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H3K27me3 epigenetic mark crucial for callus cell identity and regeneration capacity [RNA-seq]

ABSTRACT: Plant callus cells possess a remarkable ability to regenerate organs that often differ from their respective origins or even entire new individuals. Yet, the mechanisms underlying their pluripotent state remain elusive. We propose a strategy that involves two independent mechanisms to endow callus cells with pluripotency: (1) maintaining a unique transcriptional profile, characterised by the expression of genes from diverse developmental pathways that allows rapid response to developmental cues; (2) preventing premature differentiation through H3K27 methylation-mediated silencing of key transcription factors such as WUCHEL and SPEECHLESS. This strategy relies on a mechanism to silence the pluripotency network upon regenerative stimuli, enabling a single developmental pathway to dominate. Our study reveals that the EMF2 complex, a key regulator of H3K27 tri-methylation, plays a crucial role in this process. Callus derived from the emf2 mutant, deficient in H3K27me3, exhibits severely impaired regeneration. Comparative analyses of chromatin states and transcription profiles between wild-type and emf2 calli revealed that the loss of EMF2 leads to upregulation of key transcription factors in callus, and identified the genes regulated solely by EMF2. Our findings suggest that suppressing pluripotency networks through H3K27me3 is essential for executing specific developmental programs to ensure effective regeneration.

ORGANISM(S): Arabidopsis thaliana

PROVIDER: GSE288197 | GEO | 2025/01/29

REPOSITORIES: GEO

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Project description:Epigenetic priming factors establish a permissive epigenetic landscape which is not required until a later developmental or physiological time point, temporally uncoupling the presence of these factors with their phenotypic effects. One classic example of epigenetic priming is in the context of bivalent chromatin, found in pluripotent stem cells and early embryos at key developmental gene promoters marked by both activating-associated H3K4me3 and repressive-associated H3K27me3 histone modifications. It is currently unknown how these bivalent domains are targeted, or precisely how they impact on lineage commitment. Here we show that the small heterodimerising non-enzymatic DNA binding proteins Developmental Pluripotency Associated 2 (Dppa2) and 4 (Dppa4) act as epigenetic priming factors to establish bivalency at a subset of developmental genes. Dppa2/4 localise to the +1 nucleosome position of bivalent genes and while they are not required for pluripotency in embryonic stem cells (ESCs), double knockout cells fail to exit pluripotency and to differentiate efficiently, with delays in upregulating bivalently marked lineage genes. Proteomics reveal that Dppa2/4 interact on chromatin with members of the COMPASS and Polycomb complexes important for H3K4me3 and H3K27me3 deposition, respectively. Epigenetic profiling reveals a striking loss of H3K4me3, H3K27me3, and their associated enzymatic machinery at a significant subset of bivalent promoters in Dppa2/4 mutants, in addition to loss of H2A.Z and chromatin accessibility. In wild-type ESCs, these “Dppa2/4-dependent” bivalent promoters are characterised by low H3K4me3 enrichment and breadth, near-absent expression levels and initiating but not elongating RNA polymerase. Notably, Dppa2/4-dependent promoters are less evolutionarily conserved suggesting that they lack additional safeguard measures to maintain bivalency at these genes in the absence of Dppa2/4. Concomitantly with the loss of bivalency, Dppa2/4-dependent bivalent promoters gain DNA methylation and consequently are no longer able to be effectively activated upon ESC differentiation, leading to defects in cell fate acquisition. Our findings reveal a targeting principle for bivalency to developmental gene promoters poising them for future lineage specific gene activation.

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H3K27me3 epigenetic mark crucial for callus cell identity and regeneration capacity [RNA-seq]

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