Nucleosome Occupancy: How DNA Packaging Affects Gene Activity
By Dr. Zubair Khalid, DVM, MS, PhD ·
Key Takeaways
- Nucleosome occupancy quantifies the probability that a specific genomic locus is wrapped by a histone octamer, forming the fundamental unit of chromatin. This occupancy is a dynamic property, not a static one, and is crucial for regulating DNA accessibility.
- High nucleosome occupancy physically occludes DNA, directly inhibiting essential cellular processes such as transcription, DNA replication, and DNA repair by preventing the binding of necessary protein machinery.
- Gene regulation is profoundly influenced by nucleosome occupancy, with active promoters typically featuring a nucleosome-free region (NFR) around the transcription start site, flanked by positioned nucleosomes, facilitating transcription factor binding and RNA polymerase access.
- Nucleosome assembly and disassembly are orchestrated by histone chaperones (e.g., CAF-1, HIRA) and ATP-dependent chromatin remodelers (e.g., SWI/SNF, ISWI families), which dynamically modulate occupancy to control DNA accessibility.
- Factors influencing nucleosome occupancy include intrinsic DNA sequence preferences (e.g., AA/TT dinucleotides favoring bending), post-translational histone modifications (e.g., acetylation reducing histone-DNA interaction strength), and competition with sequence-specific DNA-binding proteins.
- Experimental determination of nucleosome occupancy is primarily achieved through MNase-seq, which digests linker DNA to isolate nucleosome-protected fragments, and ATAC-seq, which identifies accessible chromatin regions inversely correlated with occupancy.
The human genome contains roughly 6.4 billion base pairs of DNA, which, if stretched end to end, would extend about two meters. Yet this entire length is packed into a nucleus that is typically only 5 to 10 micrometers in diameter. This extraordinary feat of compaction is achieved through the hierarchical organization of DNA into chromatin, the complex of DNA and proteins that fills the nucleus. At the first and most fundamental level of this packaging lies the nucleosome, a bead-like structure that wraps a segment of DNA around a core of histone proteins. The extent to which DNA at any given location is wrapped into nucleosomes—a property known as nucleosome occupancy—is not uniform across the genome. It varies dramatically from one region to the next, and these variations have profound consequences for how genes are read, copied, and repaired.
What Is Nucleosome Occupancy?
Nucleosome occupancy is defined as the fraction of DNA molecules in a population of cells that are wrapped around a histone octamer at a specific genomic position. If every cell in a population has a nucleosome covering a particular stretch of DNA, that region has an occupancy of 1.0 (or 100%). If no cells have a nucleosome there, the occupancy is 0. If half the cells have a nucleosome and half do not, the occupancy is 0.5. This quantitative measure is distinct from the binary question of whether a nucleosome exists somewhere in the genome; it asks specifically how likely a given base pair is to be occupied.
The Nucleosome: The Basic Unit of Chromatin
To understand occupancy, one must first understand the nucleosome itself. As described in the Nucleosome Structure entry, a nucleosome consists of 147 base pairs of DNA wrapped in 1.65 left-handed superhelical turns around an octamer of four core histone proteins: H2A, H2B, H3, and H4. Two copies of each histone form the octamer, creating a spool-like structure. The DNA is held in place primarily through electrostatic interactions between the negatively charged phosphate backbone of DNA and positively charged lysine and arginine residues on the histones. A fifth histone, H1, binds to the linker DNA between nucleosomes and helps stabilize higher-order folding, but it is not part of the core particle.
The Nucleosome Model describes how these particles are arrayed along the DNA. In a typical chromatin fiber, nucleosomes are spaced at intervals of roughly 180 to 200 base pairs, meaning that about 147 base pairs are wrapped around the histone core and the remaining 30 to 50 base pairs serve as linker DNA connecting adjacent nucleosomes. This arrangement compacts the DNA by about a factor of six to seven relative to naked DNA, before higher-order folding into the 30-nanometer fiber and beyond.
Occupancy vs. Positioning
Nucleosome occupancy and nucleosome positioning are related but distinct concepts, and confusing them is a common source of error. Occupancy refers to the probability that a nucleosome is present at a given location. Positioning refers to the precise location of the nucleosome along the DNA sequence—that is, which 147 base pairs are wrapped around the histone octamer. A region of high occupancy may have nucleosomes positioned at many different translational frames (that is, shifted by a few base pairs in different cells), whereas a region of low occupancy may have the few nucleosomes that do form positioned at a single, exact location. Both properties are biologically important, but they are measured and interpreted differently. The Nucleosome Definition provides a formal treatment of the particle itself, while occupancy and positioning describe its distribution across the genome.
Why Nucleosome Occupancy Matters
The wrapping of DNA around histones is not a neutral packaging event. It physically occludes the DNA from proteins that need to read its sequence. The nucleosome surface covers nearly the entire length of the wrapped DNA, making the underlying bases inaccessible to sequence-specific DNA-binding proteins. This simple geometric fact has far-reaching implications for every DNA-templated process in the cell.
Gene Regulation
Transcription, the process by which RNA polymerase copies a gene into messenger RNA, requires the polymerase to access the promoter region and the gene body. RNA polymerase II, the enzyme responsible for transcribing protein-coding genes, is a large complex that cannot easily traverse a nucleosome. Moreover, the first step in transcription—the binding of general transcription factors to the core promoter—requires that the promoter DNA be free of nucleosomes. Consequently, the occupancy of nucleosomes at promoters is a major determinant of whether a gene can be transcribed.
The relationship between occupancy and transcription is not simply "low occupancy means the gene is on." Rather, the precise pattern of occupancy matters. Many active promoters in yeast and mammals are characterized by a nucleosome-free region (NFR) immediately upstream of the transcription start site, flanked by well-positioned nucleosomes. This NFR provides a landing pad for the transcription preinitiation complex. In contrast, inactive genes often have high nucleosome occupancy across their promoters, blocking access to the transcriptional machinery.
DNA Replication and Repair
Nucleosome occupancy also affects DNA replication. The replication machinery must unwind the double helix and synthesize new strands, but it cannot do so through a nucleosome without first removing or destabilizing it. The replication fork therefore encounters nucleosomes as a physical barrier. Cells have evolved mechanisms to disassemble nucleosomes ahead of the fork and reassemble them behind it, but the process is not instantaneous, and regions of high occupancy can slow replication fork progression.
Similarly, DNA repair pathways require access to damaged bases. Nucleotide excision repair, which removes bulky lesions such as those caused by ultraviolet light, operates much more efficiently on naked DNA than on nucleosomal DNA. The repair machinery must either wait for spontaneous nucleosome sliding or actively recruit chromatin remodelers to expose the damage. As a result, the rate of DNA repair—and therefore the mutation rate—varies across the genome as a function of nucleosome occupancy. Regions of high occupancy tend to have lower repair rates and higher mutation rates, a phenomenon that shapes the mutational landscape of cancer genomes.
How Nucleosomes Are Assembled and Remodeled
Nucleosome occupancy is not a static property. It is dynamically regulated by a suite of protein complexes that assemble, disassemble, slide, and exchange nucleosomes. These processes collectively determine the occupancy landscape at any given moment.
Histone Chaperones
The assembly of a nucleosome requires the delivery of histone proteins to DNA. Histones are highly basic proteins that would aggregate nonspecifically with DNA if left to their own devices. Histone chaperones are proteins that bind histones and escort them to the site of assembly, preventing inappropriate interactions and ensuring that assembly occurs at the right place and time.
The best-studied chaperone is the chromatin assembly factor 1 (CAF-1), which assembles nucleosomes onto newly replicated DNA during S phase. CAF-1 binds to the replication machinery and deposits H3-H4 tetramers onto the daughter strands immediately behind the replication fork. Another chaperone, histone regulator A (HIRA), assembles nucleosomes in a replication-independent manner, allowing nucleosome turnover in non-dividing cells. The histone chaperone ASF1 (anti-silencing function 1) hands H3-H4 dimers to both CAF-1 and HIRA, serving as a central hub in histone supply.
The disassembly of nucleosomes is equally important. During transcription, the FACT (facilitates chromatin transcription) complex destabilizes nucleosomes ahead of the elongating RNA polymerase, removing H2A-H2B dimers and allowing the polymerase to pass. FACT then reassembles the nucleosome behind the polymerase, restoring the chromatin structure. This "push and pull" of histone exchange means that nucleosome occupancy at actively transcribed genes is in constant flux.
ATP-Dependent Chromatin Remodelers
The second major class of regulators is the ATP-dependent chromatin remodelers. These are multi-subunit complexes that use the energy of ATP hydrolysis to alter nucleosome structure. They fall into four families in eukaryotes: SWI/SNF, ISWI, CHD, and INO80. Each family has distinct activities.
SWI/SNF family remodelers, such as yeast SWI/SNF and human BAF complexes, primarily slide or eject nucleosomes. They can create nucleosome-free regions by pushing nucleosomes away from a binding site or by completely removing them. This activity is often required for gene activation, as it opens up promoters and enhancers for transcription factor binding.
ISWI family remodelers, in contrast, tend to space nucleosomes evenly. They slide nucleosomes along DNA but do not eject them. This activity is important for establishing the regular nucleosome arrays seen in bulk chromatin and for assembling nucleosomes after replication.
CHD family remodelers are diverse. Some, like yeast Chd1, slide nucleosomes and promote their assembly. Others, like human CHD4 (part of the NuRD complex), are associated with transcriptional repression and may compact chromatin.
INO80 family remodelers are unique in their ability to exchange histone variants. The INO80 complex can replace the canonical histone H2A with the variant H2A.Z, which alters nucleosome stability. H2A.Z-containing nucleosomes are less stable and are often found flanking nucleosome-free regions at active promoters.
The net effect of these remodelers is that nucleosome occupancy is continuously modulated. A nucleosome can be assembled, slid along the DNA, partially unwrapped, or completely evicted in a matter of seconds to minutes. This dynamism is essential for the cell to respond quickly to environmental signals.
Factors That Influence Nucleosome Occupancy
Given the importance of occupancy, it is natural to ask what determines whether a given stretch of DNA will be wrapped around a histone octamer. The answer is multifaceted, involving both intrinsic properties of the DNA sequence and extrinsic factors such as histone modifications and protein competition.
DNA Sequence and Nucleosome Positioning Sequences
The DNA sequence itself influences nucleosome occupancy. This is because the double helix is not a rigid, uniform rod. Certain dinucleotide steps, particularly AA, TT, and TA, are easier to bend in the direction required for wrapping around the histone octamer. Conversely, stretches of poly(dA:dT) are stiff and resist bending, making them poor nucleosome formers. These sequence preferences are relatively weak—each base pair contributes only a small free energy difference—but over a 147-base-pair nucleosome, they can sum to a significant effect.
Genomic regions that are intrinsically favorable or unfavorable for nucleosome formation are called nucleosome positioning sequences. The best-characterized example is the 5S ribosomal RNA gene from the frog Xenopus, which has a strong intrinsic preference for a single nucleosome position. In yeast, poly(dA:dT) tracts are commonly found in promoters, where they help maintain nucleosome-free regions. The Nucleosome vs Nucleotide distinction is relevant here: a nucleotide is a single base, whereas a nucleosome encompasses 147 of them, and the sequence context across that entire span matters.
However, DNA sequence alone is not sufficient to explain the occupancy landscape. The intrinsic preferences are modest, and they can be overridden by trans-acting factors. In fact, genome-wide studies have shown that the correlation between predicted and actual nucleosome occupancy is only moderate, indicating that other factors play substantial roles.
Histone Modifications
Histone proteins are subject to a wide array of post-translational modifications, including acetylation, methylation, phosphorylation, and ubiquitination. These modifications occur primarily on the N-terminal tails of the histones, which protrude from the nucleosome core. They can alter nucleosome stability directly by changing the electrostatic charge of the histones, or indirectly by recruiting proteins that remodel chromatin.
Acetylation is the best-understood modification with respect to occupancy. Acetyl groups neutralize the positive charge on lysine residues, weakening the interaction between the histone tail and the negatively charged DNA. This can promote nucleosome unwrapping and increase DNA accessibility. Histone acetyltransferases (HATs) such as Gcn5 and p300 add acetyl groups, while histone deacetylases (HDACs) remove them. In general, high levels of acetylation are associated with low nucleosome occupancy and active transcription.
Methylation has more variable effects depending on which lysine is methylated and to what degree. Methylation of H3K4 (lysine 4 of histone H3) is associated with active promoters and is often found at the edges of nucleosome-free regions. Methylation of H3K9 and H3K27 is associated with heterochromatin and transcriptional repression, and these marks recruit proteins that promote nucleosome assembly and compaction. The Histone Nucleosome entry provides further detail on how these modifications are read by effector proteins.
Competition with DNA-Binding Proteins
A third major determinant of occupancy is competition. Transcription factors and other sequence-specific DNA-binding proteins can displace nucleosomes by binding to their recognition sites. The outcome of this competition depends on the relative affinities of the nucleosome and the transcription factor for the DNA, as well as on the kinetics of binding.
In many cases, the binding of a transcription factor is the initiating event that leads to nucleosome eviction. The factor binds to its site in the linker DNA or at the edge of a nucleosome, then recruits chromatin remodelers to push the nucleosome away. This is how many inducible genes are activated: a signal triggers the binding of a transcription factor, which then remodels the local chromatin to create a nucleosome-free region.
This competition also explains why nucleosome occupancy is often lower at transcription factor binding sites than at random genomic locations. The sites are occupied by proteins much of the time, preventing nucleosome formation. The Nucleosome Concept encompasses this idea of a dynamic equilibrium between nucleosomes and other DNA-binding proteins.
Methods to Measure Nucleosome Occupancy
Measuring nucleosome occupancy requires determining, at each position in the genome, what fraction of cells have a nucleosome. This is technically challenging because it requires both high resolution (to distinguish adjacent nucleosomes) and quantitative accuracy (to measure fractional occupancy). Several complementary techniques have been developed.
MNase-seq
The gold-standard method for measuring nucleosome occupancy is MNase-seq. Micrococcal nuclease (MNase) is an enzyme that preferentially cleaves linker DNA between nucleosomes, leaving the 147-base-pair nucleosome core protected. The experimental workflow is as follows:
- Isolate nuclei from cells and digest chromatin with MNase. The amount of enzyme and digestion time must be carefully titrated. A typical reaction uses 0.1 to 1 unit of MNase per microgram of DNA, incubated at 37°C for 5 to 15 minutes. Over-digestion will degrade nucleosomal DNA; under-digestion will leave linker DNA intact.
- Stop the reaction by adding EDTA (to chelate the calcium ions required for MNase activity) and place on ice.
- Purify the digested DNA. The mononucleosome fraction (approximately 147 base pairs) is isolated by agarose gel electrophoresis.
- Prepare a sequencing library and perform high-throughput sequencing.
- Map the sequencing reads to the reference genome. The density of reads at each position reflects the frequency of nucleosome protection, which is proportional to occupancy.
MNase-seq provides a genome-wide view of nucleosome occupancy at base-pair resolution. However, it has limitations. MNase has some sequence bias, cleaving AT-rich regions more readily, which can create artifacts. Additionally, the technique measures the average occupancy across millions of cells, obscuring cell-to-cell variability.
ATAC-seq
Assay for Transposase-Accessible Chromatin using sequencing (ATAC-seq) is a complementary method that measures chromatin accessibility rather than nucleosome occupancy directly. The technique uses a hyperactive Tn5 transposase that inserts sequencing adapters into accessible (nucleosome-free) DNA. The workflow is:
- Lysed nuclei are incubated with the Tn5 transposase for 30 minutes at 37°C.
- The transposase simultaneously fragments the DNA and ligates adapters in a process called tagmentation.
- The tagged DNA is purified, amplified by PCR (typically 10 to 12 cycles), and sequenced.
Regions of low nucleosome occupancy produce many sequencing reads, while regions of high occupancy produce few. ATAC-seq can also reveal nucleosome positioning because the transposase creates a characteristic ~147-base-pair periodicity in read density at nucleosome-occupied regions. The advantage of ATAC-seq is that it requires very few cells (as few as 500) and is faster than MNase-seq. Its disadvantage is that it measures accessibility, which is related to but not identical with occupancy.
ChIP-seq for Histone Marks
Chromatin immunoprecipitation followed by sequencing (ChIP-seq) can measure the occupancy of specific histone modifications. The workflow is:
- Crosslink proteins to DNA using formaldehyde (typically 1% formaldehyde for 10 minutes at room temperature).
- Shear the chromatin by sonication into fragments of 200 to 600 base pairs.
- Immunoprecipitate with an antibody specific to the histone modification of interest.
- Reverse the crosslinks, purify the DNA, and sequence it.
ChIP-seq for histone modifications provides information about where modified nucleosomes are located, which correlates with occupancy but also reports on the functional state of the chromatin. For example, ChIP-seq for H3K4me3 marks active promoters, while H3K27me3 marks repressed regions. This technique is essential for linking occupancy to gene activity but does not directly measure the fraction of cells with a nucleosome at each position.
Nucleosome Occupancy and Gene Expression
The connection between nucleosome occupancy and gene expression is best understood by examining the architecture of promoters and enhancers.
Promoter Architecture
A typical RNA polymerase II promoter in a metazoan consists of a core promoter (containing the transcription start site and binding sites for general transcription factors) surrounded by regulatory elements. The nucleosome occupancy pattern at active promoters is remarkably consistent: a nucleosome-free region of about 150 base pairs surrounds the transcription start site, flanked by well-positioned nucleosomes at approximately -1 and +1 positions relative to the start site.
The +1 nucleosome is particularly important. It is the first nucleosome downstream of the transcription start site and is enriched for the histone variant H2A.Z. This nucleosome is often partially unwrapped, allowing RNA polymerase to initiate transcription. The -1 nucleosome, upstream of the start site, is also dynamic and can be evicted during transcriptional activation.
In contrast, inactive promoters often lack a clear nucleosome-free region. Instead, they are covered by nucleosomes that occlude the transcription start site. The transition from inactive to active states involves the remodeling of this nucleosome landscape, typically initiated by the binding of activator proteins to enhancer elements.
Enhancer-Promoter Communication
Enhancers are regulatory DNA elements that can activate transcription from a promoter over long distances, sometimes hundreds of kilobases away. Nucleosome occupancy at enhancers is also dynamic. Active enhancers are characterized by low nucleosome occupancy, high levels of H3K4me1 and H3K27ac, and the presence of the pioneer transcription factors that can bind nucleosomal DNA.
The mechanism by which enhancers communicate with promoters is not fully understood, but it involves the physical looping of the intervening DNA. This looping brings the enhancer into proximity with the promoter, and the low nucleosome occupancy at both elements facilitates the assembly of the transcriptional machinery. Nucleosome occupancy in the intervening region may also matter: regions of high occupancy can form barriers that prevent enhancer-promoter interactions, while low occupancy may facilitate looping.
A classic example of occupancy-regulated gene expression is the GAL gene cluster in yeast. When glucose is present, the GAL1 promoter is occupied by nucleosomes and the gene is off. When galactose is added, the activator Gal4 binds to upstream activating sequences, recruits the SWI/SNF remodeler, and evicts the nucleosomes from the promoter. This creates a nucleosome-free region that allows the general transcription machinery to assemble. The entire process takes minutes and is fully reversible when galactose is removed.
In mammalian cells, inducible genes such as FOS and JUN show similar dynamics. These immediate-early genes have promoters that are poised with a nucleosome-free region and a paused RNA polymerase. Upon stimulation, the polymerase is released and the gene is transcribed. The nucleosome occupancy at these promoters changes only modestly, reflecting the fact that they are already in a permissive state.
Common Misconceptions and Pitfalls
Several misconceptions about nucleosome occupancy are common among students and even practicing scientists. Being aware of these pitfalls will help you interpret data and design experiments correctly.
Occupancy vs. Positioning
The most common error is conflating occupancy with positioning. A region can have high occupancy but poor positioning, meaning that nucleosomes are present in most cells but at different positions. Conversely, a region can have low occupancy but strong positioning, meaning that the few nucleosomes that form are always at the same location. These two properties are measured differently and have different biological consequences. When reading a nucleosome map, always ask whether the data report the probability of nucleosome presence (occupancy) or the precision of nucleosome location (positioning).
Dynamic Nature of Chromatin
A second misconception is that nucleosome occupancy is a static property. In reality, nucleosomes are constantly being assembled, disassembled, slid, and exchanged. The occupancy measured in a population of cells is a time-averaged snapshot of a highly dynamic system. A nucleosome that appears to be stably positioned in a population may be turning over rapidly in individual cells. This dynamism is essential for gene regulation, allowing rapid responses to environmental changes.
Population Averages
A third pitfall is ignoring cell-to-cell variability. Most occupancy measurements are performed on millions of cells, and the resulting data represent an average. If a promoter has an occupancy of 0.5, this could mean that all cells have a partially unwrapped nucleosome, or that half the cells have a fully wrapped nucleosome and half have none. These two scenarios have very different biological implications. Single-cell techniques, such as single-cell ATAC-seq, are beginning to address this issue, but they remain technically challenging and are not yet routine.
Summary of Core Concepts
- Nucleosome occupancy is the fraction of cells in which a given DNA position is wrapped around a histone octamer.
- Occupancy is distinct from positioning, which describes the precise location of nucleosomes.
- High occupancy blocks access to DNA, inhibiting transcription, replication, and repair.
- Nucleosome occupancy is dynamically regulated by histone chaperones and ATP-dependent remodelers.
- DNA sequence, histone modifications, and competition with DNA-binding proteins all influence occupancy.
- MNase-seq, ATAC-seq, and ChIP-seq are the primary experimental methods for measuring occupancy.
- Promoters and enhancers of active genes typically have low nucleosome occupancy.
Resources for Exploration
For further study, several public databases provide genome-wide nucleosome occupancy maps. The ENCODE project hosts nucleosome and chromatin accessibility data for human and mouse cell lines. The Saccharomyces cerevisiae genome browser at the University of California, Santa Cruz provides high-resolution nucleosome maps for yeast. The Nucleosome Chromatin entry offers an overview of how nucleosomes organize into higher-order structures, and Nucleosome Sliding explains the mechanisms by which remodelers move nucleosomes along DNA.
Frequently Asked Questions
What is nucleosome occupancy?
Nucleosome occupancy is the probability that a specific DNA region is wrapped around a histone octamer, measured as the fraction of cells in a population that have a nucleosome at that position. It ranges from 0 (no nucleosome in any cell) to 1 (nucleosome in every cell).
How is nucleosome occupancy measured?
The most common method is MNase-seq, which uses micrococcal nuclease to digest unprotected linker DNA, leaving nucleosome-protected fragments that are then sequenced. ATAC-seq measures chromatin accessibility, which inversely correlates with occupancy. ChIP-seq for histone modifications provides information about the location and state of nucleosomes.
Why is nucleosome occupancy important?
Nucleosome occupancy determines whether DNA is accessible to proteins that need to read its sequence. High occupancy blocks transcription factors and RNA polymerase, inhibiting gene expression. It also affects DNA replication and repair, influencing mutation rates across the genome.
What is the difference between nucleosome occupancy and positioning?
Occupancy is the probability that a nucleosome is present at a given location. Positioning is the precise location of the nucleosome along the DNA sequence. High occupancy can occur with poor positioning, and low occupancy can occur with strong positioning.
Can nucleosome occupancy change?
Yes. Nucleosome occupancy is highly dynamic. ATP-dependent chromatin remodelers can slide or eject nucleosomes, histone chaperones can assemble or disassemble them, and transcription factors can compete with nucleosomes for DNA binding. Changes in occupancy occur on timescales from seconds to minutes.
What factors determine nucleosome occupancy?
Three main factors: (1) DNA sequence, particularly the presence of flexible dinucleotides that favor wrapping or stiff poly(dA:dT) tracts that resist it; (2) histone modifications, such as acetylation that weakens histone-DNA interactions; and (3) competition with DNA-binding proteins, which can displace nucleosomes from their binding sites.
How does nucleosome occupancy affect gene expression?
Low occupancy at promoters creates nucleosome-free regions that allow the transcriptional machinery to assemble. High occupancy blocks access to the promoter and inhibits transcription. The precise pattern of occupancy—including the positions of the +1 and -1 nucleosomes—determines the transcriptional state of a gene.
Further Reading
- Lay FD, Kelly TK, Jones PA. Nucleosome Occupancy and Methylome Sequencing (NOMe-seq). Methods in molecular biology (Clifton, N.J.). 2018. PubMed 29224149
- Li Y et al. Human exonization through differential nucleosome occupancy. Proceedings of the National Academy of Sciences of the United States of America. 2018. PubMed 30104384
- Liu H et al. CHROMATIN REMODELING 11-dependent nucleosome occupancy affects disease resistance in rice. Plant physiology. 2023. PubMed 37403194
- Oberbeckmann E et al. Absolute nucleosome occupancy map for the Saccharomyces cerevisiae genome. Genome research. 2019. PubMed 31694866
- Jabre I et al. Differential nucleosome occupancy modulates alternative splicing in Arabidopsis thaliana. The New phytologist. 2021. PubMed 33135169
- Andreu-Vieyra CV, Liang G. Nucleosome occupancy and gene regulation during tumorigenesis. Advances in experimental medicine and biology. 2013. PubMed 22956498