Elucidation of control principles for a plant regeneration switch

March 24, 2026

WIND1 controls cell fate transition by histone deacetylation/acetylation

The RIKEN CSRS has discovered a regulatory principle by which the wound-responsible transcription factor WIND1, acting as a switch that enable plants to regenerate tissues and somatic embryos, reprograms developmental fate.

Several key transcription factors that promote plant regeneration have been identified. In the case of WIND1, it has been shown to stimulate callus formation, regeneration of shoots, vascular reconnection, and defense response that protect against pathogens. However, the detailed molecular mechanisms by which a single transcription factor reprograms developmental fate have remained unclear.

In this study, the research group first established an experimental system in which WIND1 efficiently induce somatic embryogenesis, then they investigated how WIND1 converts developmental fate from shoots to somatic embryos in Arabidopsis thaliana. The results revealed that WIND1 regulates both histone acetylation and deacetylation, two opposing epigenetic modifications. Through this dual regulation,  WIND1 suppresses the original shoot developmental programme, while simultaneously promoting the expression of key genes required to establish a new developmental fate as somatic embryos.

The findings are expected to the sustainable production of food and valuable plant-derived materials, such as mass propagation and crop improvement using tissue culture technologies, as well as to the development of a novel approach for controlling gene expression.

 

Original article
Molecular Plant doi: 10.1016/j.molp.2026.03.005
A. Iwase, A. Takebayashi, F. Hung, A. Kawamura, Y. Ç. Ince, Y . Kadota, S. Inagaki, T. Suzuki, K. Shirasu, K. Sugimoto,
"WIND1 controls cell fate transition through coordinately integrating histone acetylation and deacetylation-mediated transcriptional reprogramming during somatic embryogenesis".
Contact
Akira Iwase; Senior Research Scientist
Keiko Sugimoto; Team Director
Cell Function Research Team