Abstract
Heat shock transcription factor A2 (HsfA2) plays an important role in regulating induction of defenses against different types of oxidative stress (Plant J. 2006). Here, we identified a cis-element and regulatory factor involved in the induction of HsfA2 expression in response to oxidative stress. The transient reporter assay using luciferase reporter constructs with different fragments of HsfA2 promoter showed that the deletion of the sequence from -191 bp to -108 bp markedly reduced the luciferase activity under high-light. This promoter region contained HSE elements, suggesting that some Hsfs mediate the induction of HsfA2 expression. Next, to identify the Hsfs regulating the expression of HsfA2, we took advantage of the chimeric repressor silencing technology (CRES-T). We found that ectopic expression of the chimeric HsfA1d or HsfA1e repressor significantly suppressed the induction of HsfA2 expression in response to high-light. We are currently investigating that transcriptionally regulation of HsfA2 via HSE by HsfA1d/A1e and the effect of loss-of-function and overexpression of HsfA1d and/or HsfA1e on the phenotype in Arabidopsis under oxidative stress.
