Abstract
BackgroundAbscisic acid (ABA) plays an important role in plant abiotic stress responses, and ABA INSENSITIVE 4 (ABI4) is a pivotal transcription factor in the ABA signaling pathway. In Arabidopsis, ABI4 negatively regulates salt tolerance; however, the mechanism through which ABI4 regulates plant salt tolerance is poorly understood. Our previous study showed that ABI4 directly binds to the promoter of the VITAMIN C DEFECTIVE 2 (VTC2) gene, inhibiting the transcription of VTC2 and ascorbic acid (AsA) biosynthesis.ResultsIn the present study, we found that treatment with exogenous AsA could alleviate salt stress sensitivity of ABI4-overexpressing transgenic plants. The decreased AsA content and increased reactive oxygen species (ROS) levels in ABI4-overexpressing seedlings under salt treatment indicated that AsA-promoted ROS scavenging was related to ABI4-mediated salt tolerance. Gene expression analysis showed that ABI4 was induced at the early stage of salt stress, giving rise to reduced VTC2 expression. Accordingly, the abundance of the VTC2 protein decreased under the same salt stress conditions, and was absent in the ABI4 loss-of-function mutants, suggesting that the transcriptional inhibition of ABI4 on VTC2 resulted in the attenuation of VTC2 function. In addition, other encoding genes in the AsA biosynthesis and recycling pathways showed different responses to salt stress, demonstrating that AsA homeostasis is complicated under salinity stress.ConclusionsThis study elucidates the negative modulation of ABI4 in salt stress tolerance through the regulation of AsA biosynthesis and ROS accumulation in plants.
Highlights
Abscisic acid (ABA) plays an important role in plant abiotic stress responses, and ABA INSENSITIVE 4 (ABI4) is a pivotal transcription factor in the ABA signaling pathway
Ascorbic acid contributes to ABI4-regulated salt stress sensitivity Ascorbic acid has an important effect on the scavenging of the accumulated reactive oxygen species (ROS) under salt stress to enhance the tolerance of plants [6]
We previously showed that ABI4 inhibits ascorbic acid (AsA) biosynthesis [10], so we further analyzed the role of AsA in the ABI4-mediated response to salt stress by supplying exogenous AsA. 3-day-old seedlings of Col-0, two recessive knockout alleles of ABI4 and two ABI4-overexpressing lines with C-terminal truncated peptide lines (OEM1 and OEM5) [39] were transferred to 1/2 Murashige and (MS) medium containing 40 μmol AsA only or 100 mM NaCl supplied with or without AsA
Summary
Abscisic acid (ABA) plays an important role in plant abiotic stress responses, and ABA INSENSITIVE 4 (ABI4) is a pivotal transcription factor in the ABA signaling pathway. Our previous study showed that ABI4 directly binds to the promoter of the VITAMIN C DEFECTIVE 2 (VTC2) gene, inhibiting the transcription of VTC2 and ascorbic acid (AsA) biosynthesis. Ascorbic acid (AsA) plays an important role in plant growth and development [1, 2]. Salt stress limits plant growth and development, and plants have evolved a variety of adaptive mechanisms to deal with it. Many studies have reported that the exogenous supply of AsA can improve the resistance to salt stress in various plants such as corn, rice, and wheat [26,27,28], indicating that AsA has a positive role in salt tolerance in plants
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