Abstract

Heat shock transcription factors (HSFs) play critical roles in several types of environmental stresses. However, the detailed regulatory mechanisms in response to salt stress are still largely unknown. In this study, we examined the salt-induced transcriptional responses of ThHSFA1-ThWRKY4 in Tamarix hispida and their functions and regulatory mechanisms in salt tolerance. ThHSFA1 protein acts as an upstream regulator that can directly activate ThWRKY4 expression by binding to the heat shock element (HSE) of the ThWRKY4 promoter using yeast one-hybrid (Y1H), chromatin immunoprecipitation (ChIP), and dual-luciferase reporter assays. ThHSFA1 and ThWRKY4 expression was significantly induced by salt stress and abscisic acid (ABA) treatment in the roots and leaves of T. hispida. ThHSFA1 is a nuclear-localized protein with transactivation activity at the C-terminus. Compared to nontransgenic plants, transgenic plants overexpressing ThHSFA1 displayed enhanced salt tolerance and exhibited reduced reactive oxygen species (ROS) levels and increased antioxidant enzyme activity levels under salt stress. Therefore, we further concluded that ThHSFA1 mediated the regulation of ThWRKY4 in response to salt stress in T. hispida.

Highlights

  • Salinity and secondary soil salinization have become serious ecological environmental problems worldwide, affecting plant growth and production by causing osmotic imbalance, mineral deficiency, and overall toxicity [1]

  • Similar to many other transcription factors (TFs), Heat shock transcription factors (HSFs) contain a conserved N-terminal DNA-binding domain (DBD), which can bind to cis-acting heat shock element (HSE) recognition sequences in their target gene promoters [14]

  • We found that the positive yeast clone harboring an HSF gene grew better than the other yeast clones

Read more

Summary

Introduction

Salinity and secondary soil salinization have become serious ecological environmental problems worldwide, affecting plant growth and production by causing osmotic imbalance, mineral deficiency, and overall toxicity [1]. The salt and drought tolerance of AtHsfA6a-overexpressing plants is enhanced via the abscisic acid (ABA) signaling pathway, and these plants exhibit increased expression of downstream stress-responsive genes [10]. In addition to the roles of these HSFs in herbaceous plants, Populus euphratica PeHSF overexpression in tobacco maintains leaf ROS homeostasis and enhances antioxidant enzyme activity levels under salt stress conditions [4]. Transgenic plants overexpressing cotton GhWRKY6-like gene or sweet potato IbWRKY2 display enhanced salt tolerance by regulating the ABA signaling pathway and ROS scavenging [30,32]. The expression of FtWRKY46 from buckwheat, DgWRKY4 and DgWRKY5 from chrysanthemum, and GarWRKY5 from cotton in transgenic plants was shown to confer enhanced tolerance to salt stress by modulating ROS clearance, antioxidant enzyme activity, and stress-related gene expression [6,33,34,35]. ThHSFA1 and ThWRKY4 are involved in the same physiological and molecular regulatory pathways of the salt stress response

Identification of ThHSFA1 as an Upstream Regulator of ThWRKY4
ThHSFA1
ThHSFA1 Binds the ThWRKY4 Promoter and Activates the Expression of ThWRKY4
ThHSFA1 Enhances Tolerance to Salt Stress
ThHSFA1 Confers Salinity Tolerance by Regulating ROS Homeostasis
Plant Materials and Stress Treatments
RNA Extraction and RT-qPCR Analysis
Y1H Assay
ChIP Assay
Dual-Luciferase Reporter Assay
Bioinformatics Analysis of ThHSFA1
Subcellular Localization and Transcriptional Activation Analysis of ThHSFA1
Generation of Transgenic Plants
Salt Stress Tolerance Assay
4.10. Histochemical Staining and Physiological Trait Measurements
Conclusions
Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.