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

Chromatin is the molecular framework that determines how DNA is packaged and interpreted inside a cell. Long strands of DNA are wrapped around proteins called histones, and chemical modifications attached to those histones help identify regions that should be read, paused or silenced. This system enables cells carrying the same genome to develop into radically different forms, such as neurons, liver cells, roots or leaves. When chromatin regulation fails, genes can become active or inactive at the wrong time, contributing to conditions including cancer and other diseases.

The chemical marks involved in this process are thought to have been present in the Last Eukaryotic Common Ancestor, or LECA, a single-celled organism that lived approximately two billion years ago and gave rise to modern animals, plants, fungi and protists. Many of the enzymes that add or remove histone modifications are still shared across these lineages. Yet most detailed knowledge of how the system works has come from a small collection of laboratory organisms, including humans, mice, fruit flies, baker’s yeast and the model plant Arabidopsis thaliana. The new study extends that view to branches of the eukaryotic tree that have largely been missing from chromatin research.

“The cell’s instructions for activating genes are essentially the same in a human, a sea anemone and a soil amoeba,” says Arnau Sebé-Pedrós, an ICREA Research Professor at the CRG and senior author of the study. “But the instructions for silencing genes and other genomic elements like transposons have been continuously evolving since our last common eukaryotic ancestor. Different branches of life have developed different molecular toolkits to do the same thing.”

To make the comparison possible, the researchers developed iChIP2, an expanded version of a chromatin-profiling method. The technique uses molecular barcodes to label chromatin from multiple species and analyze the samples together in a single experiment. This design makes it possible to compare histone modifications under consistent experimental conditions while working with very small quantities of biological material. The approach is particularly valuable for organisms that are difficult to grow or that have not previously had their epigenetic states mapped.

The team used iChIP2 to examine twelve histone modifications across twelve phylogenetically diverse species. The collection included the soil amoeba Acanthamoeba castellanii, the freshwater amoeba Naegleria gruberi, the ciliate Tetrahymena thermophila, the chytrid fungus Spizellomyces punctatus, baker’s yeast Saccharomyces cerevisiae, the ichthyosporean Creolimax fragrantissima, the marine predator Bigelowiella natans, the alga Guillardia theta, the plants Arabidopsis thaliana and Physcomitrium patens, the social amoeba Dictyostelium discoideum and the sea anemone Nematostella vectensis. Several of these species had never undergone detailed chromatin mapping.

Across the organisms, active genes carried a highly similar chromatin signature. Histone modifications associated with transcription tended to cluster around the beginning of a gene and extend across the gene body, indicating that the basic molecular language for gene activation has remained stable since early eukaryotic evolution. Repressed genes, however, displayed strikingly different patterns. Some species used separate modifications to silence transposable elements and inactive genes, while others combined multiple repressive marks on the same stretches of DNA. In Acanthamoeba, a modification commonly associated with active genes in animals appeared to have been repurposed for gene repression.

The researchers propose that much of this diversity reflects an evolutionary struggle between host genomes and parasitic genetic material. Transposable elements, often called jumping genes, can copy or move themselves to new positions in a genome, potentially disrupting genes or altering chromosome structure. Endogenized viruses and other mobile sequences can also persist within genetic material and evolve ways to escape cellular defenses. In humans, transposable-element-derived sequences make up approximately half of the genome. Because these elements differ between lineages, the systems used to suppress them may also have diverged.

“If a species loses its repressive mechanisms completely, it can’t tolerate parasitic elements like transposable elements or endogenized viruses,” Sebé-Pedrós says. “The result is that it’s no longer there. It’s dead.” Over hundreds of millions of years, this pressure may have produced a series of lineage-specific solutions, with chromatin marks and the enzymes that control them repeatedly adapted, combined or reassigned. Some mechanisms originally evolved to restrain mobile DNA may later have been recruited to regulate ordinary genes and other genomic regions.

The results arrive as projects such as the Earth BioGenome Project and the Wellcome Sanger Institute’s Tree of Life programme accelerate the sequencing of species from across the planet. Genome sequences reveal an organism’s genetic parts list, but they do not fully explain when those genes are active or how potentially harmful sequences are controlled. By enabling chromatin comparisons across unfamiliar species, iChIP2 could help add this regulatory layer to future biodiversity studies. The researchers say that examining more branches of life may reveal additional strategies for controlling DNA—and clarify how the molecular systems underlying health, disease and genome stability evolved.

Subject of Research: Comparative evolution of chromatin regulation and histone modifications across diverse eukaryotic species.

Article Title: Diversity and evolution of chromatin regulatory states across eukaryotes

Web References: https://doi.org/10.1038/s41588-026-02672-1

References: Nature Genetics, “Diversity and evolution of chromatin regulatory states across eukaryotes,” DOI: 10.1038/s41588-026-02672-1.

Image Credits: Sean Montgomery/Centro de Regulación Genómica

Keywords: chromatin, histone modifications, gene regulation, epigenetics, eukaryotes, transposable elements, endogenized viruses, genome evolution, iChIP2, comparative genomics