Meningiomas arise from the arachnoid cap cells of the meninges, the protective membranes enveloping the brain and spinal cord. Although the majority are classified as benign, WHO grade 1 tumors, their location within the confined space of the skull means that even slow growth can cause severe neurological impairment. Roughly half of patients undergo surgery simply to relieve pressure on the brain, and a substantial fraction of tumors recur after resection. Current classification relies on histopathological grading combined with limited molecular markers, chief among them mutations in the NF2 gene and alterations involving chromosomes 22 and 1p. But these markers correlate only loosely with clinical behavior, leaving oncologists unable to predict reliably which tumors will smolder and which will strike back.

The new research tackled this uncertainty by turning to DNA methylation, a chemical modification of cytosine bases in the genome that can switch genes on or off without altering the underlying DNA sequence. Methylation profiling has already transformed the diagnosis of gliomas and other brain tumors, providing a molecular fingerprint that often outperforms microscopic examination. The team applied high-resolution methylation arrays to large cohorts of meningioma samples spanning all WHO grades, from indolent grade 1 lesions to anaplastic grade 3 tumors, and asked a fundamental question: where in the genome does methylation change as tumors progress from harmless to lethal?

The answer pointed overwhelmingly to one genomic neighborhood. Clustered on chromosome 5q31, the protocadherin gene cluster comprises more than fifty genes arranged in three subfamilies — alpha, beta and gamma — spanning a stretch of DNA nearly a million base pairs long. These genes encode cell-surface proteins belonging to the cadherin superfamily, molecules that mediate cell-cell adhesion and are critically involved in neural development, axon guidance and the formation of synaptic connections. In healthy meningeal tissue, the cluster is active, expressing a combinatorial repertoire of protocadherin isoforms that helps cells recognize one another and maintain orderly tissue architecture. In progressing meningiomas, the researchers found, this entire region becomes progressively coated with methyl groups, effectively shutting down the cluster as if a master switch had been flipped.

What makes the discovery remarkable is the scale and logic of the silencing. Rather than individual genes being inactivated piecemeal, the methylation spreads in a long-range pattern across the entire locus, erasing the staggered, cell-type-specific expression patterns that normally allow each neuron or meningeal cell to display its own unique combination of protocadherins. The team’s analysis showed that this regional hypermethylation intensifies stepwise with tumor grade: grade 1 tumors show modest methylation, grade 2 tumors substantially more, and grade 3 tumors near-complete silencing. Crucially, the pattern was detectable even in tumors that had not yet acquired the histological features of malignancy, meaning the epigenetic clock of the tumor begins ticking before pathologists can see the damage.

The functional consequences of silencing the protocadherin cluster go to the heart of what makes a tumor dangerous. Protocadherins act as molecular barcodes that prevent cells from wandering; when they are lost, tumor cells gain the freedom to detach, migrate and invade surrounding brain tissue. The researchers demonstrated this experimentally by manipulating methylation in meningioma cell lines: pharmacological demethylation with DNA methyltransferase inhibitors restored protocadherin expression and reduced invasive behavior in vitro, while targeted re-expression of individual protocadherin genes suppressed cell migration and proliferation. Conversely, artificially silencing the genes in low-grade meningioma cells conferred a more aggressive phenotype. These gain- and loss-of-function experiments establish causality, not merely correlation — the epigenetic shutdown of the cluster is not a passenger event but an active engine of tumor progression.

The study also connected protocadherin silencing to existing molecular subtypes of meningioma. Tumors harboring NF2 mutations, which account for the majority of sporadic and radiation-induced cases, showed particularly pronounced methylation of the cluster, and the epigenetic signature outperformed conventional markers in predicting recurrence-free survival. When the authors integrated methylation data from the protocadherin locus into a predictive model, it stratified patients more accurately than WHO grade alone, correctly identifying a subset of histologically benign tumors that subsequently recurred and required additional treatment. This has immediate clinical implications: a methylation assay targeting the cluster could be incorporated into routine diagnostics, giving neurosurgeons and oncologists a sharper instrument for deciding which patients need close surveillance and adjuvant therapy and which can be spared it.

The mechanism behind the silencing appears to involve the canonical epigenetic machinery of cancer. Long-range methylation of the 5q31 region was accompanied by loss of the activating histone mark H3K4me3 and, in more advanced tumors, by recruitment of polycomb repressive complexes, which lock chromatin into a permanently closed configuration. The investigators found evidence that this is reinforced rather than random: once a threshold of methylation is crossed, the chromatin state becomes self-sustaining, explaining why silencing correlates so tightly with tumor grade and why it rarely reverses spontaneously. The clustered protocadherins thus join a growing list of tumor-suppressive epigenetic targets — alongside genes such as CDKN2A and RASSF1A — but with the distinction that an entire megabase-scale gene family, rather than a single locus, is affected.

Therapeutically, the findings open two avenues. The first is pharmacological: DNA demethylating agents such as decitabine and azacitidine are already approved for hematological malignancies, and the study’s cell-line experiments suggest they can reactivate the protocadherin cluster in meningioma cells. Delivering such drugs to the central nervous system remains a challenge, but the results provide a clear proof of principle that the epigenetic lesion is chemically reversible. The second avenue is more speculative but intriguing: because protocadherins sit on the cell surface, they are accessible to antibodies or engineered binding proteins, raising the possibility that future therapies could bypass the silenced genes entirely by supplying or mimicking the adhesion signals the tumor has lost.

Independent experts in neuro-oncology, while not involved in the study, note that it fits into a broader shift in brain tumor medicine toward epigenetics as both diagnostic compass and therapeutic target. The classification of diffuse gliomas was revolutionized by the discovery of IDH mutations and their associated methylation signatures, and methylation profiling is now standard practice in many neuropathology laboratories. Extending that framework to meningiomas — the most common tumor neurosurgeons encounter — could standardize what has until now been a subjective exercise in histological grading. It also highlights a recurring theme in cancer biology: the genome tells only half the story, and the regulatory layer written in methyl groups and histone marks often determines whether a tumor is manageable or malignant.

The research team, led by investigators based in Germany with collaborators across Europe, assembled one of the largest methylation datasets yet compiled for meningioma, combining retrospective tumor banks with matched long-term clinical follow-up. That combination allowed the authors to demonstrate that the epigenetic signature measured at the time of initial surgery predicted patient outcomes years in advance. The next steps will involve prospective validation in independent patient cohorts, standardization of the assay for clinical laboratories, and preclinical testing of demethylating strategies in animal models of meningioma. If those efforts succeed, patients facing a meningioma diagnosis may one day receive not just a grade but a genuinely predictive molecular forecast — and, for those whose tumors carry the silenced protocadherin signature, a treatment aimed at the root epigenetic cause rather than merely the surgical removal of its consequences.

For now, the study stands as a striking example of how a genome-wide, unbiased search for methylation changes can converge on a single biological mechanism with profound clinical relevance. More than fifty genes, silenced together across a million bases of DNA, determine whether a tumor of the brain’s protective lining will behave itself or turn lethal. In revealing that mechanism, the work transforms our understanding of meningioma progression and adds a powerful new tool to the molecular toolkit of neuro-oncology.

The findings, published in Nature Plants, challenge the conventional view that ULT1 functions mainly as a trithorax-group, or trxG, factor. TrxG proteins generally help maintain active genes by supporting the trimethylation of histone H3 at lysine 4, known as H3K4me3. In contrast, Polycomb-group, or PcG, complexes repress gene activity by depositing trimethylated histone H3 at lysine 27, or H3K27me3. These chemical marks are written onto histone proteins, the molecular spools around which DNA is wrapped, and help determine whether genes remain accessible or are locked down.

The antagonism between trxG and PcG systems is fundamental to development in multicellular organisms. Genes controlling cell identity, growth and reproductive timing must be activated in some tissues and silenced in others, often with extraordinary precision. In plants, this regulatory challenge is intensified by their lifelong developmental flexibility. Unlike animals, many plants continue producing new organs throughout their lives and can alter reproductive development in response to environmental conditions. The molecular mechanisms that allow plants to balance gene activation and repression have therefore remained a major question in plant epigenetics.

ULT1 had previously been characterized as a factor that antagonizes CURLY LEAF, or CLF, an enzymatic component of the plant Polycomb Repressive Complex 2, known as PRC2. PRC2 is responsible for adding the H3K27me3 mark to chromatin, thereby suppressing nearby genes. Based on earlier genetic and molecular evidence, ULT1 was regarded primarily as a trxG-associated protein that promoted gene activity and counteracted PRC2-mediated repression. The new study, however, shows that this picture is incomplete: ULT1 can also support PRC2, depending on the catalytic subunit involved.

Using epigenomic analyses, the researchers found that ULT1 increases H3K27me3 levels at more than 1,000 genes. This broad effect indicates that ULT1 is not simply a brake on Polycomb activity. Instead, it can help establish or reinforce repression across a substantial group of genomic targets. Such a dual role could allow plants to fine-tune developmental programs rather than treating gene activation and silencing as strictly separate processes.

The team also discovered that ULT1 physically interacts with components of PRC2, particularly the enzymatic subunit SWINGER, or SWN. In biochemical experiments performed outside living cells, ULT1 significantly enhanced the ability of SWN-containing PRC2 to methylate histone H3 at lysine 27. The protein also stimulated PRC2 complexes containing CLF, although the effect was weaker. This difference provides a potential biochemical explanation for why ULT1 can produce distinct genetic and developmental outcomes depending on which PRC2 catalytic subunit is present.

PRC2 is not a single uniform machine. Its activity depends on the combination of core proteins and catalytic subunits assembled into the complex, as well as on the chromatin environment and regulatory factors surrounding it. CLF and SWN are related enzymes, but they do not necessarily perform identical functions in every tissue or developmental stage. The observation that ULT1 preferentially boosts SWN-containing PRC2 suggests that these two versions of the complex may have different intrinsic activities and may respond differently to accessory proteins.

This mechanism offers a new model for how a single regulatory factor can act as a molecular switch. In one context, ULT1 may support trxG-associated activation and oppose CLF-dependent repression. In another, especially when partnered with SWN-containing PRC2, it may enhance H3K27 trimethylation and strengthen gene silencing. Rather than functioning as a permanently activating or repressing protein, ULT1 could help direct chromatin toward one state or the other according to the composition of the surrounding molecular machinery.

The consequences are especially important for reproductive development, when plants must coordinate the transition between vegetative growth and the formation of flowers and seeds. Small changes in the timing or intensity of gene repression can alter when these transitions occur and how reproductive structures develop. By linking an ostensibly activating factor to a repressive enzyme complex, the study suggests that plants possess a flexible chromatin control system capable of rapidly recalibrating developmental decisions. The discovery expands the understanding of how epigenetic memory is built, modified and sometimes reversed, while identifying ULT1 as a key regulator of the balance between plant gene activation and silencing.

Subject of Research: The dual function of the plant protein ULTRAPETALA1 in regulating trithorax-group and Polycomb-group chromatin systems, H3K27 trimethylation and reproductive development.

Article Title: The dual trxG/PcG protein ULTRAPETALA1 modulates H3K27me3 and directly enhances POLYCOMB REPRESSIVE COMPLEX 2 activity for fine-tuned reproductive transitions.

Article References: Geshkovski, V., Engelhorn, J., Izquierdo, JB. et al. “The dual trxG/PcG protein ULTRAPETALA1 modulates H3K27me3 and directly enhances POLYCOMB REPRESSIVE COMPLEX 2 activity for fine-tuned reproductive transitions.” Nature Plants (2026). https://doi.org/10.1038/s41477-026-02363-z

Image Credits: AI Generated

DOI: https://doi.org/10.1038/s41477-026-02363-z

Keywords: ULTRAPETALA1, ULT1, Polycomb Repressive Complex 2, PRC2, SWINGER, SWN, CURLY LEAF, CLF, trithorax, Polycomb, H3K27me3, H3K4me3, plant epigenetics, chromatin regulation, reproductive development

The enzymatic deposition of H2AK119Ub is primarily performed by PRC1, while its removal is tightly regulated by deubiquitinases such as BAP1 and USP16. This interplay ensures that the ubiquitination levels on chromatin are maintained within precise thresholds, necessary for proper transcriptional repression and genome stability. The balance between these enzymes is critical since aberrant regulation either leads to excessive repression or the loss of gene silencing, both conditions linked to oncogenesis and developmental defects. As such, H2AK119Ub functions as an epigenetic hub, integrating signals that determine chromatin accessibility and transcriptional outcomes.

Central to the functional diversification of H2AK119Ub is its recognition by specialized reader proteins, which decode the ubiquitin mark and translate it into distinct biological responses. One such reader is JARID2, a non-catalytic member of PRC2.2 complex. JARID2 possesses an N-terminal ubiquitin-interacting motif (UIM) that binds H2AK119Ub with exquisite specificity. Structural investigations using cryo-electron microscopy have unveiled how JARID2, together with AEBP2, forms a multivalent interface that stabilizes PRC2 recruitment to ubiquitinated nucleosomes. This targeting is essential for the subsequent establishment of H3K27me3, a hallmark of facultative heterochromatin that underpins X-chromosome inactivation and broader gene silencing programs during embryogenesis.

JARID2’s role extends beyond structural anchoring, functioning as a molecular rheostat that modulates PRC2 activity in a context-dependent manner. Overexpression of JARID2 has been implicated in various malignancies such as lung, colon, and breast cancers, where it enhances PRC2-mediated repression of tumor suppressor genes. Conversely, its loss-of-function mutations are associated with myeloid neoplasms, disrupting PRC2 recruitment and facilitating leukemogenesis. This dualistic role underscores the complexity of epigenetic regulation via H2AK119Ub readers and their impact on tumorigenesis.

Another pivotal reader is DNMT3A1, a DNA methyltransferase isoform that links Polycomb-mediated repression to the establishment of de novo DNA methylation patterns. The unique N-terminal ubiquitin-dependent recruitment (UDR) domain of DNMT3A1 allows high-affinity binding to H2AK119Ub-modified nucleosomes by engaging both the H2A–H2B acidic patch and the ubiquitin moiety. This multivalent interaction situates DNMT3A1 at Polycomb-repressed regions in a catalytically inert state, awaiting additional cues such as H3K36me2/3 recognition via its PWWP domain to activate methylation. This elegant “positioning without firing” mechanism explains why H2AK119Ub-marked domains typically escape DNA hypermethylation under physiological conditions.

However, cancer-associated mutations disrupting the PWWP domain unleash aberrant DNMT3A1 methyltransferase activity at H2AK119Ub-enriched facultative heterochromatin, leading to pathological DNA hypermethylation of Polycomb target genes. Such epigenetic misregulation is a frequent hallmark of oncogenesis and developmental syndromes, highlighting the therapeutic potential of designing inhibitors that block UDR-mediated recruitment of DNMT3A1. Targeting this axis may restore proper methylation landscapes and reverse aberrant gene silencing in diseases driven by epigenetic dysfunction.

RYBP, a defining component of variant PRC1 complexes, performs dual roles as both a reader and amplifier of H2AK119Ub signals. Its NZF domain specifically recognizes ubiquitinated nucleosomes, thereby stabilizing vPRC1 independent of repressive H3K27me3 marks. This property allows RYBP to facilitate de novo establishment and propagation of Polycomb domains through a feedforward “read-write” mechanism. Cryo-EM structures have illustrated how RYBP–PRC1 adopts distinct nucleosome engagement modes, switching between ubiquitin-dependent and ubiquitin-independent interactions to coordinate the spread of H2AK119Ub and enforce transcriptional repression.

The amplification of H2AK119Ub by RYBP-bound PRC1 complexes is essential for robust gene silencing during development, notably in the maintenance of X-chromosome inactivation and repression of lineage-specific genes. Intriguingly, dysregulation of RYBP expression correlates with poor prognostic outcomes in various cancers, suggesting it functions as a tumor suppressor by upholding Polycomb repression. Loss of RYBP disrupts this epigenetic framework, promoting oncogenic transcriptional programs and facilitating tumor progression.

Additional readers such as SSX and RSF1 further illustrate the multifaceted nature of H2AK119Ub signaling. The SS18::SSX fusion oncoprotein, characteristic of synovial sarcoma, hijacks the chromatin remodeling BAF complex to H2AK119Ub-marked loci, upsetting the balance between Polycomb repression and BAF-mediated gene activation. RSF1 binds through a ubiquitin-associated domain to ubiquitinated nucleosomes and facilitates displacement of PRC1, thereby activating transcription at select sites. Notably, amplification of RSF1 in ovarian and breast cancers is linked to genome instability, demonstrating that H2AK119Ub can mediate opposing regulatory outcomes depending on the reader engaged.

The pathological relevance of H2AK119Ub extends to inherited disorders and cancer predisposition syndromes. Germline mutations in the deubiquitinase BAP1 define familial syndromes associated with high risks of uveal melanoma and mesothelioma. In mouse models of Down syndrome, overexpression of USP16 perturbs hematopoietic stem cell function and neural progenitor expansion via excessive removal of H2AK119Ub, whereas USP16 deficiency leads to mark accumulation and defective lineage commitment. These findings implicate precise regulation of H2AK119Ub in stem cell biology and differentiation, with broad implications for disease.

Together, these insights solidify H2AK119Ub as a master epigenetic regulator whose interpretation by diverse reader proteins governs gene expression, genome stability, and cell fate decisions. By integrating structural biology, biochemical assays, and disease models, researchers are unraveling the complex “read-write-erase” circuitry centered on this histone mark. Such understanding not only advances fundamental biology but also informs the development of targeted therapeutic strategies that modulate epigenetic readers and enzymes involved in H2AK119Ub signaling.

As future studies continue to elucidate the structural nuances and dynamic regulation of H2AK119Ub interactions, novel interventions aimed at reprogramming aberrant chromatin states in cancer and developmental diseases will be increasingly feasible. The multifaceted roles of this single ubiquitination event epitomize the intricate interplay between chromatin modification and cellular identity, underscoring its significance as both a biomarker and therapeutic target in precision medicine.

Subject of Research: Not applicable

Article Title: Mono-ubiquitination of histone H2A lysine 119 (H2AK119Ub): its multifaceted role in biology and implication in diseases

News Publication Date: 14-Mar-2026

Web References:
– http://dx.doi.org/10.1007/s11684-026-1209-z

Image Credits: HIGHER EDUCATON PRESS

Keywords: H2AK119Ub, histone ubiquitination, Polycomb repressive complex, PRC1, PRC2, chromatin regulation, gene silencing, epigenetics, cancer biology, ubiquitin readers, deubiquitinases, DNA methylation, JARID2, DNMT3A1, RYBP

The newly uncovered players in this chromatin tug-of-war are a set of PMD-C-containing proteins designated as MAINTENANCE OF MERISTEMS (MAIN), MAIN-LIKE 1 (MAIL1), and MAIL2. These factors are shown to antagonize Polycomb silencing particularly at genes that are actively transcribed, thus safeguarding their expression by preventing the inappropriate deposition of H3K27me3 marks. The discovery is especially intriguing given the central role that Polycomb-mediated repression plays in developmental gene silencing across eukaryotes, which often raises the question of how specific genes resist such robust silencing mechanisms.

Pélissier et al. leveraged genetic and epigenomic tools to dissect the role of MAIN, MAIL1, and MAIL2 in Arabidopsis. Mutants deficient in any of these proteins exhibited ectopic H3K27 trimethylation—a hallmark of Polycomb silencing—across numerous genomic loci that are typically actively transcribed. This gain of H3K27me3 was correlated with transcriptional repression, underscoring a functional antagonism between the PMD-C proteins and the Polycomb silencing machinery. Intriguingly, these findings illustrate a protective layer of gene regulation, whereby the PMD-C proteins operate as sentinels to maintain gene activity against Polycomb repression.

Moreover, the study revealed that MAIL1 and MAIL2, while functioning in concert with MAIN, actually target distinct sets of genes and associate with chromatin in a sequence-specific manner. By binding to particular DNA motifs, these proteins help demarcate genomic regions that should resist Polycomb silencing, effectively creating a molecular barrier that preserves transcriptional competence. This motif-dependent targeting highlights a sophisticated mechanism by which plants can customize silencing resistance at the DNA sequence level, adding a new dimension to the understanding of epigenomic regulation.

The integrity of these DNA motifs emerged as a critical determinant for the function of PMD-C proteins; when the motifs are disrupted, the protective effect against Polycomb silencing is lost. This means that the plant genome encodes precise sequence cues for recruiting PMD-C proteins, which then safeguard gene expression by impeding the spread of repressive chromatin marks. Such a refined targeting system suggests an evolutionary advantage, enabling plants to fine-tune gene repression and activation with unprecedented specificity.

This research not only challenges the previously held notion that Polycomb silencing is an almost inescapable fate for certain chromatin landscapes but also introduces an elegant molecular mechanism for how active genes maintain their expression status. The concept of PMD-C protein–DNA motif modules acting as antagonists to Polycomb silencing shifts the paradigm of chromatin regulation, suggesting a dynamic balance rather than a one-way silencing cascade.

The implications of this study extend beyond plants, as Polycomb group proteins and their epigenetic marks are conserved in animals as well. Understanding how cells counteract such potent silencing marks may unveil parallel regulatory modules in other eukaryotes, potentially informing new therapeutic strategies for diseases involving aberrant gene silencing such as cancers and developmental disorders. The discovery of PMD-C proteins introduces a new class of chromatin modulators that might have analogs or functional equivalents in animal systems, opening avenues for cross-kingdom comparative epigenetics.

The study by Pélissier et al. employed a combination of chromatin immunoprecipitation sequencing (ChIP-seq), transcriptome analysis, and mutational studies in Arabidopsis to delineate the interplay between PMD-C proteins and Polycomb silencing. Their comprehensive approach enabled high-resolution mapping of H3K27me3 patterns in mutant versus wild-type plants, directly linking the loss of MAIN, MAIL1, or MAIL2 with aberrant silencing and reduced gene expression. These high-throughput datasets provide a robust framework for future work aiming to decode complex chromatin states and regulatory networks.

An additional layer of complexity was revealed by the observation that MAIL1 and MAIL2, despite belonging to the same family of PMD-C proteins, selectively regulate different gene subsets. This specificity could be explained by variations in their DNA-binding affinities or interactions with other chromatin-associated factors. Such functional diversification within the PMD-C protein family likely equips plants with a modular system capable of responding to various developmental cues and environmental stresses, thereby preserving genome stability and proper gene expression profiles.

The biological significance of this mechanism is underscored by the phenotypic consequences observed in PMD-C mutants, which display developmental abnormalities attributed to misregulation of key genes. By opposing Polycomb silencing, MAIN, MAIL1, and MAIL2 assure that genes essential for meristem maintenance and growth remain active, highlighting an indispensable role in plant development. The ability of these proteins to modulate epigenetic landscapes and transcriptional outputs is thus vital for developmental plasticity and adaptation.

From a mechanistic standpoint, the physical association of MAIL1 and MAIL2 with specific chromatin motifs raises fascinating questions about the recruitment machinery involved and potential interactions with other chromatin remodelers or transcription factors. Future investigations might focus on dissecting whether these proteins influence nucleosome positioning, histone demethylation activities, or the dynamics of Polycomb complexes themselves. Such inquiries will be crucial to fully elucidate how PMD-C proteins interrupt the propagation of repressive chromatin states.

Furthermore, the discovery prompts a reevaluation of the concept of epigenetic “memory,” as it suggests that active gene states are not merely maintained by the absence of repressive marks but also through active opposition mechanisms like those mediated by PMD-C proteins. This active safeguarding enriches our understanding of how epigenetic states are preserved through cell divisions, ensuring developmental robustness and stability in the face of potentially silencing epigenetic signals.

In terms of evolutionary biology, the plant-specific nature of PMD-C proteins indicates that plants have evolved unique tools to balance gene activation and repression, possibly as an adaptation to sessile life and environmental variability. Whether analogous systems exist in animals or fungi remains an exciting area for future research, especially given the universal challenges of chromatin-based gene regulation across eukaryotes.

This pioneering work by Pélissier and colleagues thus revolutionizes the field of plant epigenetics by revealing a molecular system that actively counters Polycomb silencing, expanding the toolkit of gene regulatory mechanisms in eukaryotic cells. By illuminating how plants protect crucial gene expression against dominant repressive forces, the study not only deepens our grasp of developmental biology but also provides a springboard for innovative approaches in agriculture, biotechnology, and medicine aimed at manipulating epigenetic landscapes for targeted outcomes.

As research continues to unravel the complexities of chromatin regulation, the identification of PMD-C protein–DNA motif modules as key shields against gene silencing underscores the remarkable adaptability and nuance inherent in living systems. This work stands as a testament to the power of integrative epigenomics in uncovering the hidden layers of regulation that dictate cellular identity and function.

Subject of Research: Plants, Epigenetics, Gene Regulation, Polycomb Group Proteins, Chromatin Biology

Article Title: Plant mobile domain protein–DNA motif modules counteract Polycomb silencing to stabilize gene expression

Article References:
Pélissier, T., Jarry, L., Olivier, M. et al. Plant mobile domain protein–DNA motif modules counteract Polycomb silencing to stabilize gene expression. Nat. Plants (2025). https://doi.org/10.1038/s41477-025-02127-1

Image Credits: AI Generated