Cytokinin Antagonizes Abscisic Acid-Mediated Inhibition of Cotyledon Greening by Promoting the Degradation of ABSCISIC ACID INSENSITIVE5 Protein in Arabidopsis

Cytokinin Antagonizes Abscisic Acid-Mediated Inhibition of Cotyledon Greening by Promoting the Degradation of ABSCISIC ACID INSENSITIVE5 Protein in Arabidopsis
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细胞分裂素通过促进拟南芥中脱落酸不敏感5蛋白的降解来拮抗脱落酸介导的子叶绿化抑制

DOI:
10.1104/pp.113.234740
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发表时间:
2014-03-01
期刊:
影响因子:
7.4
通讯作者:
Zuo, Jianru
Zuo, Jianru
中科院分区:
生物学1区
文献类型:
--
作者:
Guan, Chunmei;Wang, Xingchun;Zuo, Jianru

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在高等植物中,种子萌发之后是萌发后的生长。在萌发后生长期间的关键发育事件之一是子叶绿化,这使得幼苗能够建立光合能力。植物激素脱落酸(阿坝)通过抑制种子萌发和萌发后的生长,响应动态变化的内部和环境线索起着至关重要的作用。脱落酸不敏感5(ABI 5)是一种碱性亮氨酸拉链转录因子,在ABA介导的抑制种子萌发和萌发后生长的调节中起重要作用。相反,植物激素细胞分裂素被认为可以通过对抗脱落酸介导的抑制作用来促进种子萌发。然而,细胞分裂素抑制阿坝信号转导的基础分子机制在很大程度上是未知的。在这里,我们表明,细胞分裂素特异性拮抗ABA介导的抑制子叶绿化,对种子萌发的影响最小的拟南芥(拟南芥)。我们发现,细胞分裂素拮抗阿坝的效果是依赖于一个功能性的细胞分裂素信号通路,主要涉及细胞分裂素受体基因细胞分裂素反应1/ARABIDOPSIS组氨酸激酶4,下游组氨酸磷酸转移蛋白基因AHP 2,AHP 3,和AHP 5,和一个B型反应调节基因,ARR 12,它的遗传行为上游的ABI 5调节子叶绿化。细胞分裂素对ABI 5的转录没有明显影响。然而,细胞分裂素以细胞分裂素信号依赖的方式有效地促进ABI 5的蛋白酶体降解。这些结果定义了一个遗传途径,通过细胞分裂素特异性诱导ABI 5蛋白的降解,从而拮抗ABA介导的抑制萌发后生长。
In higher plants, seed germination is followed by postgerminative growth. One of the key developmental events during postgerminative growth is cotyledon greening, which enables a seedling to establish photosynthetic capacity. The plant phytohormone abscisic acid (ABA) plays a vital role by inhibiting seed germination and postgerminative growth in response to dynamically changing internal and environmental cues. It has been shown that ABSCISIC ACID INSENSITIVE5 (ABI5), a basic leucine zipper transcription factor, is an important factor in the regulation of the ABA-mediated inhibitory effect on seed germination and postgerminative growth. Conversely, the phytohormone cytokinin has been proposed to promote seed germination by antagonizing the ABA-mediated inhibitory effect. However, the underpinning molecular mechanism of cytokinin-repressed ABA signaling is largely unknown. Here, we show that cytokinin specifically antagonizes ABA-mediated inhibition of cotyledon greening with minimal effects on seed germination in Arabidopsis (Arabidopsis thaliana). We found that the cytokinin-antagonized ABA effect is dependent on a functional cytokinin signaling pathway, mainly involved in the cytokinin receptor gene CYTOKININ RESPONSE1/ARABIDOPSIS HISTIDINE KINASE4, downstream histidine phosphotransfer protein genes AHP2, AHP3, and AHP5, and a type B response regulator gene, ARR12, which genetically acts upstream of ABI5 to regulate cotyledon greening. Cytokinin has no apparent effect on the transcription of ABI5. However, cytokinin efficiently promotes the proteasomal degradation of ABI5 in a cytokinin signaling-dependentmanner. These results define a genetic pathway through which cytokinin specifically induces the degradation of ABI5 protein, thereby antagonizing ABA-mediated inhibition of postgerminative growth.