Epigenetics vs Epigenesis: Key Differences Explained

By Dr. Zubair Khalid, DVM, MS, PhD · 2026-08-11

Introduction to Epigenetics and Epigenesis

The terms epigenetics and epigenesis share a common Greek root—epi, meaning "above" or "upon"—and both concern the relationship between genetic information and the organism that carries it. Despite this etymological kinship, they belong to fundamentally different domains of biology. Epigenetics is a molecular discipline concerned with heritable changes in gene expression that do not involve alterations to the underlying DNA sequence. Epigenesis is a developmental concept, centuries older, that describes how a complex organism emerges progressively from an undifferentiated egg through a series of increasingly specialized structures.

The distinction matters because conflating the two leads to conceptual errors in both molecular biology and developmental biology. A student who understands epigenetics as "the study of how organisms develop" will miss the mechanistic specificity of chromatin modification, while a student who treats epigenesis as "just another word for epigenetics" will fail to grasp the historical and conceptual foundations of developmental biology. This article clarifies both terms, their mechanisms, their histories, and the experimental approaches used to study each.

Historical Origins of the Terms

The concept of epigenesis dates to Aristotle, who argued against the preformationist view that a miniature adult (a homunculus) exists fully formed within the sperm or egg. Aristotle proposed instead that the embryo acquires its structures gradually, through a process of differentiation from undifferentiated material. This idea persisted through the centuries, and in 1651 William Harvey—famous for describing blood circulation—articulated the principle as ex ovo omnia ("everything from the egg"), asserting that all animals develop from eggs through progressive formation.

The term "epigenesis" itself was coined by Caspar Friedrich Wolff in 1759, who demonstrated that chick embryos develop progressively from simple layers of tissue. The word was later adopted by developmental biologists to describe the entire process by which a zygote becomes a fully formed organism.

The term "epigenetics" is far more recent. Conrad Hal Waddington coined it in 1942, combining "epigenesis" and "genetics" to describe "the branch of biology which studies the causal interactions between genes and their products which bring the phenotype into being." Waddington was interested in how a single genome could produce many different cell types—a question that remains central to both developmental and molecular biology. However, the modern molecular definition of epigenetics emerged later, in the 1970s and 1980s, as researchers identified specific chemical modifications to DNA and histones that could influence gene expression without changing the genetic code itself.

Why the Confusion Arises

The confusion between the two terms is understandable. Waddington explicitly built "epigenetics" on the foundation of "epigenesis," and both fields address how a fixed genome generates phenotypic diversity. Moreover, epigenetic mechanisms—DNA methylation, histone modification, and non-coding RNAs—play critical roles in developmental processes, meaning that epigenesis and epigenetics often co-occur in the same biological contexts. A developing embryo relies on epigenetic marks to silence pluripotency genes and activate lineage-specific programs; this is an epigenetic process occurring within an epigenetic (developmental) context.

The distinction, however, is clear: epigenesis is a developmental process; epigenetics is a molecular mechanism. Epigenesis describes what happens as an organism develops. Epigenetics describes how gene expression is regulated without changing the DNA sequence. One can study epigenetics in a single cell type in a dish, with no development occurring at all. Conversely, one can study epigenesis using classical embryological techniques that never examine a single methylated cytosine.

Core Concepts of Epigenetics

Epigenetics refers to stable, often heritable changes in gene expression that occur without changes to the DNA sequence itself. The "epigenome" is the collection of chemical modifications to DNA and chromatin that collectively determine which genes are active in a given cell. These modifications are mitotically heritable—when a cell divides, its daughter cells inherit the same epigenetic marks—and in some cases can be transmitted across generations.

The three principal molecular mechanisms of epigenetic regulation are DNA methylation, histone modification, and non-coding RNA-mediated regulation. Each operates through distinct biochemical pathways, but they frequently cooperate to establish and maintain specific gene expression patterns.

DNA Methylation

DNA methylation is the covalent addition of a methyl group to the C5 position of cytosine residues, producing 5-methylcytosine (5mC). In mammals, this occurs almost exclusively at cytosine residues followed by guanine—so-called CpG dinucleotides. The reaction is catalyzed by DNA methyltransferases (DNMTs): DNMT3A and DNMT3B establish new methylation patterns during development (de novo methylation), while DNMT1 maintains existing patterns during DNA replication by recognizing hemimethylated CpG sites and methylating the newly synthesized strand.

The functional consequence of DNA methylation depends on genomic context. Methylation within gene promoter regions—particularly at CpG islands, which are GC-rich regions of approximately 1 kilobase found in roughly 60–70% of human gene promoters—is generally associated with transcriptional repression. Methylated CpGs recruit methyl-CpG-binding domain (MBD) proteins such as MeCP2, which in turn recruit histone deacetylases (HDACs) and other chromatin-remodeling complexes, condensing the chromatin and blocking transcription factor access.

In contrast, methylation within gene bodies is often associated with active transcription, and methylation at intergenic regions helps silence transposable elements and maintain genomic stability. Approximately 70–80% of CpG dinucleotides in the human genome are methylated, but most CpG islands at gene promoters remain unmethylated.

Histone Modifications

Histones are the protein components of chromatin. Each nucleosome consists of 147 base pairs of DNA wrapped around an octamer of four core histone proteins—H2A, H2B, H3, and H4. The N-terminal tails of these histones protrude from the nucleosome and are subject to a wide array of post-translational modifications, including acetylation, methylation, phosphorylation, ubiquitination, and sumoylation.

Histone acetylation is the best-characterized modification. Histone acetyltransferases (HATs) such as p300/CBP add acetyl groups to lysine residues on histone tails, neutralizing the positive charge of the lysine and weakening the electrostatic interaction between the histone and the negatively charged DNA backbone. This relaxes chromatin structure, making DNA more accessible to transcription factors. Histone deacetylases (HDACs) reverse this process, restoring positive charge and promoting chromatin condensation.

Histone methylation is more complex because lysine residues can be mono-, di-, or tri-methylated, and the effect depends on which residue is modified. For example, trimethylation of lysine 4 on histone H3 (H3K4me3) is associated with active gene promoters, while trimethylation of lysine 27 on histone H3 (H3K27me3) is a hallmark of facultative heterochromatin and gene silencing. The enzymes that add methyl groups are histone methyltransferases (HMTs) such as EZH2 (the catalytic subunit of Polycomb repressive complex 2, PRC2), and those that remove them are histone demethylases such as LSD1 and the JmjC-domain family.

Non-coding RNAs

Non-coding RNAs (ncRNAs) regulate gene expression at multiple levels. MicroRNAs (miRNAs) are ~22-nucleotide RNAs that bind to complementary sequences in the 3' untranslated regions (UTRs) of messenger RNAs (mRNAs), leading to mRNA degradation or translational repression. Long non-coding RNAs (lncRNAs) are transcripts longer than 200 nucleotides that can guide chromatin-modifying complexes to specific genomic loci. For example, the lncRNA XIST is essential for X-chromosome inactivation in female mammals: it coats the inactive X chromosome and recruits PRC2, which deposits H3K27me3 marks and silences the chromosome.

These mechanisms are not mutually exclusive. DNA methylation, histone modifications, and non-coding RNAs often work together in feedback loops to establish and maintain stable gene expression states. For a broader overview of how these processes operate in human biology, see Epigenetics Explained.

Core Concepts of Epigenesis

Epigenesis is the developmental theory—and the biological reality—that an organism's structure and function emerge progressively from an undifferentiated zygote through a series of increasingly complex and specialized stages. It stands in direct opposition to preformationism, the now-discredited idea that the adult form exists pre-formed in miniature within the gametes.

Historical Context: Preformationism vs Epigenesis

The preformationism–epigenesis debate dominated embryology from the 17th through the 19th centuries. Preformationists argued that all the parts of an adult organism exist in miniature within the sperm (spermists) or the egg (ovists), and that development is merely the growth and unfolding of these pre-existing structures. This view had the appeal of simplicity—it required no mysterious "formative forces" to explain how complex structures arise—but it faced a logical problem: if the adult is pre-formed in the gamete, then the gamete of that adult must contain the next generation, and so on, leading to an infinite regress of nested homunculi.

Epigenesis, by contrast, held that structures arise de novo through a process of progressive differentiation. Wolff's observations of chick embryos in 1759 provided strong evidence for this view: he saw that the embryonic gut and nervous system form from simple sheet-like layers of tissue, not from miniature pre-formed organs. Karl Ernst von Baer, in 1828, formalized the principles of germ layer formation, showing that vertebrate embryos pass through conserved stages in which the three germ layers—ectoderm, mesoderm, and endoderm—give rise to specific tissues and organs.

Modern Understanding of Developmental Biology

Modern developmental biology is thoroughly epigenetic (in the developmental sense). A single fertilized egg—the zygote—contains a complete genome but no pre-formed structures. Through the processes of cleavage, gastrulation, and organogenesis, the embryo generates hundreds of distinct cell types arranged in precise three-dimensional patterns. This requires:

1. Cell division to generate sufficient cell numbers.
2. Cell differentiation to produce distinct cell types with specialized functions.
3. Morphogenesis to organize cells into tissues and organs.
4. Pattern formation to establish spatial coordinates and positional information.

These processes are driven by the differential expression of genes—which brings us back to epigenetics. The genome of every cell in an organism is essentially identical, yet a neuron and a hepatocyte express different sets of genes. The mechanisms that establish and maintain these differences are epigenetic (molecular) mechanisms operating within an epigenetic (developmental) context. This is precisely the insight Waddington captured with his famous "epigenetic landscape" metaphor: a marble rolling down a hillside of branching valleys, where each valley represents a possible developmental fate, and the contours of the landscape are shaped by gene regulatory networks.

Mechanisms of Epigenetic Regulation

The molecular machinery of epigenetics can be organized into three functional categories: writers, readers, and erasers. These enzymes establish, interpret, and remove epigenetic marks, respectively, and their coordinated activity determines the chromatin state of any given genomic region.

Writers, Readers, and Erasers

Writers are enzymes that deposit chemical modifications onto DNA or histones. The DNMT family (DNMT1, DNMT3A, DNMT3B) writes DNA methylation marks. Histone acetyltransferases (p300, CBP, GCN5) write acetylation marks. Histone methyltransferases (EZH2, SETD2, SUV39H1) write methylation marks. Each writer enzyme typically targets specific residues and works within specific protein complexes that direct it to appropriate genomic locations.

Readers are proteins that recognize and bind to specific epigenetic marks, translating them into functional outcomes. The bromodomain is a protein domain that recognizes acetylated lysine residues; bromodomain-containing proteins such as BRD4 recruit transcriptional machinery to acetylated promoters. The chromodomain recognizes methylated lysine residues; HP1 (heterochromatin protein 1) uses its chromodomain to bind H3K9me3 and establish heterochromatin. MBD proteins such as MeCP2 bind methylated CpG dinucleotides and recruit repressive complexes.

Erasers remove epigenetic marks. Ten-eleven translocation (TET) enzymes oxidize 5-methylcytosine to 5-hydroxymethylcytosine and further derivatives, ultimately leading to DNA demethylation. Histone deacetylases (HDAC1, HDAC2, SIRT1) remove acetyl groups. Histone demethylases (LSD1, KDM5A, KDM6A) remove methyl groups from specific lysine residues.

The balance between writers, readers, and erasers is dynamic and responsive to cellular signals. For example, in embryonic stem cells, the promoters of developmental regulator genes often carry both H3K4me3 (activating) and H3K27me3 (repressing) marks—so-called "bivalent domains" that keep genes poised for activation or silencing depending on differentiation cues.

Chromatin Remodeling

Beyond covalent modifications, chromatin structure is regulated by ATP-dependent chromatin remodeling complexes. These complexes—SWI/SNF, ISWI, CHD, and INO80 families—use the energy of ATP hydrolysis to slide, eject, or restructure nucleosomes. This changes the accessibility of DNA to transcription factors and other regulatory proteins.

The SWI/SNF complex, for example, can evict nucleosomes from promoter regions, creating nucleosome-free regions that allow transcription initiation. The ISWI family, by contrast, tends to space nucleosomes evenly, promoting chromatin compaction. Mutations in SWI/SNF subunits are found in approximately 20% of human cancers, underscoring the importance of chromatin remodeling in normal gene regulation.

The interplay between histone modifications and chromatin remodeling is bidirectional: histone modifications recruit remodeling complexes, and remodeling complexes facilitate the deposition of histone modifications. This creates a self-reinforcing system that can maintain a given chromatin state through many cell divisions—a key feature of epigenetic inheritance. For more detail on how these marks are maintained across cell divisions, see Epigenetics Inherited.

Epigenesis in Development

Epigenesis, as a developmental process, encompasses the entire sequence of events from fertilization to adulthood. While the term is historical, the phenomena it describes remain the central subject of developmental biology. Understanding how an organism's form emerges requires examining cell differentiation, morphogenesis, and pattern formation.

Cell Differentiation

Cell differentiation is the process by which cells become specialized for particular functions. In mammals, the zygote is totipotent—it can give rise to all cell types of the organism, including extraembryonic tissues. As development proceeds, cells become progressively restricted in their potential: pluripotent embryonic stem cells can form all embryonic lineages but not extraembryonic tissues; multipotent adult stem cells are limited to a few related cell types; and terminally differentiated cells are committed to a single fate.

Differentiation is driven by the activation and silencing of specific sets of genes. The transcription factor MyoD, for example, is both necessary and sufficient to convert fibroblasts into skeletal muscle cells—expressing MyoD in a fibroblast activates the entire muscle gene expression program. Similarly, the transcription factor PAX6 can induce ectopic eye formation when expressed in the Drosophila leg imaginal disc.

Epigenetic mechanisms lock in these differentiated states. Once a cell commits to a particular lineage, DNA methylation and histone modifications ensure that lineage-inappropriate genes remain silenced even after the initial differentiation signals have disappeared. This is why differentiated cells are stable: a hepatocyte does not spontaneously become a neuron, even though it contains the full genome.

Morphogens and Gradients

Pattern formation—the establishment of spatial organization—relies heavily on morphogens, signaling molecules that diffuse through tissues and form concentration gradients. Cells respond to different morphogen concentrations by activating different sets of target genes, effectively reading their position within the gradient.

The classic example is the Bicoid gradient in the Drosophila embryo. Bicoid protein is synthesized from mRNA localized at the anterior pole of the egg and diffuses posteriorly, forming an exponential concentration gradient. At high concentrations, Bicoid activates the anterior-posterior patterning gene hunchback; at lower concentrations, it activates other gap genes such as giant and knirps. The result is a segmented body plan established by differential gene expression along the anterior-posterior axis.

In vertebrates, Sonic hedgehog (Shh) forms a gradient across the neural tube that specifies distinct neuronal subtypes. High Shh concentrations activate the transcription factor Gli1, specifying ventral cell fates; lower concentrations activate Gli3, specifying more dorsal fates. The cellular response to Shh is not simply binary but graded, with different thresholds activating different target genes.

These developmental processes are intimately connected to epigenetic mechanisms. The response to morphogen gradients involves the rapid activation of immediate-early genes, but the stable maintenance of cell fate requires epigenetic silencing of alternative fates. The Polycomb and Trithorax group proteins—which deposit H3K27me3 and H3K4me3, respectively—are essential for maintaining the memory of developmental decisions through subsequent cell divisions.

Evidence and Experimental Methods

Both epigenetics and epigenesis are supported by extensive experimental evidence, and each field has developed specialized techniques for probing its respective phenomena.

Classic Experiments in Epigenetics

The agouti mouse experiment is a canonical demonstration of epigenetic inheritance. The agouti gene (A) encodes a signaling molecule that influences coat color; when expressed ectopically, it produces yellow fur, obesity, and diabetes. In viable yellow agouti (Aʸ) mice, a transposable element inserted upstream of the agouti gene can be variably methylated. When the element is hypermethylated, the agouti gene is silenced and mice have brown fur and normal metabolism. When hypomethylated, the gene is expressed and mice are yellow and obese. Importantly, the methylation state is established in the mother and influences the phenotype of offspring, demonstrating that epigenetic marks can be transmitted across generations.

Monozygotic twin studies provide evidence for epigenetic divergence over time. Identical twins share the same DNA sequence, yet they often differ in disease susceptibility and physical traits. Genome-wide DNA methylation analysis of monozygotic twins shows that their epigenomes are nearly identical early in life but diverge with age, particularly at CpG islands and in genes involved in immune function and metabolism. This divergence is influenced by environmental factors such as diet, smoking, and stress. For a deeper discussion of how environmental factors shape epigenetic marks, see Change Epigenetics.

Techniques for Studying Epigenesis

Classical embryology used surgical manipulation, grafting, and ablation to study developmental potential. The Spemann-Mangold organizer experiment (1924) demonstrated that transplanting the dorsal lip of the blastopore from one newt embryo to the ventral side of another induces a second body axis, identifying this region as the "organizer" that patterns the embryo.

Modern techniques for studying epigenesis include:

1. Lineage tracing: Using genetic markers (such as Cre-recombinase under cell-type-specific promoters) to permanently label a cell and all its descendants, revealing what tissues a given progenitor contributes to.
2. Live imaging: Time-lapse microscopy of developing embryos, often using fluorescent reporters, to observe cell movements, divisions, and differentiation in real time.
3. Single-cell transcriptomics: Sequencing the mRNA content of individual cells to reconstruct developmental trajectories and identify the gene expression states that cells pass through during differentiation.
4. Grafting and transplantation: Physically moving cells or tissues to new locations to test their developmental potential and the influence of surrounding tissue.

These approaches have revealed that development is not a rigid, deterministic program but a dynamic process with substantial plasticity. Cells can change fate when transplanted to new locations (regulative development), and many tissues can regenerate after damage.

Common Pitfalls and Misconceptions

Students frequently encounter specific conceptual errors when learning about epigenetics and epigenesis. Recognizing these pitfalls is essential for mastering the material.

Interchanging the Terms

The most common error is using "epigenetics" and "epigenesis" as synonyms. This is incorrect: epigenetics is a molecular mechanism (heritable changes in gene expression without DNA sequence change), while epigenesis is a developmental process (progressive emergence of form from an undifferentiated egg). A sentence like "Epigenesis explains how DNA methylation affects gene expression" is wrong; a sentence like "Epigenetic mechanisms contribute to epigenesis during embryonic development" is correct.

A useful mnemonic: epigenetics = gene regulation; epigenesis = development. If the sentence is about methylation, histones, or chromatin, it is epigenetics. If it is about embryos, differentiation, or morphogenesis, it is epigenesis.

Overlooking the Developmental Context

A second error is treating epigenetics as purely a molecular phenomenon divorced from development. While it is true that epigenetic marks can be studied in isolated cells, the evolutionary and biological significance of epigenetics lies largely in its role in development. The same epigenetic mechanisms that silence transposable elements in somatic cells also establish and maintain cell identity during embryogenesis. Ignoring this context leads to a fragmented understanding of both fields.

Assuming Epigenetics Is Only About DNA Methylation

Many introductory treatments focus exclusively on DNA methylation, leading students to believe that this is the only epigenetic mechanism. In reality, histone modifications and non-coding RNAs are equally important, and the three systems interact extensively. A complete answer to an exam question about epigenetic mechanisms should mention all three.

Confusing Heritability with Inheritance

Epigenetic marks are heritable—they are passed from mother to daughter cells during mitosis. However, transgenerational inheritance (passing marks from parents to offspring through gametes) is much rarer and more controversial. In mammals, most epigenetic marks are erased and re-established during gametogenesis and early embryogenesis. Only a small number of loci escape this reprogramming. When a student asks whether epigenetic changes can be inherited, the answer depends on the timescale: mitotic inheritance is well-established; transgenerational inheritance is limited and context-dependent. See Epigenetics Inherited for a detailed treatment.

Misunderstanding the Stability of Epigenetic Marks

Epigenetic marks are stable but not permanent. They can be actively removed by eraser enzymes or passively lost through failure to maintain during DNA replication. This reversibility is the basis for epigenetic therapies—drugs that inhibit DNMTs (such as 5-azacytidine) or HDACs (such as vorinostat) are used to treat certain cancers by reactivating silenced tumor suppressor genes.

Practical Summary and Study Tips

The following table summarizes the key differences between epigenetics and epigenesis:

Study Tips

1. Anchor each term to its core question. Epigenetics answers "How is gene expression controlled without changing the DNA?" Epigenesis answers "How does an organism develop from an egg?"
2. Learn the mechanisms by heart. For epigenetics, memorize the writers, readers, and erasers for both DNA methylation and histone modification. For epigenesis, memorize the stages of development: cleavage, gastrulation, neurulation, organogenesis.
3. Use examples. The agouti mouse is the classic example of epigenetic inheritance; the Spemann-Mangold organizer is the classic example of developmental induction.
4. Draw the epigenetic landscape. Waddington's metaphor—a marble rolling down branching valleys—captures the relationship between epigenesis (the rolling) and epigenetics (the contours of the landscape).
5. Practice distinguishing sentences. Take a statement like "The embryo develops through progressive differentiation" (epigenesis) versus "The promoter is hypermethylated, silencing the gene" (epigenetics).

Frequently Asked Questions

What is the difference between epigenetics and epigenesis?

Epigenetics is the study of heritable changes in gene expression that do not involve changes to the DNA sequence. It operates through molecular mechanisms such as DNA methylation, histone modification, and non-coding RNAs. Epigenesis is a developmental concept describing how an organism's form emerges progressively from an undifferentiated egg through cell differentiation, morphogenesis, and pattern formation. Epigenetics is a molecular mechanism; epigenesis is a developmental process.

Are epigenetics and epigenesis the same thing?

No. They are related—epigenetic mechanisms play important roles in developmental processes—but they are distinct concepts. Epigenetics concerns gene regulation at the molecular level; epigenesis concerns the emergence of organismal form during development. The terms share a Greek root and a historical connection through Waddington, but they are not interchangeable.

How do epigenetic modifications affect gene expression?

Epigenetic modifications affect gene expression by altering chromatin structure and the accessibility of DNA to transcription factors. DNA methylation at promoter CpG islands typically represses transcription by recruiting MBD proteins and histone deacetylases. Histone acetylation relaxes chromatin and promotes transcription; histone methylation can either activate or repress depending on the specific residue and degree of methylation. Non-coding RNAs can guide chromatin-modifying complexes to specific loci or directly degrade mRNA transcripts.

What is an example of epigenesis in development?

Gastrulation is a classic example of epigenesis. During gastrulation, the simple ball of cells that constitutes the blastula reorganizes into three germ layers—ectoderm, mesoderm, and endoderm—through coordinated cell movements. These layers then give rise to all tissues and organs of the adult organism. The process is progressive: structures emerge step by step, with each stage building on the previous one.

Can epigenetic changes be inherited?

Epigenetic marks are mitotically heritable—they are faithfully copied during cell division, ensuring that daughter cells maintain the same gene expression state as the parent cell. Transgenerational inheritance (transmission through gametes to offspring) is more limited. In mammals, most epigenetic marks are erased and reset during gametogenesis and early embryogenesis, but a small number of loci, such as imprinted genes and certain transposable elements, retain their marks across generations. The agouti mouse is a well-documented example of transgenerational epigenetic inheritance.

Why do students confuse epigenetics with epigenesis?

The confusion arises from several sources: the shared Greek root (epi), the historical connection (Waddington coined "epigenetics" from "epigenesis"), and the fact that epigenetic mechanisms operate during developmental processes. Additionally, both terms address the relationship between genotype and phenotype. The key to distinguishing them is to remember that epigenetics is about gene regulation (molecular) and epigenesis is about development (organismal).

What are the main mechanisms of epigenetic regulation?

The three main mechanisms are: (1) DNA methylation—the addition of methyl groups to cytosine residues, typically repressing transcription; (2) histone modification—post-translational modifications to histone proteins, including acetylation (activation), methylation (activation or repression depending on residue), and phosphorylation; and (3) non-coding RNA-mediated regulation—including microRNAs that degrade mRNA and long non-coding RNAs that guide chromatin-modifying complexes to specific loci.

How is epigenesis studied in modern biology?

Modern developmental biology uses a combination of approaches: lineage tracing with genetic markers to track cell fates; live imaging with fluorescent reporters to observe cell behavior in real time; single-cell transcriptomics to reconstruct gene expression trajectories during differentiation; and classical embryological techniques such as grafting, ablation, and transplantation to test developmental potential and inductive interactions.

Key Takeaways

• Epigenetics is a molecular mechanism: heritable changes in gene expression without DNA sequence alteration, mediated by DNA methylation, histone modification, and non-coding RNAs.
• Epigenesis is a developmental process: the progressive emergence of organismal form from an undifferentiated egg through differentiation, morphogenesis, and pattern formation.
• The two concepts are related—epigenetic mechanisms operate during development—but they are not synonyms.
• DNA methylation is catalyzed by DNMTs and typically represses transcription when present at promoter CpG islands.
• Histone modifications are written by HATs and HMTs, read by bromodomain and chromodomain proteins, and erased by HDACs and demethylases.
• Epigenesis was historically contrasted with preformationism and was established by Wolff, von Baer, and others as the correct model of development.
• Waddington's epigenetic landscape metaphor unifies the two concepts: the landscape represents developmental potential (epigenesis), and the molecular mechanisms shaping the landscape are epigenetic (epigenetics).

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