The COP9 Signalosome regulates seed germination by facilitating protein degradation of RGL2 and ABI5 

First author: Dan Jin; Affiliations: Yale University (耶鲁大学): New Haven, USA

Corresponding author: Ning Wei

The control of seed germination and seed dormancy (种子休眠) are critical for the successful propagation of plant species, and are important agricultural traits. Seed germination is tightly controlled by the balance of gibberellin (GA) and abscisic acid (ABA), and is influenced by environmental factors. The COP9 Signalosome (CSN) is a conserved multi-subunit protein complex that is best known as a regulator of the Cullin-RING family of ubiquitin E3 ligases (CRLs). Multiple viable mutants of the CSN showed poor germination, except for csn5b-1. Detailed analyses showed that csn1-10 has a stronger seed dormancy, while csn5a-1 mutants exhibit retarded (受阻的) seed germination in addition to hyperdormancy (超休眠). Both csn5a-1 and csn1-10 plants show defects in the timely removal of the germination inhibitors: RGL2, a repressor of GA signaling, and ABI5, an effector of ABA responses. We provide genetic evidence to demonstrate that the germination phenotype of csn1-10 is caused by over-accumulation of RGL2, a substrate of the SCF (CRL1) ubiquitin E3 ligase, while the csn5a-1 phenotype is caused by over-accumulation of RGL2 as well as ABI5. The genetic data are consistent with the hypothesis that CSN5A regulates ABI5 by a mechanism that may not involve CSN1. Transcriptome analyses suggest that CSN1 has a more prominent role than CSN5A during seed maturation, but CSN5A plays a more important role than CSN1 during seed germination, further supporting the functional distinction of these two CSN genes. Our study delineates (描述) the molecular targets of the CSN complex in seed germination, and reveals that CSN5 has additional functions in regulating ABI5, thus the ABA signaling pathway.

种子萌发和种子休眠的调控对于植物物种的成功繁殖至关重要，同样也是重要的的农艺性状。种子萌发主要是受到体内赤霉素GA和脱落酸ABA之间的平衡状态所调控的，并且受到环境因子的影响。COP9信号复合体CSN是一个保守的多亚基组成的蛋白复合物，是泛素E3连接酶Cullin-RING家族CRL的调控子。除了csn5b-1突变体以外，CSN多个不致死突变体均显示出了萌发缺陷。进一步的分析显示csn1-10突变体具有更强的休眠，而csn5a-1突变体除了超休眠的表型还存在种子萌发受阻的现象。csn5a-1和csn1-10突变体均在及时清除两个萌发抑制蛋白方面存在缺陷，一个是能够抑制GA信号转导的RGL2蛋白，另一个是ABA响应的效应蛋白ABI5。遗传学的证据表明csn1-10的萌发表型主要是由于过量积累SCF (CRL1) 泛素E3连接酶的底物RGL2所导致的，而csn5a-1的表型是由于同时过量积累RGL2和ABI5所引起的。遗传学上的数据与CSN5A不通过CSN1调控ABI5的假设一致。转录组数据分析进一步显示了在种子成熟过程中，CSN1基因要比CSN5A基因具有更加重要的作用；而在种子萌发过程中，CSN5A基因要比CSN1基因发挥更加重要的作用，进一步支持了这两个CSN基因在演化过程中出现了功能的分化。本文的研究揭示了种子萌发过程中CSN复合物的分子靶标，显示CSN5还有调控ABI5的功能，进而调控ABA的信号通路。

通讯：Ning Wei (https://mcdb.yale.edu/people/ning-wei)

个人简介：北京大学，学士；伯克利大学，博士；耶鲁大学，研究科学家。

研究方向：CSN复合物在调控植物生长和发育方面的作用。

（p.s. Ning属于耶鲁大学Irish实验室的成员，Vivian Irish（真·老板）本科毕业于卫斯理大学，博士毕业于哈佛大学，博士方向为细胞和发育生物学，由于对发育遗传学比较感兴趣，博士后在剑桥大学研究果蝇，后因对于植物发育遗传学比较着迷，在耶鲁大学Ian Sussex教授指导下完成博士后工作。目前Vivian Irish博士在耶鲁大学工作，主要从事植物发育、遗传以及发育机制的演化等方面的研究。实验室网址：https://irishlab.yale.edu）

doi: https://doi.org/10.1371/journal.pgen.1007237

Journal: PLOS Genetics

Published date: 20 February, 2018

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