| Abstrak/Abstract |
Heat shock transcription factors (HSFs) regulate the responses of plants to heat stress, but their functions in heat-shock induced resistance (HSIR) are poorly understood. Here, we investigated the functions of HSFs in the resistance induced by a heat shock treatment (HST; 50 °C for 20 s) against gray mold (Botrytis cinerea) in Cucumis sativus by measuring lesion area using image processing and quantitative gene expression analysis. The HST reduced the percentage of lesion area, consistent with the upregulation of peroxidase (POX) and pathogenesis-related (PR) 1.C1 genes at 24 and 48 h after treatment, respectively. Both genes were detected after the upregulation of the heat shock transcription factor A2 (HSFA2) and B2 (HSFB2 genes. Heat shock element (HSE) motifs were found upstream of POX, PR1.C1, POX73, and POX43, and they were upregulated at 24 h after the HST. A heat shock protein 90 (HSP90) inhibitor, geldanamycin (GDA), maintained the upregulation of the HSE-containing PR, thereby reducing gray mold lesions. The GDA treatment enhanced local resistance, whereas the HST induced systemic resistance. The combination of heat shock and GDA treatments induced HSE-containing PR expression and enhanced plant resistance against B. cinerea. The HSIR mechanism involves a pathway related to systemic acquired resistance (SAR). It also involves an HSF-mediated pathway that is associated with local resistance and concealed by the SAR. This study provides novel insights into the molecular mechanisms of HSIR and an alternative approach to activate defense responses against pathogens in cucumber plants. |
