拟南芥 ATXR2 在愈伤组织向芽形成的转变过程中抑制新梢器官发生。
Arabidopsis ATXR2 represses de novo shoot organogenesis in the transition from callus to shoot formation.
机构信息
Department of Chemistry, Seoul National University, Seoul 08826, Korea; Research Institute of Basic Sciences, Seoul National University, Seoul 08826, Korea.
Plant Genomics and Breeding Institute, Seoul National University, Seoul 08826, Korea.
出版信息
Cell Rep. 2021 Nov 9;37(6):109980. doi: 10.1016/j.celrep.2021.109980.
Plants exhibit high regenerative capacity, which is controlled by various genetic factors. Here, we report that ARABIDOPSIS TRITHORAX-RELATED 2 (ATXR2) controls de novo shoot organogenesis by regulating auxin-cytokinin interaction. The auxin-inducible ATXR2 Trithorax Group (TrxG) protein temporally interacts with the cytokinin-responsive type-B ARABIDOPSIS RESPONSE REGULATOR 1 (ARR1) at early stages of shoot regeneration. The ATXR2-ARR1 complex binds to and deposits the H3K36me3 mark in the promoters of a subset of type-A ARR genes, ARR5 and ARR7, thus activating their expression. Consequently, the ATXR2/ARR1-type-A ARR module transiently represses cytokinin signaling and thereby de novo shoot regeneration. The atxr2-1 mutant calli exhibit enhanced shoot regeneration with low expression of ARR5 and ARR7, which ultimately upregulates WUSCHEL (WUS) expression. Thus, ATXR2 regulates cytokinin signaling and prevents premature WUS activation to ensure proper cell fate transition, and the auxin-cytokinin interaction underlies the initial specification of shoot meristem in callus.
植物表现出高度的再生能力，这由各种遗传因素控制。在这里，我们报告 ARABIDOPSIS TRITHORAX-RELATED 2（ATXR2）通过调节生长素-细胞分裂素相互作用来控制新梢器官发生。生长素诱导的 ATXR2 Trithorax Group（TrxG）蛋白在新梢再生的早期阶段与细胞分裂素反应型 B ARABIDOPSIS RESPONSE REGULATOR 1（ARR1）暂时相互作用。ATXR2-ARR1 复合物结合并在一组 A 型 ARR 基因（ARR5 和 ARR7）的启动子中沉积 H3K36me3 标记，从而激活它们的表达。因此，ATXR2/ARR1-A 型 ARR 模块瞬时抑制细胞分裂素信号，从而实现新梢的再生。atxr2-1 突变体愈伤组织表现出增强的新梢再生能力，ARR5 和 ARR7 的表达水平较低，这最终上调了 WUSCHEL（WUS）的表达。因此，ATXR2 调节细胞分裂素信号并防止 WUS 的过早激活，以确保适当的细胞命运转变，生长素-细胞分裂素相互作用是愈伤组织中茎分生组织初始特化的基础。
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