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Transcriptome and physiological analyses for revealing genes involved in wheat response to endoplasmic reticulum stress.

ABSTRACT: BACKGROUND:Wheat production is largely restricted by adverse environmental stresses. Under many undesirable conditions, endoplasmic reticulum (ER) stress can be induced. However, the physiological and molecular responses of wheat to ER stress remain poorly understood. We used dithiothreitol (DTT) and tauroursodeoxycholic acid (TUDCA) to induce or suppress ER stress in wheat cells, respectively, with the aim to reveal the molecular background of ER stress responses using a combined approach of transcriptional profiling and morpho-physiological characterization. METHODS:To understand the mechanism of wheat response to ER stress, three wheat cultivars were used in our pre-experiments. Among them, the cultivar with a moderate stress tolerance, Yunong211 was used in the following experiments. We used DTT (7.5?mM) to induce ER stress and TUDCA (25??g·mL-?1) to suppress the stress. Under three treatment groups (Control, DTT and DTT?+?TUDCA), we firstly monitored the morphological, physiological and cytological changes of wheat seedlings. Then we collected leaf samples from each group for RNA extraction, library construction and RNA sequencing on an Illumina Hiseq platform. The sequencing data was then validated by qRT-PCR. RESULTS:Morpho-physiological results showed DTT significantly reduced plant height and biomass, decreased contents of chlorophyll and water, increased electrolyte leakage rate and antioxidant enzymes activity, and accelerated the cell death ratio, whereas these changes were all remarkably alleviated after TUDCA co-treatment. Therefore, RNA sequencing was performed to determine the genes involved in regulating wheat response to stress. Transcriptomic analysis revealed that 8204 genes were differentially expressed in three treatment groups. Among these genes, 158 photosynthesis-related genes, 42 antioxidant enzyme genes, 318 plant hormone-related genes and 457 transcription factors (TFs) may play vital roles in regulating wheat response to ER stress. Based on the comprehensive analysis, we propose a hypothetical model to elucidate possible mechanisms of how plants adapt to environmental stresses. CONCLUSIONS:We identified several important genes that may play vital roles in wheat responding to ER stress. This work should lay the foundations of future studies in plant response to environmental stresses.

SUBMITTER: Yu X

PROVIDER: S-EPMC6509841 | biostudies-literature | 2019 May

REPOSITORIES: biostudies-literature

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Transcriptome and physiological analyses for revealing genes involved in wheat response to endoplasmic reticulum stress.

Yu Xing X Wang Tanchun T Zhu Meichen M Zhang Liting L Zhang Fengzhi F Jing Enen E Ren Yongzhe Y Wang Zhiqiang Z Xin Zeyu Z Lin Tongbao T

BMC plant biology 20190509 1

<h4>Background</h4>Wheat production is largely restricted by adverse environmental stresses. Under many undesirable conditions, endoplasmic reticulum (ER) stress can be induced. However, the physiological and molecular responses of wheat to ER stress remain poorly understood. We used dithiothreitol (DTT) and tauroursodeoxycholic acid (TUDCA) to induce or suppress ER stress in wheat cells, respectively, with the aim to reveal the molecular background of ER stress responses using a combined approa ...[more]

PMID: 31072347

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Project description:Zinc oxide nanoparticles (Nano-ZnO) are widely used in sunscreens, clothes, medicine and electronic devices. However, the potential risks of human exposure and the potential for adverse health impacts are not well understood. Previous studies have demonstrated that exposure to Nano-ZnO caused liver damage and hepatocyte apoptosis through oxidative stress, but the molecular mechanisms that are involved in Nano-ZnO-induced hepatotoxicity are still unclear. Endoplasmic reticulum (ER) is sensitive to oxidative stress, and also plays a crucial role in oxidative stress-induced damage. Previous studies showed that ER stress was involved in many chemical-induced liver injuries. We hypothesized that exposure to Nano-ZnO caused oxidative stress and ER stress that were involved in Nano-ZnO-induced liver injury. To test our hypothesis, mice were gavaged with 200 mg/kg or 400 mg/kg of Nano-ZnO once a day for a period of 90 days, and blood and liver tissues were obtained for study. Our results showed that exposure to Nano-ZnO caused liver injury that was reflected by focal hepatocellular necrosis, congestive dilation of central veins, and significantly increased alanine transaminase (ALT) and aspartate transaminase (AST) levels. Exposure to Nano-ZnO also caused depletion of glutathione (GSH) in the liver tissues. In addition, our electron microscope results showed that ER swelling and ribosomal degranulation were observed in the liver tissues from mice treated with Nano-ZnO. The mRNA expression levels of ER stress-associated genes (grp78, grp94, pdi-3, xbp-1) were also up-regulated in Nano-ZnO-treated mice. Nano-ZnO caused increased phosphorylation of RNA-dependent protein kinase-like ER kinase (PERK) and eukaryotic initiation factor 2α (eIF2α). Finally, we found that exposure to Nano-ZnO caused increased ER stress-associated apoptotic protein levels, such as caspase-3, caspase-9, caspase-12, phosphorylation of JNK, and CHOP/GADD153, and up-regulation of pro-apoptotic genes (chop and bax). These results suggest that oxidative stress and ER stress-induced apoptosis are involved in Nano-ZnO-induced hepatotoxicity in mice.

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Transcriptome and physiological analyses for revealing genes involved in wheat response to endoplasmic reticulum stress.

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Transcriptome and physiological analyses for revealing genes involved in wheat response to endoplasmic reticulum stress.

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