| Summary: | 碩士 === 國立高雄大學 === 生物科技研究所 === 101 === Heat stress belongs to abiotic stress that affects the growth and yield of plants. For chloroplast, photosystem II (PSII) is the most heat-sensitive site and the electron transport may be blocked and results in accumulation of reactive oxygen species (ROS) after heat stress. Several genes are also induced by heat stress, such as heat shock transcription factors (Hsfs), heat shock proteins (HSPs), ascorbate peroxidases (APXs) and glutathione-S- transferase (GST). Ferredoxin (Fd) is a group of electron transport proteins which involves in many metabolic processes. Study indicates AtFd1 in Arabidopsis is responsible for the cyclic electron flow, the electron transport which is suggested to act in stress. It’s indicated that replacement of Fd with a cyanobacterial flavodoxin in tobacco enhanced tolerance to stresses. However, function of AtFd1 in tolerance of heat stress is unclear. In order to reveal this issue, atfd1-transgenic Arabidopsis thaliana (ecotypes Col-0) were used to investigate heat tolerance and possible mechanism. For 40°C-treatment, the atfd1-expression pattern showed that atfd1 is a heat-inducible gene which may play an important role in heat response. Overexpression of atfd1 enhanced the heat tolerance in transgenic Arabidopsis under 10 h of 45°C- treatment. The H2O2 and malondialdehyde (MDA) content after heat treatment indicated that WT exhibited more severe damage than transgenic lines. Additionally, after 8 d-treatment in 38°C, the Fv/Fm and electron transport rate (ETR) shown no significant difference between WT and transgenic lines, while the Fo of WT was higher than those of transgenic lines, indicating the heat damage in WT was more severe than transgenic lines. The expression of stress-related genes (apx2, hsfA2, hsp101) in WT were higher than those in transgenic lines after 45°C heat treatment, whereas the expression of apx1 and gst had the opposite result. Furthermore, soluble sugar accumulation was observed after 5 d-heat treatment, and the glucose data showed that heat treatment induced more severe threat to WT. In this study, we demonstrated overexpression of AtFd1 confers heat tolerance through regulating ROS content and expression of hsfA2 and its target genes in heat response.
|
|---|
