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植物丝裂原活化蛋白激酶 TaMPK3 通过使小麦 TaPYL4 受体失稳来抑制 ABA 反应。

Mitogen-activated protein kinase TaMPK3 suppresses ABA response by destabilising TaPYL4 receptor in wheat.

机构信息

Institute of Crop Sciences, Chinese Academy of Agricultural Sciences (CAAS)/National Key Facility for Crop Gene Resources and Genetic Improvement, Key Laboratory of Biology and Genetic Improvement of Triticeae Crops, Ministry of Agriculture, Beijing, 100081, China.

National Engineering Laboratory for Wheat and Maize/Key Laboratory of Wheat Biology and Genetic Improvement, Crop Research Institute, Shandong Academy of Agricultural Sciences, Jinan, 250100, China.

出版信息

New Phytol. 2022 Oct;236(1):114-131. doi: 10.1111/nph.18326. Epub 2022 Jul 13.

Abstract

Abscisic acid (ABA) receptors are considered as the targeted manipulation of ABA sensitivity and water productivity in plants. Regulation of their stability or activity will directly affect ABA signalling. Mitogen-activated protein kinase (MAPK) cascades link multiple environmental and plant developmental cues. However, the molecular mechanism of ABA signalling and MAPK cascade interaction remains largely elusive. TaMPK3 overexpression decreases drought tolerance and wheat sensitivity to ABA, significantly weakening ABA's inhibitory effects on growth. Under drought stress, overexpression lines show lower survival rates, shoot fresh weight and proline content, but higher malondialdehyde levels at seedling stage, as well as decreased grain width and 1000 grain weight in both glasshouse and field conditions at the adult stage. TaMPK3-RNAi increases drought tolerance. TaMPK3 interaction with TaPYL4 leads to decreased TaPYL4 levels by promoting its ubiquitin-mediated degradation, whereas ABA treatment diminishes TaMPK3-TaPYL interactions. In addition, the expression of ABA signalling proteins is impaired in TaMPK3-overexpressing wheat plants under ABA treatment. The MPK3-PYL interaction module was found to be conserved across monocots and dicots. Our results suggest that the MPK3-PYL module could serve as a negative regulatory mechanism for balancing appropriate drought stress response with normal plant growth signalling in wheat.

摘要

脱落酸 (ABA) 受体被认为是植物中 ABA 敏感性和水分生产率的靶向操纵对象。它们的稳定性或活性的调节将直接影响 ABA 信号转导。丝裂原活化蛋白激酶 (MAPK) 级联反应将多种环境和植物发育线索联系起来。然而,ABA 信号转导和 MAPK 级联相互作用的分子机制在很大程度上仍未被揭示。TaMPK3 的过表达降低了干旱耐受性和小麦对 ABA 的敏感性,显著削弱了 ABA 对生长的抑制作用。在干旱胁迫下,过表达系在幼苗期表现出较低的存活率、茎鲜重和脯氨酸含量,但丙二醛水平较高,在温室和田间条件下,成株期的粒宽和千粒重均降低。TaMPK3-RNAi 提高了耐旱性。TaMPK3 与 TaPYL4 的相互作用通过促进其泛素介导的降解导致 TaPYL4 水平降低,而 ABA 处理则减弱了 TaMPK3-TaPYL 相互作用。此外,在 ABA 处理下,过表达 TaMPK3 的小麦植物中 ABA 信号蛋白的表达受到损害。在单子叶植物和双子叶植物中都发现了 MPK3-PYL 互作模块的保守性。我们的研究结果表明,MPK3-PYL 模块可以作为一种负调控机制,在小麦中平衡适当的干旱胁迫响应与正常的植物生长信号。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/49bf/9544932/add4c9c9bc38/NPH-236-114-g004.jpg

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