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JXB Advance Access published online on August 14, 2006
Journal of Experimental Botany, doi:10.1093/jxb/erl098
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© 2006 The Author(s). This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.0/uk/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
Received May 16, 2006
Accepted June 27, 2006

RESEARCH PAPER

Novel interrelationship between salicylic acid, abscisic acid, and PIP2-specific phospholipase C in heat acclimation-induced thermotolerance in pea leaves

Hong-Tao Liu 1, Yan-Yan Liu 1, Qiu-Hong Pan 1, Hao-Ru Yang 1, Ji-Cheng Zhan 1, and Wei-Dong Huang 1 *

1 College of Food Science and Nutritional Engineering, China Agricultural University, Beijing 100083, China

* To whom correspondence should be addressed.
Wei-Dong Huang, E-mail: huanggwd{at}263.net


  Abstract

Increasing evidence suggests that heat acclimation and exogenous salicylic acid (SA) and abscisic acid (ABA) may lead to the enhancement of thermotolerance in plants. In this study, the roles that free SA, conjugated SA, ABA, and phosphatidylinositol-4,5-bisphosphate (PIP2)-specific phospholipase C (PLC) play in thermotolerance development induced by heat acclimation (38 °C) were investigated. To evaluate their potential functions, three inhibitors of synthesis or activity were infiltrated into pea leaves prior to heat acclimation treatment. The results showed that the burst of free SA in response to heat acclimation could be attributed to the conversion of SA 2-O-D-glucose, the main conjugated form of SA, to free SA. Inhibition of ABA biosynthesis also resulted in a defect in the free SA peak during heat acclimation. In acquired thermotolerance assessment, the greatest weakness of antioxidant enzyme activity and the most severe heat injury (malondialdehyde content and degree of wilting) were found in pea leaves pre-treated with neomycin, a well-known inhibitor of PIP2-PLC activity. PsPLC gene expression was activated by exogenous ABA, SA treatments, and heat acclimation after pre-treatments with a SA biosynthesis inhibitor. From these results, PIP2-PLC appears to play a key role in free SA- and ABA-associated reinforcement of thermotolerance resulting from heat acclimation.

Keywords: ABA; abscisic acid; heat acclimation; pea; PIP2-PLC; SA; salicylic acid; thermotolerance.
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