Abstract
Heat shock transcriptional factor A2 (HsfA2) plays an important role in oxidative stress tolerance by expression various defence-related genes (Plant J. 2006). Recently we have reported that a heat shock element clusters (HSE I and II, III) in the 5'-flanking region of the HsfA2 gene is involved in high light (HL)-inducible HsfA2 expression. Furthermore, we revealed that HsfA1d, HsfA1e and HsfA4c regulate the induction of HsfA2 in response to HL stress. To further investigate the mode of regulation of HsfA2 expression by class A Hsfs. we generated the double knockout mutants (KO-HsfA1d/A1e, KO-HsfA1d/A4c and KO-HsfA1e/A4c) and examined the effect of these Hsfs on HsfA2 induction in response to HL. Transcript levels of HsfA2 were significantly reduced in the three Hsfs double mutants. The transient reporter assay using effector plasmids for HsfA1d or HsfA1e and reporter plasmids with HSE mutation of HsfA2 promoter revealed that HSE I is the most important in the induction of HsfA2 expression by HsfA1d or HsfA1e. We are investigating interaction of HsfA1d, HsfA1e and HsfA4c with HSE by electrophoretic mobility shift assay.
