WIND1 controls cell fate transition through coordinately integrating histone acetylation and deacetylation-mediated transcriptional reprogramming during somatic embryogenesis.

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.