ArticleMolecular plant2026
WIND1 controls cell fate transition through coordinately integrating histone acetylation and deacetylation-mediated transcriptional reprogramming during somatic embryogenesis.
Article in Molecular plant, 2026. 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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Who cites it
3 citing papers in PubMed.
- To acetylate or deacetylate? WIND1 directs opposing H3K27 modifications in plant somatic cell reprogramming.Plant molecular biology · 2026Article
- Histone deacetylases and cell-cycle regulators orchestrate cell-identity transitions during Arabidopsis root regeneration.Molecular plant · 2026Article
- Reprogramming the wound microenvironment: identity remodeling strategies for fibroblasts, keratinocytes, and macrophages.Frontiers in immunology · 2026Review
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10 authors.
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Abstract
Regeneration involves large-scale transcriptional reprogramming to drive cell identity transitions. These transcriptional changes are tightly coupled with chromatin remodeling, but the molecular mechanisms that coordinate these changes remain unclear. Here, we show that WOUND INDUCED DEDIFFERENTIATION 1 (WIND1) transcription factor promotes somatic embryogenesis by repressing pre-existing cell fate and activating new cell identity programs. WIND1 interacts with histone deacetylase HISTONE DEACETYLASE 9 and histone acetyltransferase complex component HOMOLOG OF YEAST ADA1 2a via a conserved N-terminal domain. These interactions enable WIND1 to mediate both H3K27 deacetylation and acetylation at distinct target loci, leading to repression of organ-primordium/procambium development genes such as AINTEGUMENTA and activation of embryogenesis regulators, including LEAFY COTYLEDON 2. Our study identifies WIND1 as a bifunctional chromatin regulator that integrates opposing histone acetylation dynamics to coordinate transcriptional reprogramming, providing a molecular framework for how a transcription factor directs complex cell fate transitions during regeneration.
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