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Transcriptomic analysis revealed the regulatory mechanisms of rice leaves in response to short-term Pb stress
Xin-Nan Wang1, Yue-Ying Li1, Lian-Ju Ma1
1College of Life Science, Shenyang Normal University, Shenyang 110034, China.
Abstract:
Lead (Pb) is a widely ubiquitous and highly toxic heavy metal pollutant that severely inhibits crop growth. However, the molecular regulatory mechanisms of Pb toxicity in plants remain incompletely understood. We investigated growth indices, chlorophyll content, and chlorophyll fluorescence parameters in rice leaves after 1 day of treatment with 100 μM Pb(NO₃)₂ stress, and performed transcriptomics analysis using RNA sequencing (RNA-seq) technology. The results indicated that Pb stress significantly reduced growth parameters, SPAD values, maximum photochemical efficiency (Fᵥ/Fₘ), and performance index (PIABS) in rice seedlings, as well as the electron transport efficiency of Photosystem II (PSII), as reflected by decreased φE₀ and ψ₀. In contrast, it markedly increased energy absorption per reaction center (ABS/RC), non-photochemical energy dissipation (DI₀/RC), and the quantum yield of dissipation (φD₀). Through RNA-seq analysis, 1721 differentially expressed genes (DEGs) were identified. Gene Ontology (GO) enrichment analysis showed that the most significantly enriched upregulated DEGs were oxidation-reduction processes. Gene set enrichment analysis (GSEA) and Kyoto Encyclopedia of Genes and Genomes (KEGG) joint analysis identified 8 common pathways, such as cysteine and methionine metabolism, brassinosteroid biosynthesis, and photosynthesis. All DEGs in cysteine and methionine metabolism were upregulated. Additionally, Pb stress upregulated genes encoding heat shock transcription factors and heat shock proteins, whereas genes encoding MYB and WRKY were downregulated. This study systematically revealed the transcriptome response mechanisms of rice leaves under short-term Pb stress, providing crucial data support and theoretical foundations for deepening the understanding of rice response mechanisms to heavy metal stress.
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