ESR2–HDA6 complex negatively regulates auxin biosynthesis to delay callus initiation in Arabidopsis leaf explants during tissue culture  

作　　者：Kyounghee Lee Hobin Yoon Ok-Sun Park Jongbu Lim Sang-Gyu Kim Pil Joon Seo 

机构地区：[1]Department of Chemistry,Seoul National University,Seoul 08826,Korea [2]Research Institute of Basic Sciences,Seoul National University,Seoul 08826,Korea [3]Interdisciplinary Program in Agricultural Biotechnology,Seoul National University,Seoul 08826,Korea [4]Plant Genomics and Breeding Institute,Seoul National University,Seoul 08826,Korea [5]Department of Biological Sciences,KAIST,Daejeon 34141,Korea

出　　处：《Plant Communications》2024年第7期200-214,共15页植物通讯（英文）

基　　金：supported by the Basic Science Research(NRF-2022R1A 2B5B02001266);Basic Research Laboratory(NRF-2022R1A4A 3024451)programs funded by the National Research Foundation of Korea(South Korea);the New Breeding Technologies Development Program(RS-2024-00322275)of the Rural Development Administration(South Korea).

摘　　要：Plants exhibit an astonishing ability to regulate organ regeneration upon wounding.Excision of leaf explants promotes the biosynthesis of indole-3-acetic acid(IAA),which is polar-transported to excised regions,where cell fate transition leads to root founder cell specification to induce de novo root regeneration.The regeneration capacity of plants has been utilized to develop in vitro tissue culture technologies.Here,we report that IAA accumulation near the wounded site of leaf explants is essential for callus formation on 2,4-dichlorophenoxyacetic acid(2,4-D)-rich callus-inducing medium(CIM).Notably,a high concentration of 2,4-D does not compensate for the action of IAA because of its limited efflux;rather,it lowers IAA biosynthesis via a negative feedback mechanism at an early stage of in vitro tissue culture,delaying callus initiation.The auxin negative feedback loop in CIM-cultured leaf explants is mediated by an auxin-inducible APETALA2 transcription factor,ENHANCER OF SHOOT REGENERATION 2(ESR2),along with its interacting partner HISTONE DEACETYLASE 6(HDA6).The ESR2–HDA6 complex binds directly to,and removes the H3ac mark from,the YUCCA1(YUC1),YUC7,and YUC9 loci,consequently repressing auxin biosynthesis and inhibiting cell fate transition on 2,4-D-rich CIM.These findings indicate that negative feedback regulation of auxin biosynthesis by ESR2 and HDA6 interferes with proper cell fate transition and callus initiation.

关 键 词：auxin biosynthesis negative feedback loop ESR2 HDA6 YUCCA chromatin modification 

分 类 号：Q94[生物学—植物学]