Transcriptional repression of MaRBOHs by MaHsf26 is associated with heat shock-alleviated chilling injury in banana fruit

Both heat shock factors (Hsfs) and reactive oxygen species (ROS) are widely perceived to be involved in chilling stress response. However, the particular mechanism of Hsfs mediated-ROS metabolism related to chilling stress remains largely unknown, especially during chilling injury development of postharvest economically cold-sensitive fruit such as banana. In this study, we found that heat shock treatment (HST) could effectively alleviate postharvest banana chilling injury and reduce ROS accumulation during storage. The expression levels of several respiratory burst oxidase homolog (RBOH) genes, encoding ROS-producing enzymes, increased consistently with the progression, whereas were inhibited upon HST. Significantly, we identified an Hsfs MaHsf26, which exhibited a opposite expression pattern as that of MaRBOHs, as the putative binding protein of MaRBOHB-like1, MaRBOHE-like and MaRBOHF-like promoters using yeast one-hybrid (Y1H) screening analysis. Further electrophoretic mobility shift assay (EMSA) and dual luciferase reporter (DLR) analysis displayed MaHsf26 suppressed the transcriptions of MaRBOHB-like1, MaRBOHE-like and MaRBOHF-like through binding to the heat shock elements (HSE) in their promoters, respectively. In general, our results suggested that MaHsf26 plays as a transcriptional repressor of ROS generation by suppressing the transcriptions of MaRBOHs and thereby involving in the HST-mitigated chilling injury in postharvest banana fruit.