Cadmium (Cd), as a widely investigated heavy metal, demonstrates severe toxicity to plant growth and development. However, the roles of energy metabolism, and protein degradation caused by autophagy in plant Cd tolerance remain poorly characterized. This study reveals that Cd-exposure simultaneously affects both the glycolytic and autophagic in Arabidopsis thaliana. Cd-exposure enhances autophagy by upregulating the mRNA and protein level of AtATG7 and finally promotes the autophagy-induced energy burst. Another hand, Cd-exposure induces the accumulation of AtGAPDH and AtENO2, further boosting energy production during glycolysis. Through treatments with the autophagic modulators rapamycin and 3-methyladenine, and the autophagy-deficient mutant Atatg7, it was found that Cd-exposure establishes a link between autophagy and glycolysis through the autophagic degradation of AtHK2. Furthermore, using non-invasive micro-test technology, both the autophagic degradation of AtHK2 and the enhancement of glycolysis significantly promote Cd²⁺ efflux in Arabidopsis. Finally, the changes of ATP level demonstrate that the synergistic mediation of autophagy and glycolysis provides sufficient energy for the efflux of Cd2 + under Cd-exposure. These findings elucidate the molecular mechanisms underlying Cd tolerance in Arabidopsis through synergistic regulation of autophagy and glycolysis pathways, and offer crucial theoretical foundations and novel perspectives for developing plant-based remediation strategies for Cd-contaminated soils.
Autophagy and glycolysis synergistically mediate Cd²⁺ transport to enhance Cd tolerance in Arabidopsis.
Hanchen Tang,Shoujian Zang,Xing-Yue Hong,Ruiyuan Jiang,Hezi Huang,Shengwei Hu,Mengqi Wu,Qinghua Li,Jicheng Wang,Ling Sun,Yupeng Zhang,Dekai Chen,Hailei Zheng
Published 2025 in Journal of Hazardous Materials
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- Publication year
2025
- Venue
Journal of Hazardous Materials
- Publication date
2025-08-23
- Fields of study
Biology, Medicine, Environmental Science
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- Source metadata
Semantic Scholar, PubMed
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