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Histone deacetylation regulates de novo shoot regeneration.

Haruka TemmanTakuya SakamotoMinoru UedaKaoru SugimotoMasako MigihashiKazunari YamamotoYayoi Tsujimoto-InuiHikaru SatoMio K ShibutaNorikazu NishinoTomoe NakamuraHiroaki ShimadaYukimi Y TaniguchiSeiji TakedaMitsuhiro AidaTakamasa SuzukiMotoaki SekiSachihiro Matsunaga
Published in: PNAS nexus (2023)
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 HDA19 , 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 ENHANCER OF SHOOT REGENERATION 1 and CUP-SHAPED COTYLEDON 2 play important roles in shoot apical meristem formation. Histones at the loci of these genes were hyperacetylated and markedly upregulated in hda19 . Transient ESR1 or CUC2 overexpression impaired shoot regeneration, as observed in hda19 . Therefore, HDA19 mediates direct histone deacetylation of CUC2 and ESR1 loci to prevent their overexpression at the early stages of shoot regeneration.
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