Abstract
Ph.D.
In plants, salicylic acid (SA) is a signaling molecule that regulates disease resistance responses such as systemic acquired resistance (SAR) and the hypersensitive response (HR), and has been implicated in both basal and acquired thermotolerance. It has also been shown that SA enhances heat-induced Hsp/Hsc70 accumulation in plants. In this study, temperature studies revealed that heat shock (HS) at 40 °C for 30 min significantly induced Hsp/Hsc70 accumulation in 3-week old tomato (UC82B) seedlings. Time- and dose-responsive studies showed that 0.1 mM SA for 17 hrs was unable to induce Hsp/Hsc70 but in combination with HS significantly (P > 0.001) potentiated this response. To investigate the mechanism of SA-mediated, heat-induced Hsp/Hsc70 potentiation, tomato seedlings were treated with either SA alone, HS or both, before analyses of hsp70 mRNA, Hsf DNA-binding and gene expression of hsp70, hsfAl, hsfA2 and hsfEll. SA alone established Hsf DNA-binding, but was not accompanied by increased Hsp70 accumulation or expression of hsp70 mRNA. SA had no significant effect on hsfA2 and hsf81 gene expression, but increased the basal levels of hsfAl. In heat-shocked plants, Hsf DNA-binding was enhanced, and increased hsfAl, hsfA2 and hsfB1 expression preceded accumulation of Hsp70. The combined treatment of SA and HS resulted in potentiated Hsf DNA-binding, enhanced expression of hsp70, hsfAl, hsfA2 and hsfB1, leading to potentiated levels of Hsp/Hsc70. Since increased hsp70 and hsf gene expression coincided with increased levels of Hsp70 accumulation, it is likely that the SA-mediated potentiation of Hsp70 is due to the ability of SA to regulate Hsfs during HS. This study therefore proposes a mechanism for the potentiation of Hsp70 by SA in the presence of heat, which might contribute to our understanding of the role SA plays in the heat shock response and thermotolerance.