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激活蛋白激酶 C 受体 1 拮抗脱落酸不敏感 5 介导的拟南芥种子萌发和萌发后生长的抑制作用。

Receptor for Activated C Kinase 1 counteracts ABSCISIC ACID INSENSITIVE5-mediated inhibition of seed germination and post-germinative growth in Arabidopsis.

机构信息

Department of Biology, Southern University of Science and Technology, Shenzhen 518055, China.

Shenzhen Key Laboratory of Plant Genetic Engineering and Molecular Design, Institute of Plant and Food Science, Department of Biology, Southern University of Science and Technology, Shenzhen 518055, China.

出版信息

J Exp Bot. 2024 Jul 10;75(13):3932-3945. doi: 10.1093/jxb/erae153.

Abstract

ABSCISIC ACID INSENSITIVE5 (ABI5), a key regulator of the abscisic acid (ABA) signalling pathway, plays a fundamental role in seed germination and post-germinative development. However, the molecular mechanism underlying the repression function of ABI5 remains to be elucidated. In this study, we demonstrate that the conserved eukaryotic WD40 repeat protein Receptor for Activated C Kinase 1 (RACK1) is a novel negative regulator of ABI5 in Arabidopsis. The RACK1 loss-of-function mutant is hypersensitive to ABA, while this phenotype is rescued by a mutation in ABI5. Moreover, overexpression of RACK1 suppresses ABI5 transcriptional activation activity for ABI5-targeted genes. RACK1 may also physically interact with ABI5 and facilitate its degradation. Furthermore, we found that RACK1 and the two substrate receptors CUL4-based E3 ligases (DWA1 and DWA2) function together to mediate the turnover of ABI5, thereby efficiently reducing ABA signalling in seed germination and post-germinative growth. In addition, molecular analyses demonstrated that ABI5 may bind to the promoter of RACK1 to repress its expression. Collectively, our findings suggest that RACK1 and ABI5 might form a feedback loop to regulate the homeostasis of ABA signalling in acute seed germination and early plant development.

摘要

脱落酸不敏感 5(ABI5)是脱落酸(ABA)信号通路的关键调节剂,在种子萌发和萌发后发育中起着重要作用。然而,ABI5 抑制功能的分子机制仍有待阐明。在这项研究中,我们证明了保守的真核 WD40 重复蛋白蛋白激酶激活物受体 1(RACK1)是拟南芥 ABI5 的一种新的负调控因子。RACK1 功能丧失突变体对 ABA 敏感,而 ABI5 突变可挽救这种表型。此外,RACK1 的过表达抑制了 ABI5 对 ABI5 靶向基因的转录激活活性。RACK1 还可能与 ABI5 相互作用并促进其降解。此外,我们发现 RACK1 和两种底物受体 CUL4 基 E3 连接酶(DWA1 和 DWA2)共同作用,介导 ABI5 的周转,从而有效降低种子萌发和萌发后生长过程中的 ABA 信号转导。此外,分子分析表明 ABI5 可能与 RACK1 的启动子结合,抑制其表达。总之,我们的研究结果表明,RACK1 和 ABI5 可能形成一个反馈回路,以调节急性种子萌发和早期植物发育过程中 ABA 信号的动态平衡。

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