| Summary: | 碩士 === 國立臺灣大學 === 植物科學研究所 === 102 === The heat stress (HS) response (HSR) is a conserved mechanism developed to increase the expression of heat shock proteins (HSPs) via a heat shock factor (HSF)-dependent mechanism. As well, signaling by the stress phytohormone abscisic acid (ABA) is involved in acquired thermotolerance. Analysis of Arabidopsis (Arabidopsis thaliana) microarray databases revealed that the expression of HSFA6b, a class-A HSF, was increased with salinity, osmotic and cold but not HS. Here, we show that HSFA6b plays a pivotal role in the response to ABA and in thermotolerance in Arabidopsis. Intriguingly, in previous studies showed salt-inducible HSFA6b expression was downregulated in ABA-insensitive and -deficient mutants, and exogenous ABA application restored its expression in ABA-deficient plants, so the ABA signal is required for proper HSFA6b expression. Consequently, transcriptional activation assay of protoplasts showed that ABA treatment and coexpression of an ABA-signaling master effector, ABRE-binding protein 1 (AREB1), could activate the HSFA6b promoter. In addition, DREB2A, HSP18.2 and APX2 were regulated by heat shock factor A6b that enhanced their expression. Analysis of ABA responses in drought and salt tolerance in HSFA6b-null, -overexpression and -dominant–negative mutants indicated that HSFA6b is a positive regulator participating in ABA-mediated salt and drought resistance. Thermoprotection tests showed that HSFA6b was required for thermotolerance acquisition. Our study reveals a network in which HSFA6b operates as a downstream regulator of the ABA-mediated stress response and is required for HS resistance. This new ABA-signaling pathway is integrated into the complex HSR network in planta.
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