Recretohalophyte Tamarix TrSOS1 confers higher salt tolerance to transgenic plants and yeast than glycophyte soybean GmSOS1
Cong Cheng, Yongmei Liu, Xun Liu, Jing An, Li Jiang, Bingjun Yu
Journal:ENVIRONMENTAL AND EXPERIMENTAL BOTANY
IF:3.71
DOI:10.1016/j.envexpbot.2019.06.006
PMID:
Published:2019-06-15
research field:植物生理学分子遗传学生物技术
Abstract
The SOS1 ( S alt O verly S ensitive 1 ) gene has been widely investigated in plants including many glycophytes and a few euhalophytes. The encoded plasma membrane Na + /H + antiporter, SOS1, is mainly responsible for transporting Na + outside the cell and reducing the Na + content in plants under salt stress, and has been considered a key determinant in conferring plant salt tolerance . However, studies on the function of the SOS1 gene from recretohalophyte Tamarix have not yet been reported. In this work, the TrSOS1 gene was first transformed into Arabidopsis wild type and the sos1 mutant mediated by Agrobacterium tumefaciens and the soybean hairy root-composite plant by A. rhizogenes . Then, alongside the glycophyte soybean GmSOS1 gene as a reference, the TrSOS1 gene, including genes derived by site-directed mutagenesis, were transformed into Saccharomyces cerevisiae wild type and mutants. The differences in growth phenotype and physiological responses under salt stress were compared. The results showed that, overexpression of the TrSOS1 gene in Arabidopsis wild type and sos1 mutant could significantly improve transgenic plant growth and reduce Na + content and Na + /K + ratio in the shoots. As a result, the secondary oxidative stress was also alleviated by reducing the O 2 − · production rate, H 2 O 2 and malondialdehyde (MDA) contents in the shoots, thereby displaying enhanced salt tolerance and the complementary effects on the sos1 mutant were more prominent. The overexpression of TrSOS1 in yeast mutants ( ena1nha1 or ena1nhx1 ) also suppressed salt sensitivity by reducing the cellular Na + content and Na + /K + ratio, especially for the plasma membrane antiporter NHA1 mutant, ena1nha1. In terms of the yeast mutant complementation, the effects of overexpressing the intact TrSOS1 or mutated TrSOS1 A238V ge
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