ArticleProceedings of the National Academy of Sciences of the United States of America2025
A chromatin-linked CPL2-PHD2/3 module sustains multiple DNA methylation pathways and Polycomb silencing.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed.
- Ecological Memory in Plants: Epigenetic Integration of Abiotic Stress and Climate Change.Plants (Basel, Switzerland) · 2026Review
- A chromatin-linked CPL2-PHD2/3 module sustains multiple DNA methylation pathways and Polycomb silencing.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Plant LHP1 as a Context-Dependent Regulator of Polycomb-Associated Chromatin.Physiologia plantarumReview
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9 authors.
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Abstract
While multiple chromatin-based epigenetic pathways are well characterized, their genome-wide coordination and hierarchical interplay remain poorly understood. We previously identified the BAH-PHD-CPL2 complex, where AIPP3 binds H3K27me3 via its BAH domain and, in concert with PHD2 and PHD3 (PHD2/3), recruits CPL2 to repress transcription by dephosphorylating RNA Polymerase II. Here, we show that CPL2 and PHD2/3 form a distinct module (CPL2-PHD2/3) that safeguards CHH DNA methylation and silences CHH-methylated sites at transposable elements (TEs) through engagement of multiple DNA methylation pathways. The CPL2-PHD2/3 module physically associates with SUVH4 and SUVH5 (SUVH4/5) to preserve SUVH4/5-CMT2-mediated CHH methylation at a subset of H3K9me2-marked regions. Chromatin enrichment of PHD3 likewise enables the module to sustain RNA-directed DNA methylation (RdDM)-mediated CHH DNA methylation at sites bearing H3K9me2, H3K27me3, or neither. Thus, CPL2-PHD2/3 emerges as a previously underappreciated, multifunctional regulator of plant DNA methylation networks. Unexpectedly, its gene repression function is uncoupled from DNA methylation. CPL2-PHD2/3 represses Polycomb-marked genes by interacting with LHP1 or recognizing hypomethylated H3K4. While it cooperates with LHP1 at a subset of targets, it also independently silences many more genes that LHP1 alone cannot repress, both sets of genes being critical for proper development. This dual, yet largely LHP1-insufficient, repression mode singles out CPL2-PHD2/3 as the essential executor of Polycomb silencing. Together, our findings establish CPL2-PHD2/3 as a chromatin-responsive integrator that spans DNA methylation and Polycomb-associated repression, providing a unifying mechanism for epigenetic control of both TEs and genes across diverse chromatin landscapes.
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