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Abstract
背景回顾：Plants exhibit an astonishing ability to regulate organ regeneration upon wounding. Excision of leaf explants promotes biosynthesis of indole-3-acetic acid (IAA), which is polar-transported to excised regions, where cell fate transition leads to specification of root founder cells to induce de novo root regeneration. The regeneration capacity of plants has been utilized to develop in vitro tissue culture technology.
主要发现：Here, we report that IAA accumulation near wounded site of leaf explants is essential for induction of callus on 2,4-dichlorophenoxyacetic acid (2,4-D)-rich callus-inducing medium (CIM).
结果1-负反馈调节：Notably, a high concentration of a synthetic auxin, 2,4-D, does not compensate for IAA action 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.
结果2-ESR2-HDA6：The auxin negative feedback loop in CIM-cultured leaf explants is mediated by an auxin-inducible AP2 transcription factor, ENHANCER OF SHOOT REGENERATION 2 (ESR2), and its interacting partner HISTONE DEACETYLASE 6 (HDA6).
结果3-ESR2-HDA6-YUC1/7/9：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.
结论：These findings indicate that negative feedback regulation of auxin biosynthesis by ESR2 and HDA6 interferes with proper cell fate transition and callus initiation.
摘 要
植物具有在遭受创伤时进行器官再生的神奇能力。叶片外植体的切除会促进IAA的生物合成，从而被转运到切除伤口处，促进细胞命运转变，从而特化出根基细胞并诱导从头根再生。植物的再生能力已经被用于开发体外组织培养技术。本文中，作者发现叶片外植体创口位置的IAA积累对于CIM培养基上2，4-D介导的愈伤诱导至关重要。高浓度的2，4-D由于不能及时外排，从而并不能补偿IAA的作用；相反，2，4-D会通过一个负反馈机制在组织培养早期降低IAA的生物合成，从而延迟愈伤起始。CIM培养基上叶片外植体中的生长素负反馈环是由一个生长素诱导的AP2转录因子ESR2及其互作蛋白HDA6共同介导的。ESR2–HDA6复合体能够直接结合到YUC1/7/9基因位点上并移除H3ac标记，从而能够在富含2，4-D的CIM培养基上抑制生长素生物合成，抑制细胞命运转变。本文的研究结果揭示了由ESR2和HDA6介导的生长素生物合成负反馈调控，从而干扰正确的细胞命运转变及愈伤起始机制。
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