Autophagy confers aluminum tolerance by enhancing the antioxidant capacity and promoting oxidized protein degradation in wheat (Triticum aestivum.) roots

Abstract

Aluminum (Al) usually disturbs redox homeostasis and causes irreversible oxidative damage to biomolecules in plants, efficiently removing damaged and toxic macromolecules is essential to Al tolerance. Here, we investigated the role of autophagy, a conserved cellular degradation pathway, in plant Al tolerance using two wheat genotypes with different Al sensitivity. Compared to the sensitive genotype, Al significantly upregulated the expression of autophagy-related genes (ATGs) and enhanced the formation of autophagosomes. Reinforcing autophagy by rapamycin substantially alleviated the inhibition of root growth by Al stress, accompanied by low levels of reactive oxygen species (ROS) accumulation and oxidative damage in wheat roots; whereas inhibition of autophagy by 3-methyladenine (3-MA) aggravated the adverse impacts of Al toxicity. Further experiments showed that Al significantly triggered the accumulation of oxidized proteins, particularly in the sensitive genotype. The content of Al-induced oxidized proteins was reduced by rapamycin but further increased by 3-MA in wheat roots. Wheat plants treated with the inhibitor of vacuole H+-ATPase, concanamycin A, were more sensitive to Al stress and accumulated higher levels of oxidatively-damaged proteins compared to Al treatment. These results reveal that autophagy-mediated redox homeostasis and the clearance of oxidatively damaged proteins play a crucial role in plant's tolerance to Al stress.