Ectopic over-expression of HaFT-1, a 14-3-3 Protein from Haloxylon ammodendron, leads to enhanced acquired thermotolerance of transgenic Arabidopsis

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Abstract

Abstract Haloxylon ammodendron, an important shrub for desert afforestation, can adapt to harsh ecological environments such as drought, saline and extreme high temperature. Therefore, the study of H. ammodendron stress adaptation mechanism is of great practical significance for ecological improvement in desert areas. Previously, a heat stress (HS) responsive H. ammodendron 14-3-3 protein gene HaFT-1 with HS memory characteristics found in transcriptome was cloned and its transgenic Arabidopsis lines were obtained. In this study, its role in HS tolerance was further investigated. qRT-PCR analysis showed that HS priming enhanced the expression of HaFT-1 under the second HS and subsequent recovery treatment, indicating expression of HaFT-1 had transcriptional memory to HS. Subcellular localization showed that YFP-HaFT-1 fusion protein located in the cytoplasm of protoplasts. The survival rates of HaFT-1 overexpression seedlings were higher than that of WT after priming-and-triggering and non-primed control treatments. Cell death staining showed that cell death in HaFT-1 overexpression lines was more significantly inhibited than that in WT seedlings when treated with HS. Transcriptome analysis showed that energy generation, protein metabolism, signal transduction, biosynthesis, proline metabolism, autophagy, chlorophyll metabolism, and peroxisome were related to resistance of HaFT-1 transgenic plants to the second HS. Growth physiology analysis showed that priming-and-triggering treatment in HaFT-1 overexpression Arabidopsis promoted regulation on proline content and strengthened reactive oxygen species (ROS) scavenging activity. These results demonstrated that overexpression of HaFT-1 strengthened not only HS priming but also tolerance to the second HS of transgenic Arabidopsis, suggesting HaFT-1 as a positive regulator in acquired thermotolerance.

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last seen: 2026-05-19T01:45:01.086888+00:00