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ZmNF-YA1 Contributes to Maize Thermotolerance by Regulating Heat Shock Response. | LitMetric

ZmNF-YA1 Contributes to Maize Thermotolerance by Regulating Heat Shock Response.

Int J Mol Sci

Key Laboratory of Plant Development and Environment Adaptation Biology, Ministry of Education, School of Life Sciences, Shandong University, Qingdao 266237, China.

Published: June 2024


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Article Abstract

(maize) is a staple food, feed, and industrial crop. Heat stress is one of the major stresses affecting maize production and is usually accompanied by other stresses, such as drought. Our previous study identified a heterotrimer complex, ZmNF-YA1-YB16-YC17, in maize. ZmNF-YA1 and ZmNF-YB16 were positive regulators of the drought stress response and were involved in maize root development. In this study, we investigated whether ZmNF-YA1 confers heat stress tolerance in maize. The mutant and overexpression lines were used to test the role of ZmNF-YA1 in maize thermotolerance. The mutant was more temperature-sensitive than the wild-type (WT), while the overexpression lines showed a thermotolerant phenotype. Higher malondialdehyde (MDA) content and reactive oxygen species (ROS) accumulation were observed in the mutant, followed by WT and overexpression lines after heat stress treatment, while an opposite trend was observed for chlorophyll content. RNA-seq was used to analyze transcriptome changes in and its wild-type control W22 in response to heat stress. Based on their expression profiles, the heat stress response-related differentially expressed genes (DEGs) in compared to WT were grouped into seven clusters via -means clustering. Gene Ontology (GO) enrichment analysis of the DEGs in different clades was performed to elucidate the roles of ZmNF-YA1-mediated transcriptional regulation and their contribution to maize thermotolerance. The loss function of led to the failure induction of DEGs in GO terms of protein refolding, protein stabilization, and GO terms for various stress responses. Thus, the contribution of ZmNF-YA1 to protein stabilization, refolding, and regulation of abscisic acid (ABA), ROS, and heat/temperature signaling may be the major reason why overexpression enhanced heat tolerance, and the mutant showed a heat-sensitive phenotype.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11173165PMC
http://dx.doi.org/10.3390/ijms25116275DOI Listing

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