Loading…

Histone deacetylation regulates de novo shoot regeneration

During de novo plant organ regeneration, auxin induction mediates the formation of a pluripotent cell mass called callus, which regenerates shoots upon cytokinin induction. However, molecular mechanisms underlying transdifferentiation remain unknown. Here, we showed that the loss of , a histone deac...

Full description

Saved in:
Bibliographic Details
Published in:PNAS nexus 2023-02, Vol.2 (2), p.pgad002-pgad002
Main Authors: Temman, Haruka, Sakamoto, Takuya, Ueda, Minoru, Sugimoto, Kaoru, Migihashi, Masako, Yamamoto, Kazunari, Tsujimoto-Inui, Yayoi, Sato, Hikaru, Shibuta, Mio K, Nishino, Norikazu, Nakamura, Tomoe, Shimada, Hiroaki, Taniguchi, Yukimi Y, Takeda, Seiji, Aida, Mitsuhiro, Suzuki, Takamasa, Seki, Motoaki, Matsunaga, Sachihiro
Format: Article
Language:English
Subjects:
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:During de novo plant organ regeneration, auxin induction mediates the formation of a pluripotent cell mass called callus, which regenerates shoots upon cytokinin induction. However, molecular mechanisms underlying transdifferentiation remain unknown. Here, we showed that the loss of , a histone deacetylase (HDAC) family gene, suppresses shoot regeneration. Treatment with an HDAC inhibitor revealed that the activity of this gene is essential for shoot regeneration. Further, we identified target genes whose expression was regulated through HDA19-mediated histone deacetylation during shoot induction and found that and play important roles in shoot apical meristem formation. Histones at the loci of these genes were hyperacetylated and markedly upregulated in . Transient or overexpression impaired shoot regeneration, as observed in . Therefore, HDA19 mediates direct histone deacetylation of and loci to prevent their overexpression at the early stages of shoot regeneration.
ISSN:2752-6542
2752-6542
DOI:10.1093/pnasnexus/pgad002