The Type-B Cytokinin Response Regulator ARR1 Inhibits Shoot Regeneration in an ARR12-Dependent Manner in Arabidopsis
The Type-B Cytokinin Response Regulator ARR1 Inhibits Shoot Regeneration in an ARR12-Dependent Manner in Arabidopsis
复制标题
B 型细胞分裂素反应调节器 ARR1 以 ARR12 依赖性方式抑制拟南芥芽再生
DOI：
10.1105/tpc.19.00022
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发表时间：
2020-07-01
期刊：
影响因子：
11.6
通讯作者：
Xiang, Fengning
中科院分区：
文献类型：
--
作者：
Liu, Zhenhua;Dai, Xuehuan;Xiang, Fengning
ARR1是b型ARR，被定义为体外茎再生的重要抑制剂，以arr12依赖的方式调节WUS和CLV3的表达，直接激活IAA17。外源细胞分裂素对离体芽再生至关重要。参与细胞分裂素信号转导途径的蛋白质，包括b型拟南芥应答调节因子（ARRs），参与拟南芥（ARABIDOPSIS thaliana）的茎再生。部分b型arr（如ARR1、ARR12）通过直接激活WUSCHEL （WUS）表达促进茎部再生；然而，b型ARRs如何抑制茎再生尚不清楚。在这里，我们发现ARR12是愈伤组织形成和茎再生的中心促进剂，而ARR1是这一过程的强烈抑制剂，抵消了ARR12的积极作用。ARR1通过与ARR12竞争CLV3启动子的结合，间接抑制CLAVATA3 （CLV3）的表达，从而抑制CLAVATA3 （CLV3）的愈伤组织形成和茎再生。同时，ARR1通过转录激活生长素反应抑制基因INDOLE-3-ACETIC ACID INDUCIBLE17抑制茎再生，从而间接抑制WUS的表达。因此，b型arr对愈伤组织的形成和茎部再生有不同的影响。我们的研究揭示了连接细胞分裂素信号、CLV3调节剂和生长素信号的新分子途径，并揭示了细胞分裂素调节芽再生的机制。
ARR1, a type-B ARR, is defined as an important inhibitor of in vitro shoot regeneration that modulates the expression of WUS and CLV3 in an ARR12-dependent manner, and directly activates IAA17. Exogenous cytokinin is critical for in vitro shoot regeneration. Proteins involved in the cytokinin signal transduction pathway, including type-B ARABIDOPSIS RESPONSE REGULATORs (ARRs), participate in shoot regeneration in Arabidopsis (Arabidopsis thaliana). Some type-B ARRs (e.g., ARR1 and ARR12) promote shoot regeneration by directly activating WUSCHEL (WUS) expression; however, it is unclear how type-B ARRs inhibit shoot regeneration. Here, we show that ARR12 is a central enhancer of callus formation and shoot regeneration, whereas ARR1 is a strong inhibitor of this process that counteracts the positive effect of ARR12. ARR1 indirectly represses CLAVATA3 (CLV3) expression in an ARR12-dependent manner via competing with ARR12 for binding to the CLV3 promoter, which contributes to its ARR12-dependent inhibitory effect on callus formation and shoot regeneration. In parallel, ARR1 inhibits shoot regeneration through transcriptional activation of INDOLE-3-ACETIC ACID INDUCIBLE17, an auxin response repressor gene, and the consequent indirect repression of WUS expression. Thus, type-B ARRs have diverse effects on callus formation and shoot regeneration. Our study reveals novel molecular pathways linking cytokinin signaling, the CLV3 regulator, and auxin signaling, and sheds light on the mechanism underlying cytokinin-regulated shoot regeneration.