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参与脱落酸信号通路以调节……的早期生长和发育。 (原文中“of”后面缺少具体内容)

involved in the abscisic acid signaling pathway to regulate the early growth and development of .

作者信息

Xie Xiaoyang, Wei Lei, Han Hongyuan, Jing Bingnian, Liu Yuqing, Zhou Yong, Li Ningjie, Li Xiao, Wang Wei

机构信息

Key Laboratory of Natural Products, Henan Academy of Sciences, Zhengzhou, Henan Province, China.

State Key Laboratory of Cotton Biology, School of Life Sciences, Henan University, Kaifeng, Henan Province, China.

出版信息

PeerJ. 2024 Nov 26;12:e18460. doi: 10.7717/peerj.18460. eCollection 2024.

DOI:10.7717/peerj.18460
PMID:39619177
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11606324/
Abstract

BACKGROUND

Living organisms possess the remarkable capacity to swiftly adapt to fluctuations in their environment. In the context of cell signal transduction, a significant challenge lies in ensuring the effective perception of external signals and the execution of appropriate responses. To investigate this phenomenon, a recent study utilized as a model plant and induced stress by administering abscisic acid (ABA), a plant hormone, to elucidate the involvement of leucine-rich repeat receptor-like kinase1 (LRR1) in ABA signaling pathways.

METHODS

Homozygous T-DNA insertion alleles for and were isolated. Quantitative real-time PCR (qRT-PCR) was performed to confirm the expression of the gene. Subcellular localization and beta-glucuronidase (GUS) tissue labeling techniques were utilized to determine the expression pattern of the gene in cells and tissues. Yeast two-hybrid complementation, bimolecular fluorescence complementation assay, and GST pull-down assays were conducted to validate the interaction of LRR1 proteins.

RESULTS

Phenotypic analyses revealed that and mutants are less sensitive to the inhibitory effects of ABA on germination and cotyledon greening that is seen in WT. Mutants and kinase 7 (KIN7) exhibited resistance to ABA and displayed normal growth patterns under control conditions. The double mutant showed reduced responsiveness to ABA. Conversely, overexpression lines and demonstrated heightened sensitivity to ABA, resulting in severe growth reduction. qRT-PCR assay indicated that exogenous application of ABA led to significant down-regulation of , , and transcription factors in material compared to wild-type WT material. An investigation was conducted to determine the expression pattern and transcriptional level of in Arabidopsis. The results revealed ubiquitous expression of across all developmental stages and tissue tested. Subcellular localization assays confirmed the presence of LRR1 on the plasma membrane of cells. Furthermore, BiFC assay, yeast two-hybrid complementation, and GST pull-down assays demonstrated an interaction between LRR1 and PYL6 . These findings provide substantial insights into the involvement of in the ABA signaling pathway while regulating seed germination and cotyledon greening during early development in Arabidopsis. This study significantly advances our understanding regarding the correlation between and ABA signaling pathways with potential applications for enhancing crop stress resistance.

摘要

背景

生物具有迅速适应环境波动的非凡能力。在细胞信号转导的背景下,一个重大挑战在于确保有效感知外部信号并执行适当的反应。为了研究这一现象,最近的一项研究利用[植物名称未给出]作为模式植物,并通过施用脱落酸(ABA)(一种植物激素)诱导胁迫,以阐明富含亮氨酸重复序列的受体样激酶1(LRR1)在ABA信号通路中的作用。

方法

分离了[植物名称未给出]的纯合T-DNA插入等位基因。进行定量实时PCR(qRT-PCR)以确认[基因名称未给出]基因的表达。利用亚细胞定位和β-葡萄糖醛酸酶(GUS)组织标记技术来确定[基因名称未给出]基因在细胞和组织中的表达模式。进行酵母双杂交互补、双分子荧光互补分析和GST下拉分析以验证LRR1蛋白之间的相互作用。

结果

表型分析表明,[突变体名称未给出]突变体对ABA对发芽和子叶绿化的抑制作用不如野生型(WT)敏感。突变体[突变体名称未给出]和激酶7(KIN7)对ABA具有抗性,并且在对照条件下表现出正常的生长模式。双突变体[双突变体名称未给出]对ABA的反应性降低。相反,过表达株系[过表达株系名称未给出]对ABA表现出更高的敏感性,导致严重的生长抑制。qRT-PCR分析表明,与野生型WT材料相比,外源施用ABA导致[材料名称未给出]材料中[转录因子名称未给出]、[转录因子名称未给出]和[转录因子名称未给出]转录因子的显著下调。对拟南芥中[基因名称未给出]的表达模式和转录水平进行了研究。结果显示,[基因名称未给出]在所有测试的发育阶段和组织中均有普遍表达。亚细胞定位分析证实LRR1存在于细胞的质膜上。此外,双分子荧光互补分析、酵母双杂交互补和GST下拉分析表明LRR1与PYL6之间存在相互作用。这些发现为[基因名称未给出]在ABA信号通路中的作用提供了重要见解,同时调节拟南芥早期发育过程中的种子萌发和子叶绿化。这项研究显著推进了我们对[基因名称未给出]与ABA信号通路之间相关性的理解,具有增强作物抗逆性的潜在应用价值。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe33/11606324/86f31ad341b1/peerj-12-18460-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe33/11606324/6bf30aec50c3/peerj-12-18460-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe33/11606324/6d15865892b3/peerj-12-18460-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe33/11606324/dfea9a9e1358/peerj-12-18460-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe33/11606324/95a6e6f5d22b/peerj-12-18460-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe33/11606324/f46f06a014e1/peerj-12-18460-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe33/11606324/0889d5aaa5c2/peerj-12-18460-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe33/11606324/14a1b2b5ccfb/peerj-12-18460-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe33/11606324/86f31ad341b1/peerj-12-18460-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe33/11606324/6bf30aec50c3/peerj-12-18460-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe33/11606324/6d15865892b3/peerj-12-18460-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe33/11606324/dfea9a9e1358/peerj-12-18460-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe33/11606324/95a6e6f5d22b/peerj-12-18460-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe33/11606324/f46f06a014e1/peerj-12-18460-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe33/11606324/0889d5aaa5c2/peerj-12-18460-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe33/11606324/14a1b2b5ccfb/peerj-12-18460-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe33/11606324/86f31ad341b1/peerj-12-18460-g008.jpg

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