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Overexpression of the Stress-Inducible SsMAX2 Promotes Drought and Salt Resistance via the Regulation of Redox Homeostasis in Arabidopsis

Recent studies have demonstrated that strigolactones (SLs) also participate in the regulation of stress adaptation; however, the regulatory mechanism remains elusive. In this study, the homolog of More Axillary Branches 2, which encodes a key component in SL signaling, in the perennial oil plant Sap...

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Autores principales: Wang, Qiaojian, Ni, Jun, Shah, Faheem, Liu, Wenbo, Wang, Dongdong, Yao, Yuanyuan, Hu, Hao, Huang, Shengwei, Hou, Jinyan, Fu, Songling, Wu, Lifang
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6412474/
https://www.ncbi.nlm.nih.gov/pubmed/30781340
http://dx.doi.org/10.3390/ijms20040837
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author Wang, Qiaojian
Ni, Jun
Shah, Faheem
Liu, Wenbo
Wang, Dongdong
Yao, Yuanyuan
Hu, Hao
Huang, Shengwei
Hou, Jinyan
Fu, Songling
Wu, Lifang
author_facet Wang, Qiaojian
Ni, Jun
Shah, Faheem
Liu, Wenbo
Wang, Dongdong
Yao, Yuanyuan
Hu, Hao
Huang, Shengwei
Hou, Jinyan
Fu, Songling
Wu, Lifang
author_sort Wang, Qiaojian
collection PubMed
description Recent studies have demonstrated that strigolactones (SLs) also participate in the regulation of stress adaptation; however, the regulatory mechanism remains elusive. In this study, the homolog of More Axillary Branches 2, which encodes a key component in SL signaling, in the perennial oil plant Sapium sebiferum was identified and functionally characterized in Arabidopsis. The results showed that the expression of SsMAX2 in S. sebiferum seedlings was stress-responsive, and SsMAX2 overexpression (OE) in Arabidopsis significantly promoted resistance to drought, osmotic, and salt stresses. Moreover, SsMAX2 OE lines exhibited decreased chlorophyll degradation, increased soluble sugar and proline accumulation, and lower water loss ratio in response to the stresses. Importantly, anthocyanin biosynthesis and the activities of several antioxidant enzymes, such as superoxide dismutase (SOD), peroxidase (POD), and ascorbate peroxidase (APX), were enhanced in the SsMAX2 OE lines, which further led to a significant reduction in hydrogen peroxide levels. Additionally, the SsMAX2 OE lines exhibited higher expression level of several abscisic acid (ABA) biosynthesis genes, suggesting potential interactions between SL and ABA in the regulation of stress adaptation. Overall, we provide physiological and biochemical evidence demonstrating the pivotal role of SsMAX2 in the regulation of osmotic, drought, and salt stress resistance and show that MAX2 can be a genetic target to improve stress tolerance.
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spelling pubmed-64124742019-04-05 Overexpression of the Stress-Inducible SsMAX2 Promotes Drought and Salt Resistance via the Regulation of Redox Homeostasis in Arabidopsis Wang, Qiaojian Ni, Jun Shah, Faheem Liu, Wenbo Wang, Dongdong Yao, Yuanyuan Hu, Hao Huang, Shengwei Hou, Jinyan Fu, Songling Wu, Lifang Int J Mol Sci Article Recent studies have demonstrated that strigolactones (SLs) also participate in the regulation of stress adaptation; however, the regulatory mechanism remains elusive. In this study, the homolog of More Axillary Branches 2, which encodes a key component in SL signaling, in the perennial oil plant Sapium sebiferum was identified and functionally characterized in Arabidopsis. The results showed that the expression of SsMAX2 in S. sebiferum seedlings was stress-responsive, and SsMAX2 overexpression (OE) in Arabidopsis significantly promoted resistance to drought, osmotic, and salt stresses. Moreover, SsMAX2 OE lines exhibited decreased chlorophyll degradation, increased soluble sugar and proline accumulation, and lower water loss ratio in response to the stresses. Importantly, anthocyanin biosynthesis and the activities of several antioxidant enzymes, such as superoxide dismutase (SOD), peroxidase (POD), and ascorbate peroxidase (APX), were enhanced in the SsMAX2 OE lines, which further led to a significant reduction in hydrogen peroxide levels. Additionally, the SsMAX2 OE lines exhibited higher expression level of several abscisic acid (ABA) biosynthesis genes, suggesting potential interactions between SL and ABA in the regulation of stress adaptation. Overall, we provide physiological and biochemical evidence demonstrating the pivotal role of SsMAX2 in the regulation of osmotic, drought, and salt stress resistance and show that MAX2 can be a genetic target to improve stress tolerance. MDPI 2019-02-15 /pmc/articles/PMC6412474/ /pubmed/30781340 http://dx.doi.org/10.3390/ijms20040837 Text en © 2019 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Article
Wang, Qiaojian
Ni, Jun
Shah, Faheem
Liu, Wenbo
Wang, Dongdong
Yao, Yuanyuan
Hu, Hao
Huang, Shengwei
Hou, Jinyan
Fu, Songling
Wu, Lifang
Overexpression of the Stress-Inducible SsMAX2 Promotes Drought and Salt Resistance via the Regulation of Redox Homeostasis in Arabidopsis
title Overexpression of the Stress-Inducible SsMAX2 Promotes Drought and Salt Resistance via the Regulation of Redox Homeostasis in Arabidopsis
title_full Overexpression of the Stress-Inducible SsMAX2 Promotes Drought and Salt Resistance via the Regulation of Redox Homeostasis in Arabidopsis
title_fullStr Overexpression of the Stress-Inducible SsMAX2 Promotes Drought and Salt Resistance via the Regulation of Redox Homeostasis in Arabidopsis
title_full_unstemmed Overexpression of the Stress-Inducible SsMAX2 Promotes Drought and Salt Resistance via the Regulation of Redox Homeostasis in Arabidopsis
title_short Overexpression of the Stress-Inducible SsMAX2 Promotes Drought and Salt Resistance via the Regulation of Redox Homeostasis in Arabidopsis
title_sort overexpression of the stress-inducible ssmax2 promotes drought and salt resistance via the regulation of redox homeostasis in arabidopsis
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6412474/
https://www.ncbi.nlm.nih.gov/pubmed/30781340
http://dx.doi.org/10.3390/ijms20040837
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