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Elucidating the downstream pathways triggered by H2S signaling in Arabidopsis thaliana under drought stress via transcriptome analysis
Hydrogen sulfide (H 2 S) is a crucial signaling molecule in plants. Recent studies have shown that H 2 S plays an equally important role as nitric oxide (NO) and hydrogen peroxide (H 2 O 2 ) in plant signaling. Previous studies have demonstrated the involvement of H 2 S in regulating drought and oth...
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Published in: | Plant signaling & behavior 2024-12, Vol.19 (1), p.2411911 |
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Main Authors: | , , , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Online Access: | Get full text |
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Summary: | Hydrogen sulfide (H
2
S) is a crucial signaling molecule in plants. Recent studies have shown that H
2
S plays an equally important role as nitric oxide (NO) and hydrogen peroxide (H
2
O
2
) in plant signaling. Previous studies have demonstrated the involvement of H
2
S in regulating drought and other stressful environmental conditions, but the exact downstream molecular mechanisms activated by the H
2
S signaling molecule remain unclear. In this study, we conducted a comprehensive genome-wide transcriptomic analysis of both wild type (WT) and double mutant (lcd/des1). Arabidopsis thaliana plants were exposed to 40% polyethylene glycol (PEG) to induce drought stress and 20 µM sodium hydrosulfide (NaHS). The resulting transcriptome data were analyzed for differentially significant genes and their statistical enrichments in the Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways. The results indicated significant upregulation of genes related to photosynthesis, carbon fixation, plant secondary metabolite biosynthesis, inositol and phosphatidylinositol signaling pathways, and stress-responsive pathways in mutant plants under drought stress. Mutant plants with impaired H
2
S signaling mechanisms displayed greater susceptibility to drought stress compared to wild-type plants. In summary, all findings highlight the pivotal role of H
2
S signaling in stimulating other drought-responsive signaling pathways. |
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ISSN: | 1559-2324 1559-2316 1559-2324 |
DOI: | 10.1080/15592324.2024.2411911 |