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热响应性促分裂原活化蛋白激酶对生长素信号抑制因子IAA8的磷酸化作用导致花发育缺陷。

Phosphorylation of auxin signaling repressor IAA8 by heat-responsive MPKs causes defective flower development.

作者信息

Kim Sun Ho, Hussain Shah, Pham Huyen Trang Thi, Kadam Ulhas Sopanrao, Bahk Sunghwa, Ramadany Zakiyah, Lee Jeongwoo, Song Young Hun, Lee Kyun Oh, Hong Jong Chan, Chung Woo Sik

机构信息

Division of Applied Life Science (BK21 Four program), Plant Molecular Biology and Biotechnology Research Center, Gyeongsang National University, Jinju 52828, Republic of Korea.

Depatment of Applied Biology and Chemistry, Seoul National University, Seoul 08826, Republic of Korea.

出版信息

Plant Physiol. 2024 Dec 2;196(4):2825-2840. doi: 10.1093/plphys/kiae470.

DOI:10.1093/plphys/kiae470
PMID:39240752
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11638004/
Abstract

Heat stress is a substantial and imminent threat to plant growth and development. Understanding its adverse effects on plant development at the molecular level is crucial for sustainable agriculture. However, the molecular mechanism underlying how heat stress causes developmental defects in flowers remains poorly understood. Here, we identified Indole-3-Acetic Acid 8 (IAA8), a repressor of auxin signaling, as a substrate of mitogen-activated protein kinases (MPKs) in Arabidopsis thaliana, and found that MPK-mediated phosphorylation of IAA8 inhibits flower development. MPKs phosphorylated three residues of IAA8: S74, T77, and S135. Interestingly, transgenic plants overexpressing a phospho-mimicking mutant of IAA8 (IAA8DDD OX) exhibited defective flower development due to high IAA8 levels. Furthermore, MPK-mediated phosphorylation inhibited IAA8 polyubiquitination, thereby significantly increasing its stability. Additionally, the expression of key transcription factors involved in flower development, such as bZIP and MYB genes, was significantly perturbed in the IAA8DDD OX plants. Collectively, our study demonstrates that heat stress inhibits flower development by perturbing the expression of flower development genes through the MPK-mediated phosphorylation of IAA8, suggesting that Aux/IAA phosphorylation enables plants to fine-tune their development in response to environmental stress.

摘要

热胁迫是对植物生长发育的重大且紧迫的威胁。在分子水平上了解其对植物发育的不利影响对于可持续农业至关重要。然而,热胁迫如何导致花发育缺陷的分子机制仍知之甚少。在这里,我们鉴定出吲哚 - 3 - 乙酸8(IAA8),一种生长素信号转导的抑制因子,作为拟南芥中丝裂原活化蛋白激酶(MPK)的底物,并发现MPK介导的IAA8磷酸化抑制花发育。MPK使IAA8的三个残基磷酸化:S74、T77和S135。有趣的是,过表达IAA8的磷酸模拟突变体(IAA8DDD OX)的转基因植物由于IAA8水平过高而表现出花发育缺陷。此外,MPK介导的磷酸化抑制IAA8多聚泛素化,从而显著提高其稳定性。另外,参与花发育的关键转录因子如bZIP和MYB基因的表达在IAA8DDD OX植物中受到显著干扰。总的来说,我们的研究表明,热胁迫通过MPK介导的IAA8磷酸化干扰花发育基因的表达来抑制花发育,这表明Aux/IAA磷酸化使植物能够根据环境胁迫微调其发育。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dcc3/11638004/c7ee5aaae0a3/kiae470f8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dcc3/11638004/a4c221f5db36/kiae470f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dcc3/11638004/ab762fedcd7c/kiae470f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dcc3/11638004/6cf4899147c0/kiae470f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dcc3/11638004/64e008c6049e/kiae470f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dcc3/11638004/1bd49924cffe/kiae470f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dcc3/11638004/f358e117bafb/kiae470f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dcc3/11638004/890786a2a7e2/kiae470f7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dcc3/11638004/c7ee5aaae0a3/kiae470f8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dcc3/11638004/a4c221f5db36/kiae470f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dcc3/11638004/ab762fedcd7c/kiae470f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dcc3/11638004/6cf4899147c0/kiae470f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dcc3/11638004/64e008c6049e/kiae470f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dcc3/11638004/1bd49924cffe/kiae470f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dcc3/11638004/f358e117bafb/kiae470f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dcc3/11638004/890786a2a7e2/kiae470f7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dcc3/11638004/c7ee5aaae0a3/kiae470f8.jpg

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Pharmacophore-Oriented Identification of Potential Leads as CCR5 Inhibitors to Block HIV Cellular Entry.
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