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Research Project: Nutritional Role of Phytochemicals

Location: Children's Nutrition Research Center

Title: Crucial role of Arabidopsis glutaredoxin S17 in heat stress response revealed by transcriptome analysis

Author
item RAO, XIAOLAN - Hubei University
item CHENG, NINGHUI - Children'S Nutrition Research Center (CNRC)
item MATHEW, INY - Children'S Nutrition Research Center (CNRC)
item HIRSCHI, KENDAL - Children'S Nutrition Research Center (CNRC)
item Nakata, Paul

Submitted to: Functional Plant Biology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 8/21/2022
Publication Date: 9/14/2022
Citation: Rao, X., Cheng, N., Mathew, I.E., Hirschi, K.D., Nakata, P.A. 2022. Crucial role of Arabidopsis glutaredoxin S17 in heat stress response revealed by transcriptome analysis. Functional Plant Biology. 50(1):58-70. https://doi.org/10.1071/FP22002.
DOI: https://doi.org/10.1071/FP22002

Interpretive Summary: Heat stress is a major environmental condition that negatively affects agricultural production each year. Thus, making plants more tolerant to heat would help reduce crop loss. Before we can design rational strategies to combat heat stress we must first gain a better understanding of how the plant senses temperature, transmits this information, and responds to the increase in temperature. Previously we reported a mutant plant that no longer expressed a specific glutathione reductase. This mutant plant was less tolerant to heat stress. As a step toward understanding the importance of this gene in heat stress we measured what genes increased in expression and which genes decreased in expression during heat stress in both wild type and mutant plants. We were able to identify several genes that had reduced expression in the mutant plant during heat stress. These genes included those encoding heat stress factors, auxin response proteins, and plant signaling proteins. Of special note were a family of receptor-like kinase genes that are involved in cellular communication and abiotic stress signaling pathways. It is possible that these receptor-like kinase genes serve as a key component of the plants heat stress response signaling pathway.

Technical Abstract: Climate change and the associated abiotic stresses can have detrimental effects on plant growth and development. Heat stress (HS), for example, results in an accumulation of reactive oxygen species (ROS) leading to oxidative damage within the cells of plants. As a result, plants have evolved complex regulatory networks to dampen the damaging effects caused by fluctuations in temperature. However, the mechanisms by which the plant is able to perceive changes in ambient temperature, transmit this information, and initiate a temperature-induced response are not fully understood. Previously, we showed that heterologous expression of an Arabidopsis thaliana monothiol glutaredoxin AtGRXS17 enhanced thermotolerance in various crops, while disruption of AtGRXS17 expression caused hypersensitivity to permissive temperature. In this study, we extend our investigation into the effect of AtGRXS17 and HS on plant growth and development. Although atgrxs17 plants were found to exhibit a slight decrease in hypocotyl elongation, shoot meristem development, and root growth compared to wild type when grown at 22 degree C, these growth phenotypic differences became more pronounced when growth temperatures were raised to 28 degree C. Transcriptome analysis revealed significant changes in genome-wide gene expression in atgrxs17 plants compared to wild type under conditions of heat stress. The expression of genes related to heat stress factors, auxin response, cellular communication, and abiotic stress were altered in atgrxs17 mutant plants in response to heat stress. Interestingly, a family of receptor-like kinase (RLK) involved in cellular communication and abiotic stress signaling pathways were found to be down-regulated in Atsgrxs17 compared to wild type when grown at 28 degree C. This finding raises the possibility that these RLKs might serve as a key link between ROS and extra- and intra-cellular signaling pathways in response to HS.