COP1 mediates dark-specific degradation of microtubule-associated protein WDL3 in regulating Arabidopsis hypocotyl elongation.

COP1 mediates dark-specific degradation of microtubule-associated protein WDL3 in regulating Arabidopsis hypocotyl elongation.
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COP1介导微管相关蛋白WDL3的暗特异性降解调节拟南芥下胚轴伸长

DOI:
10.1073/pnas.1708087114
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发表时间:
2017-11-14
影响因子:
11.1
通讯作者:
Mao T
Mao T
中科院分区:
综合性期刊1区
文献类型:
--
作者:
Lian N;Liu X;Wang X;Zhou Y;Li H;Li J;Mao T

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意义光形态发生酶1(COP1)是一种E3泛素连接酶,是植物幼苗光形态建成的中心抑制因子。在过去的二十年里,已经确定了许多核定位的COP1底物;然而,COP1是否针对细胞质因子进行泛素化和降解在很大程度上仍不清楚。在这项研究中,我们发现COP1与微管相关蛋白WDL3以暗依赖的方式在皮质微管相互作用。因此,COP1针对WDL3进行26S蛋白酶体介导的降解,以控制黄化拟南芥幼苗的下胚轴伸长。总体而言,我们的研究揭示了COP1的细胞质底物,它在介导下胚轴细胞伸长过程中发挥微管相关蛋白的功能。结构性光形态发生酶1(COP1)是一种广为人知的E3泛素连接酶,是植物生长和光形态发生发育的中枢调节因子,包括下胚轴的伸长。众所周知,在黑暗中,COP1以许多促进光形态发生的因子为靶点,在细胞核内泛素化和降解。然而,越来越多的证据表明,在暗培养的幼苗中,COP1的一部分也定位在细胞核外,但这种定位的生理功能仍不清楚。在这项研究中,我们证明了COP1直接靶向并介导WDL3蛋白的降解,WDL3蛋白是微管相关蛋白(MAP)WVD2/WDL家族的成员,参与调节拟南芥幼苗下胚轴细胞的伸长。我们发现COP1与WDL3在体内以暗依赖的方式在皮质微管相互作用。此外,我们的数据表明,COP1在体外直接泛化WDL3,WDL3蛋白在WT幼苗中被降解,但在黑暗中在Cop1突变体中含量丰富。一致地,wdl3突变的引入减弱了,而wdl3的过度表达增强了,在黑暗中,Cop1突变体的短下胚轴表型。综上所述,本研究揭示了COP1在调节黄化下胚轴中细胞质定位的MAP的蛋白质周转方面的功能,从而为COP1介导的下游因子的降解控制幼苗光形态建成提供了见解。
Significance CONSTITUTIVE PHOTOMORPHOGENIC 1 (COP1) is an E3 ubiquitin ligase acting as a central repressor of seedling photomorphogenesis in plants. Many nuclear-localized COP1 substrates have been identified in the last two decades; however, whether COP1 targets cytoplasmic factors for ubiquitination and degradation remains largely unknown. In this study, we show that COP1 interacts with a microtubule-associated protein, WAVE-DAMPENED 2-LIKE 3 (WDL3), in a dark-dependent manner at cortical microtubules. Thus, COP1 targets WDL3 for 26S proteasome-mediated degradation to control hypocotyl elongation in etiolated Arabidopsis seedlings. Collectively, our study uncovers a cytoplasmic substrate of COP1 that functions as a microtubule-associated protein in mediating hypocotyl cell elongation. CONSTITUTIVE PHOTOMORPHOGENIC 1 (COP1), a well-known E3 ubiquitin ligase, functions as a central regulator of plant growth and photomorphogenic development in plants, including hypocotyl elongation. It has been well-established that, in darkness, COP1 targets many photomorphogenesis-promoting factors for ubiquitination and degradation in the nucleus. However, increasing evidence has shown that a proportion of COP1 is also localized outside the nucleus in dark-grown seedlings, but the physiological function of this localization remains largely unclear. In this study, we demonstrate that COP1 directly targets and mediates the degradation of WAVE-DAMPENED 2-LIKE 3 (WDL3) protein, a member of the microtubule-associated protein (MAP) WVD2/WDL family involved in regulating hypocotyl cell elongation of Arabidopsis seedlings. We show that COP1 interacts with WDL3 in vivo in a dark-dependent manner at cortical microtubules. Moreover, our data indicate that COP1 directly ubiquitinates WDL3 in vitro and that WDL3 protein is degraded in WT seedlings but is abundant in the cop1 mutant in the dark. Consistently, introduction of the wdl3 mutation weakened, whereas overexpression of WDL3 enhanced, the short-hypocotyl phenotype of cop1 mutant in darkness. Together, this study reveals a function of COP1 in regulating the protein turnover of a cytosol-localized MAP in etiolated hypocotyls, thus providing insights into COP1-mediated degradation of downstream factors to control seedling photomorphogenesis.
DOI: 10.1016/j.cub.2004.12.026
发表时间: 2004-12-29
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