Author:
Zhou Zixin,Wang Juan,Yu Qinghui,Lan Haiyan
Abstract
Abstract
Background
Our previous studies revealed that CgbHLH001 transcription factor (TF) played an important role in abiotic stress tolerance, suggesting that its promoter was a potential target in response to stress signals. In addition, the regulatory mechanism of CgbHLH001 TF is still limited.
Results
In the present study, a 1512 bp of 5’-flanking sequence of CgbHLH001 gene was identified, and the sequence carried quite a few of cis-acting elements. The gene promoter displayed strong activity and was induced by multiple abiotic stress. A series of 5’-deletions of the promoter sequence resulted in a gradual decrease in its activity, especially, the 5’ untranslated region (UTR) was necessary to drive promoter activity. Further, CgbHLH001 promoter drove its own gene overexpression ectopically at the transcriptional and translational levels, which in turn conferred the stress tolerance to transgenic Arabidopsis. Transcriptome analysis showed that salt stress induced a large number of genes involved in multiple biological regulatory processes. Differentially expressed genes (DEGs) that mediate phytohormone signal transduction and mitogen-activated protein kinase (MAPK) signaling pathway were widely induced and mostly upregulated under salt stress, and the transcription levels in PbHLH::bHLH-overexpressing transgenic lines were higher than that of 35S::bHLH overexpression.
Conclusions
The CgbHLH001 promoter exhibited a positive response to abiotic stress and its 5’ UTR sequence enhanced the regulation of gene expression to stress. A few important pathways and putative key genes involved in salt tolerance were identified, which can be used to elucidate the mechanism of salt tolerance and decipher the regulatory mechanism of promoters to develop an adaptation strategy for desert halophytes.
Funder
National Natural Science Foundation of China
Open Fund of Xinjiang Uygur Autonomous Region
Publisher
Springer Science and Business Media LLC
Cited by
3 articles.
订阅此论文施引文献
订阅此论文施引文献,注册后可以免费订阅5篇论文的施引文献,订阅后可以查看论文全部施引文献