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NUA和ESD4在种子萌发过程中对脱落酸信号传导起负调控作用。

NUA and ESD4 negatively regulate ABA signaling during seed germination.

作者信息

Cui Xiaona, Lv Mengyang, Cao Yuanyuan, Li Ziwen, Liu Yan, Ren Zhenzhen, Zhang Hairong

机构信息

College of Life sciences, Henan Agricultural University, Zhengzhou, 450002, China.

State Key Laboratory of Wheat and Maize Crop Science, Henan Agricultural University, Zhengzhou, 450002, China.

出版信息

Stress Biol. 2022 Sep 13;2(1):38. doi: 10.1007/s44154-022-00062-1.

DOI:10.1007/s44154-022-00062-1
PMID:37676575
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10442006/
Abstract

The phytohormone abscisic acid (ABA) plays important roles in plant growth, development and adaptative responses to abiotic stresses. SNF1-related protein kinase 2s (SnRK2) are key components that activate the ABA core signaling pathway. NUCLEAR PORE ANCHOR (NUA) is a component of the nuclear pore complex (NPC) that involves in deSUMOylation through physically interacting with the EARLY IN SHORT DAYS 4 (ESD4) SUMO protease. However, it is not clear how NUA functions with SnRK2 and ESD4 to regulate ABA signaling. In our study, we found that nua loss-of-function mutants exhibited pleiotropic ABA-hypersensitive phenotype. We also found that ABA-responsive genes remarkably up-regulated in nua by exogenous ABA. The nua snrk2.2 snrk2.3 triple mutant and nua abi5 double mutant partially rescued the ABA-hypersensitive phenotype of nua, thereby suggesting that NUA is epistatic to SnRK2s. Additionally, we observed that esd4-3 mutant was also ABA-hypersensitive. NUA and ESD4 were further demonstrated to physically interact with SnRK2s and negatively regulate ABA signaling by reducing SnRK2s stability. Taken together, our findings uncover a new regulatory mechanism that can modulate ABA signaling.

摘要

植物激素脱落酸(ABA)在植物生长、发育以及对非生物胁迫的适应性反应中发挥着重要作用。蔗糖非发酵1相关蛋白激酶2(SnRK2)是激活ABA核心信号通路的关键组分。核孔锚定蛋白(NUA)是核孔复合体(NPC)的一个组分,通过与早花4(ESD4)小泛素样修饰蛋白酶物理相互作用参与去SUMO化作用。然而,尚不清楚NUA如何与SnRK2和ESD4共同作用来调控ABA信号传导。在我们的研究中,我们发现NUA功能缺失突变体表现出多效性的ABA超敏感表型。我们还发现,外源ABA处理后,ABA响应基因在NUA中显著上调。NUA、SnRK2.2和SnRK2.3三突变体以及NUA、ABI5双突变体部分挽救了NUA的ABA超敏感表型,从而表明NUA对SnRK2具有上位性。此外,我们观察到esd4 - 3突变体也对ABA超敏感。进一步证明,NUA和ESD4与SnRK2物理相互作用,并通过降低SnRK2的稳定性来负调控ABA信号传导。综上所述,我们的研究结果揭示了一种可调节ABA信号传导的新调控机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3471/10442006/4a1858581ed1/44154_2022_62_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3471/10442006/ef1e1ccfc809/44154_2022_62_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3471/10442006/a2db7e9a56b7/44154_2022_62_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3471/10442006/bb5cd20c5e31/44154_2022_62_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3471/10442006/d1519e5402f5/44154_2022_62_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3471/10442006/1a761feccb60/44154_2022_62_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3471/10442006/4a1858581ed1/44154_2022_62_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3471/10442006/ef1e1ccfc809/44154_2022_62_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3471/10442006/a2db7e9a56b7/44154_2022_62_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3471/10442006/bb5cd20c5e31/44154_2022_62_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3471/10442006/d1519e5402f5/44154_2022_62_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3471/10442006/1a761feccb60/44154_2022_62_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3471/10442006/4a1858581ed1/44154_2022_62_Fig6_HTML.jpg

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