101. Possible role of autophagy in microbial volatile pollutant-induced starch degradation and expression of hypoxia responsive genes.
- Author
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Huang CC, Chang CH, Thi Truong TT, Wang WG, Lin CH, Chiang CY, Obayashi I, and Huang HJ
- Subjects
- Volatile Organic Compounds metabolism, Gene Expression Regulation, Plant drug effects, Air Pollutants toxicity, Hypoxia metabolism, Autophagy drug effects, Starch metabolism, Arabidopsis genetics, Arabidopsis metabolism
- Abstract
Autophagy is thought to be critically involved in the regulation of nutrient metabolism and gene expression. Nevertheless, little is known about its role in regulating starch metabolism and hypoxia responsive genes in plants exposed to microbial volatile pollutants. In the present study, we found that exposure of Arabidopsis to Enterobacter aerogene (E. aerogene) volatile pollutants induced autophagy, as indicated by autophagosome formation. The exposure also caused upregulation of autophagy-associated genes, such as ATGs, NBR1, ATI1, and ATG8e-regulating transcription factors. Additionally, exposure to E. aerogenes volatile pollutants induced starch degradation in the roots of Arabidopsis seedlings. Finally, we found that ATG7-deficiency negatively affected the expression of hypoxia-responsive genes (i.e HRE1, HRA1, and ADH1) and starch degradation induced by E. aerogenes volatile pollutants. Overall, our study reveals that microbial volatile pollutants can induce starch degradation and autophagy, which participates in the regulation of some hypoxia-responsive genes and starch metabolism. These findings help to define the role of autophagy in plant nutrient metabolism and regulation of gene expression under microbial volatile pollutant exposure. The insights gained may contribute to agricultural management when living organisms face challenges from microbial volatile pollutants., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2025 Elsevier Ltd. All rights reserved.)
- Published
- 2025
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