. ### What methods are used to study epigenetic inheritance? Several methods are used to study epigenetic inheritance. Bisulfite sequencing maps DNA methylation at single-base resolution. Chromatin immunoprecipitation followed by sequencing (ChIP-seq) identifies histone modifications and protein-DNA interactions. The assay for transposase-accessible chromatin using sequencing (ATAC-seq) maps open chromatin regions. For inheritance studies, these methods are applied to germ cells, gametes, and offspring across multiple generations to track the transmission of epigenetic marks. ## Key Takeaways - Epigenetics encompasses DNA methylation, histone modification, and non-coding RNA mechanisms that produce heritable changes in gene expression without altering DNA sequence. - Transgenerational epigenetic inheritance occurs when epigenetic marks survive reprogramming, with plants showing more robust inheritance than mammals. - Epimutation rates are 10⁴ to 10⁵ times higher than genetic mutation rates, generating abundant heritable phenotypic variation for natural selection to act upon. - Evidence from natural populations of *Arabidopsis*, Darwin's finches, and sticklebacks demonstrates that epigenetic variation correlates with environmental adaptation. - Epigenetic changes are reversible and less stable than genetic mutations, making them suited for rapid, short-term adaptation rather than long-term evolutionary change. - Epigenetic and genetic evolution are complementary: epigenetic variation can provide rapid responses, while genetic assimilation can stabilize beneficial epigenetic states. - Studying epigenetic evolution requires genome-wide profiling methods including bisulfite sequencing, ChIP-seq, and ATAC-seq, applied across generations in appropriate model systems. ## Further Reading - Mendizabal I et al. *Epigenetics and evolution*. Integrative and comparative biology. 2014. [PubMed 24838745](https://doi.org/10.1093/icb/icu040) - Seebacher F, Krause J. *Epigenetics of Social Behaviour*. Trends in ecology & evolution. 2019. [PubMed 31153645](https://doi.org/10.1016/j.tree.2019.04.017) - Ashe A, Colot V, Oldroyd BP. *How does epigenetics influence the course of evolution?*. Philosophical transactions of the Royal Society of London. Series B, Biological sciences. 2021. [PubMed 33866814](https://doi.org/10.1098/rstb.2020.0111) - Xavier MJ et al. *Transgenerational inheritance: how impacts to the epigenetic and genetic information of parents affect offspring health*. Human reproduction update. 2019. [PubMed 31374565](https://doi.org/10.1093/humupd/dmz017) - Muyle A et al. *Epigenetics drive the evolution of sex chromosomes in animals and plants*. Philosophical transactions of the Royal Society of London. Series B, Biological sciences. 2021. [PubMed 33866802](https://doi.org/10.1098/rstb.2020.0124) - Diez CM, Roessler K, Gaut BS. *Epigenetics and plant genome evolution*. Current opinion in plant biology. 2014. [PubMed 24424204](https://doi.org/10.1016/j.pbi.2013.11.017) ## Related Topics - [Epigenetics Affect Behavior](/knowledge/molecular-biology/epigenetics-affect-behavior) - [Epigenetics Affect Me with Meds](/knowledge/molecular-biology/epigenetics-affect-me-with-meds) - [Epigenetics Affect Mental Health](/knowledge/molecular-biology/epigenetics-affect-mental-health) - [Epigenetic Inheritance](/knowledge/molecular-biology/epigenetic-inheritance) - [Epigenetics Explained](/knowledge/molecular-biology/epigenetics-explained)
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