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First published online November 3, 2006; 10.1104/pp.106.091322

Plant Physiology 143:251-262 (2007)
© 2007 American Society of Plant Biologists

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ENVIRONMENTAL STRESS AND ADAPTATION TO STRESS

A Heat-Inducible Transcription Factor, HsfA2, Is Required for Extension of Acquired Thermotolerance in Arabidopsis1,[W],[OA]

Yee-yung Charng*, Hsiang-chin Liu2, Nai-yu Liu2, Wen-tzu Chi2, Chun-neng Wang, Shih-hsun Chang and Tsu-tsuen Wang

Agricultural Biotechnology Research Center, Academia Sinica, Taipei 11529, Taiwan, ROC (Y.-y.C., H.-c.L., N.-y.L., W.-t.C., C.-n.W., S.-h.C.); and Department of Horticulture, National Taiwan University, Taipei 10617, Taiwan, ROC (S.-h.C., T.-t.W.)

The expression of heat shock proteins (Hsps) induced by nonlethal heat treatment confers acquired thermotolerance (AT) to organisms against subsequent challenges of otherwise lethal temperature. After the stress signal is removed, AT gradually decays, with decreased Hsps during recovery. AT of sufficient duration is critical for sessile organisms such as plants to survive repeated heat stress in their environment, but little is known regarding its regulation. To identify potential regulatory components, we took a reverse genetics approach by screening for Arabidopsis (Arabidopsis thaliana) T-DNA insertion mutants that show decreased thermotolerance after a long recovery (2 d) under nonstress conditions following an acclimation heat treatment. Among the tested mutants corresponding to 48 heat-induced genes, only the heat shock transcription factor HsfA2 knockout mutant showed an obvious phenotype. Following pretreatment at 37°C, the mutant line was more sensitive to severe heat stress than the wild type after long but not short recovery periods, and this could be complemented by the introduction of a wild-type copy of the HsfA2 gene. Quantitative hypocotyl elongation assay also revealed that AT decayed faster in the absence of HsfA2. Significant reduction in the transcript levels of several highly heat-inducible genes was observed in HsfA2 knockout plants after 4 h recovery or 2 h prolonged heat stress. Immunoblot analysis showed that Hsa32 and class I small Hsp were less abundant in the mutant than in the wild type after long recovery. Our results suggest that HsfA2 as a heat-inducible transactivator sustains the expression of Hsp genes and extends the duration of AT in Arabidopsis.


1 This work was supported by the National Science Council (grant nos. 91–3112–P–001–036–Y and 94–2311–B–001–058) and by Academia Sinica, Taiwan, ROC.

2 These authors contributed equally to the paper.

The author responsible for distribution of materials integral to the findings presented in this article in accordance with the policy described in the Instructions for Authors (www.plantphysiol.org) is: Yee-yung Charng (yycharng{at}gate.sinica.edu.tw).

[W] The online version of this article contains Web-only data.

[OA] Open Access articles can be viewed online without a subscription.

www.plantphysiol.org/cgi/doi/10.1104/pp.106.091322

* Corresponding author; e-mail yycharng{at}gate.sinica.edu.tw; fax 886–2–2651–5600.

Received October 13, 2006; accepted October 28, 2006; published November 3, 2006.




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