The Transcription Factor INDUCER OF CBF EXPRESSION1 Interacts with ABSCISIC ACID INSENSITIVE5 and DELLA Proteins to Fine-Tune Abscisic Acid Signaling during Seed Germination in Arabidopsis
The Transcription Factor INDUCER OF CBF EXPRESSION1 Interacts with ABSCISIC ACID INSENSITIVE5 and DELLA Proteins to Fine-Tune Abscisic Acid Signaling during Seed Germination in Arabidopsis
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转录因子 INDUCER OF CBF EXPRESSION1 与 ABCISIC ACID INSENSITIVE5 和 DELLA 蛋白相互作用，在拟南芥种子萌发过程中微调脱落酸信号传导。
DOI：
10.1105/tpc.18.00825
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发表时间：
2019-07-01
期刊：
影响因子：
11.6
通讯作者：
Yu, Diqiu
中科院分区：
文献类型：
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作者：
Hu, Yanru;Han, Xiao;Yu, Diqiu
ABCISIC ACID INSENSITIVE5 (ABI5) 是脱落酸 (ABA) 信号通路的重要调节因子，参与抑制拟南芥 (Arabidopsis thaliana) 种子萌发和萌发后生长。 ABI5 在翻译后水平受到精确调节；然而，ABI5 及其相互作用的转录因子的转录调控机制仍然很大程度上未知。在这里，我们发现 CBF EXPRESSION1 诱导剂 (ICE1) 与 ABI5 有物理关联。 ICE1 在种子萌发过程中负向调节 ABA 反应，并直接抑制 ABA 反应的晚期胚胎发生 ABUNDANT6 (EM6) 和 EM1 表达。遗传分析表明ice1突变体的ABA超敏感表型需要ABI5。 ICE1 干扰 ABI5 的转录活性以介导下游调节子。重要的是，ICE1 还与 DELLA 蛋白相互作用，后者在 ABA 信号传导过程中刺激 ABI5。 ICE1 的破坏部分恢复了 della 突变体 gai-t6 rga-t2 rgl1-1 rgl2-1 的 ABA 低敏感表型，表明 ICE1 在 ABA 信号传导中与 DELLA 发挥拮抗作用。一致地，DELLA 蛋白抑制 ICE1 的转录功能以及 ICE1 对 ABI5 的拮抗作用。总的来说，我们的研究表明，ICE1 拮抗 ABI5 和 DELLA 活性，以在种子萌发过程中维持适当的 ABA 信号传导水平，从而提供了关于 ABA 信号传导如何通过涉及 ABI5 及其相互作用伙伴的转录复合物进行微调的机制理解。
ABSCISIC ACID INSENSITIVE5 (ABI5) is a crucial regulator of abscisic acid (ABA) signaling pathways involved in repressing seed germination and postgerminative growth in Arabidopsis (Arabidopsis thaliana). ABI5 is precisely modulated at the posttranslational level; however, the transcriptional regulatory mechanisms underlying ABI5 and its interacting transcription factors remain largely unknown. Here, we found that INDUCER OF CBF EXPRESSION1 (ICE1) physically associates with ABI5. ICE1 negatively regulates ABA responses during seed germination and directly suppresses ABA-responsive LATE EMBRYOGENESIS ABUNDANT6 (EM6) and EM1 expression. Genetic analysis demonstrated that the ABA-hypersensitive phenotype of the ice1 mutant requires ABI5. ICE1 interferes with the transcriptional activity of ABI5 to mediate downstream regulons. Importantly, ICE1 also interacts with DELLA proteins, which stimulate ABI5 during ABA signaling. Disruption of ICE1 partially restored the ABA-hyposensitive phenotype of the della mutant, gai-t6 rga-t2 rgl1-1 rgl2-1, indicating that ICE1 functions antagonistically with DELLA in ABA signaling. Consistently, DELLA proteins repress ICE1's transcriptional function and the antagonistic effect of ICE1 on ABI5. Collectively, our study demonstrates that ICE1 antagonizes ABI5 and DELLA activity to maintain the appropriate level of ABA signaling during seed germination, providing a mechanistic understanding of how ABA signaling is fine-tuned by a transcriptional complex involving ABI5 and its interacting partners.