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Transgenic Arabidopsis overexpressing MsSNAT enhances salt tolerance via the increase in autophagy, and the reestablishment of redox and ion homeostasis

Author:
Zhao, Gan, Yu, Xiuli, Lou, Wang, Wei, Siqi, Wang, Ren, Wan, Qun, Shen, Wenbiao
Source:
Environmental and experimental botany 2019 v.164 pp. 20-28
ISSN:
0098-8472
Subject:
Arabidopsis, Medicago sativa, acetyltransferases, alfalfa, antioxidant genes, autophagy, chlorophyll, enzyme activity, gene expression regulation, gene overexpression, growth retardation, homeostasis, hydrogen, melatonin, root growth, roots, salt stress, salt tolerance, serotonin, sodium, sodium chloride, synthetic genes, transcription (genetics), transgenic plants
Abstract:
Whether or how alfalfa serotonin N-acetyltransferase gene (MsSNAT; a melatonin synthetic gene) enhances salinity tolerance is still elusive. In this report, the wild-type and the transgenic Arabidopsis plants overexpressing MsSNAT were adopted. Compared to the wild-type, two transgenic Arabidopsis lines enhanced endogenous melatonin production in response to NaCl stress. Meanwhile, the primary root growth inhibition and chlorophyll degradation caused by NaCl stress were differentially alleviated. These were accompanied with the enhanced autophagy in two transgenic lines, as evidenced by the number of autophagosomes in roots and up-regulated some Autophagy-related (ATG) genes. Redox homeostasis was reestablished, since representative antioxidant genes and corresponding enzymatic activities were intensified in the transgenic Arabidopsis plants overexpressing alfalfa SNAT, compared to the stressed wild-type. Importantly, NaCl-triggered ion imbalance was differentially abolished in transgenic lines, which was consistent with the transcriptional profiles of representative genes related to ion homeostasis, including sodium hydrogen exchanger 1 (NHX1) and salt overly sensitive1 (SOS1). Collectively, our results revealed that MsSNAT-dependent melatonin enhanced salt tolerance via the increase in autophagy, and reestablishment of redox and ion homeostasis.
Agid:
6393142