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HO与Ca之间的正向相互作用介导了褪黑素诱导的西瓜(L.)CBF途径和耐寒性。

Positive Interaction between HO and Ca Mediates Melatonin-Induced CBF Pathway and Cold Tolerance in Watermelon ( L.).

作者信息

Chang Jingjing, Guo Yanliang, Li Jiayue, Su Zhuangzhuang, Wang Chunxia, Zhang Ruimin, Wei Chunhua, Ma Jianxiang, Zhang Xian, Li Hao

机构信息

State Key Laboratory of Crop Stress Biology for Arid Areas, College of Horticulture, Northwest A&F University, Xianyang 712100, China.

State Key Laboratory of Vegetable Germplasm Innovation, Tianjin 300384, China.

出版信息

Antioxidants (Basel). 2021 Sep 14;10(9):1457. doi: 10.3390/antiox10091457.

DOI:10.3390/antiox10091457
PMID:34573090
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8471466/
Abstract

Cold stress is a major environmental factor that detrimentally affects plant growth and development. Melatonin has been shown to confer plant tolerance to cold stress through activating the C-REPEAT BINDING FACTOR (CBF) pathway; however, the underlying modes that enable this function remain obscure. In this study, we investigated the role of HO and Ca signaling in the melatonin-induced CBF pathway and cold tolerance in watermelon ( L.) through pharmacological, physiological, and genetic approaches. According to the results, melatonin induced HO accumulation, which was associated with the upregulation of () during the early response to cold stress in watermelon. Besides, melatonin and HO induced the accumulation of cytoplasmic free Ca ([Ca]) in response to cold. This was associated with the upregulation of () in watermelon. However, blocking of Ca influx channels abolished melatonin- or HO-induced CBF pathway and cold tolerance. Ca also induced expression and HO accumulation in early response to cold stress in watermelon. Inhibition of HO production in watermelon by RBOH inhibitor or in Arabidopsis by knockout compromised melatonin-induced [Ca] accumulation and melatonin- or Ca-induced CBF pathway and cold tolerance. Overall, these findings indicate that melatonin induces -dependent HO generation in early response to cold stress. Increased HO promotes [Ca] accumulation, which in turn induces HO accumulation via , forming a reciprocal positive-regulatory loop that mediates melatonin-induced CBF pathway and subsequent cold tolerance.

摘要

冷胁迫是一种严重影响植物生长发育的环境因素。褪黑素已被证明可通过激活C-重复结合因子(CBF)途径赋予植物对冷胁迫的耐受性;然而,实现这一功能的潜在模式仍不清楚。在本研究中,我们通过药理学、生理学和遗传学方法,研究了HO和Ca信号在褪黑素诱导的西瓜(Citrullus lanatus (Thunb.) Matsum. & Nakai)CBF途径和耐寒性中的作用。结果表明,褪黑素诱导HO积累,这与西瓜在冷胁迫早期响应中NADPH氧化酶(NADPH oxidase, RBOH)的上调有关。此外,褪黑素和HO在冷胁迫下诱导细胞质游离Ca2+([Ca2+]cyt)积累,这与西瓜中RBOH的上调有关。然而,阻断Ca2+内流通道消除了褪黑素或HO诱导的CBF途径和耐寒性。Ca2+在西瓜冷胁迫早期响应中也诱导RBOH表达和HO积累。用RBOH抑制剂抑制西瓜中HO的产生或通过AtRBOH F基因敲除抑制拟南芥中HO的产生,会损害褪黑素诱导的[Ca2+]cyt积累以及褪黑素或Ca2+诱导的CBF途径和耐寒性。总体而言,这些发现表明,褪黑素在冷胁迫早期响应中诱导依赖于RBOH的HO生成。HO增加促进[Ca2+]cyt积累,进而通过RBOH诱导HO积累,形成一个相互正向调节环,介导褪黑素诱导的CBF途径和随后的耐寒性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f50d/8471466/5d0de95baf72/antioxidants-10-01457-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f50d/8471466/e368a6a2bcfb/antioxidants-10-01457-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f50d/8471466/225d9bedf0e5/antioxidants-10-01457-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f50d/8471466/01f5fc18960e/antioxidants-10-01457-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f50d/8471466/e97ca80b8eae/antioxidants-10-01457-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f50d/8471466/a20605bb6eb5/antioxidants-10-01457-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f50d/8471466/92f42036d748/antioxidants-10-01457-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f50d/8471466/3b11ff2f2168/antioxidants-10-01457-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f50d/8471466/6e2ecc045d06/antioxidants-10-01457-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f50d/8471466/5d0de95baf72/antioxidants-10-01457-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f50d/8471466/e368a6a2bcfb/antioxidants-10-01457-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f50d/8471466/225d9bedf0e5/antioxidants-10-01457-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f50d/8471466/01f5fc18960e/antioxidants-10-01457-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f50d/8471466/e97ca80b8eae/antioxidants-10-01457-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f50d/8471466/a20605bb6eb5/antioxidants-10-01457-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f50d/8471466/92f42036d748/antioxidants-10-01457-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f50d/8471466/3b11ff2f2168/antioxidants-10-01457-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f50d/8471466/6e2ecc045d06/antioxidants-10-01457-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f50d/8471466/5d0de95baf72/antioxidants-10-01457-g009.jpg

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