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HOS15在拟南芥干旱胁迫期间影响DIL9蛋白稳定性。

HOS15 impacts DIL9 protein stability during drought stress in Arabidopsis.

作者信息

Zareen Shah, Ali Akhtar, Park Junghoon, Kang Sang-Mo, Lee In-Jung, Pardo Jose M, Yun Dae-Jin, Xu Zheng-Yi

机构信息

Department of Biomedical Science & Engineering, Konkuk University, Seoul, 05029, South Korea.

Plant Global Stress Research Center, Konkuk University, Seoul, 05029, South Korea.

出版信息

New Phytol. 2025 Mar;245(6):2553-2568. doi: 10.1111/nph.20398. Epub 2025 Jan 31.

Abstract

HIGH EXPRESSION OF OSMOTICALLY RESPONSIVE GENE 15 (HOS15) acts as a substrate receptor of E3 ligase complex, which plays a negative role in drought stress tolerance. However, whether and how HOS15 participates in controlling important transcriptional regulators remains largely unknown. Here, we report that HOS15 physically interacts with and tightly regulates DROUGHT-INDUCED LIKE 19 (DIL9) protein stability. Moreover, application of exogenous abscisic acid (ABA) stabilizes the interaction between DIL9 and HOS15, leading to ABA-induced proteasomal degradation of DIL9 by HOS15. Genetic analysis revealed that DIL9 functions downstream to HOS15 and that the drought tolerance of hos15-2 plants was impaired in dil9/hos15 double mutants. Notably, DIL9 is directly associated with the promoter regions of ABF transcription factors and facilitates their expression, which is pivotal in enhancing ABA-dependent drought tolerance. Collectively, these findings demonstrate that HOS15 consistently degrades DIL9 under normal condition, while stress (drought/ABA) promotes the DIL9 activity for binding to the promoter regions of ABFs and positively regulates their expression in response to dehydration.

摘要

渗透压响应基因15(HOS15)的高表达作为E3连接酶复合体的底物受体,在干旱胁迫耐受性中起负向作用。然而,HOS15是否以及如何参与调控重要的转录调节因子在很大程度上仍不清楚。在此,我们报道HOS15与干旱诱导类蛋白19(DIL9)发生物理相互作用并严格调控其蛋白稳定性。此外,外源脱落酸(ABA)的施用稳定了DIL9与HOS15之间的相互作用,导致HOS15介导ABA诱导的DIL9经蛋白酶体降解。遗传分析表明DIL9在HOS15下游发挥作用,并且在dil9/hos15双突变体中hos15-2植株的耐旱性受损。值得注意的是,DIL9与ABF转录因子的启动子区域直接相关并促进其表达,这在增强ABA依赖的耐旱性中起关键作用。总体而言,这些发现表明,在正常条件下HOS15持续降解DIL9,而胁迫(干旱/ABA)促进DIL9与ABF启动子区域结合的活性,并在脱水响应中正向调节其表达。

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