Phosphorylation of SPT5 by CDKD;2 is required for VIP5 recruitment and normal flowering in Arabidopsis thaliana.

Phosphorylation of SPT5 by CDKD;2 is required for VIP5 recruitment and normal flowering in Arabidopsis thaliana.
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CDKD;2 磷酸化 SPT5 是拟南芥中 VIP5 募集和正常开花所必需的。

DOI:
10.1105/tpc.16.00568
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发表时间:
2017
期刊:
影响因子:
11.6
通讯作者:
Ding Yong
Ding Yong
中科院分区:
生物学1区
文献类型:
--
作者:
Lu Chengyuan;Tian Yongke;Wang Shiliang;Su Yanhua;Mao Ting;Huang Tongtong;Chen Qingqing;Xu Zuntao;Ding Yong

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Ty 5同源物的延伸因子抑制因子(Spt 5)是转录和组蛋白甲基化的调节因子。在人类中,P-TEFb(一种由细胞周期蛋白依赖性激酶9(CDK 9)和细胞周期蛋白T组成的蛋白激酶)对SPT 5的磷酸化与RNA聚合酶II相关因子1(PAF 1)复合物相互作用。然而,SPT 5磷酸化的机制在植物中并不清楚。在此,我们研究了拟南芥中SPT 5的功能,发现spt 5突变体在长日照和短日照条件下都能提早开花。SPT 5与CDK活化激酶4(CAK 4; CDKD;2)相互作用,并在苏氨酸处被CDKD;2特异性磷酸化。磷酸化的SPT 5结合春化独立性5(VIP 5),这是PAF 1复合物的一个亚基。遗传分析表明VIP 5作用于SPT 5和CDKD的下游; SPT 5或CDKD; 2功能的缺失导致开花提前,因为FLC转录本的数量减少。重要的是,CDKD; 2和SPT 5是VIP 5沉积和组蛋白3赖氨酸4三甲基化增强所必需的。总之,我们的研究结果提供了深入了解拟南芥延伸因子SPT 5通过蛋白质的翻译后修饰招募PAF 1复合物的机制,并表明SPT 5通过CDKD的磷酸化;2使其能够招募VIP 5来调节拟南芥中的染色质和转录。
The elongation factor suppressor of Ty 5 homolog (Spt5) is a regulator of transcription and histone methylation. In humans, phosphorylation of SPT5 by P-TEFb, a protein kinase composed of Cyclin-dependent kinase 9 (CDK9) and cyclin T, interacts with the RNA polymerase II-associated factor1 (PAF1) complex. However, the mechanism of SPT5 phosphorylation is not well understood in plants. Here, we examine the function of SPT5 inArabidopsis thalianaand find thatspt5mutant flowers early under long-day and short-day conditions. SPT5 interacts with the CDK-activating kinase 4 (CAK4; CDKD;2) and is specifically phosphorylated by CDKD;2 at threonines. The phosphorylated SPT5 binds VERNALIZATION INDEPENDENCE5 (VIP5), a subunit of the PAF1 complex. Genetic analysis showed thatVIP5acts downstream ofSPT5andCDKD;2. Loss ofSPT5orCDKD;2function results in early flowering because of decreased amounts ofFLOWERING LOCUS C(FLC) transcript. Importantly,CDKD;2andSPT5are required for the deposition of VIP5 and the enhancement of trimethylation of histone 3 lysine 4 in the chromatin of theFLClocus. Together, our results provide insight into the mechanism by which the Arabidopsis elongation factor SPT5 recruits the PAF1 complex via the posttranslational modification of proteins and suggest that the phosphorylation of SPT5 by CDKD;2 enables it to recruit VIP5 to regulate chromatin and transcription in Arabidopsis.