Silencing of ATG2 and ATG7 promotes programmed cell death in wheat via inhibition of autophagy under salt stress

Salt stress, as an abiotic stress, limits crops production worldwide. Autophagy and programmed cell death (PCD) have been functionally linked to plant adaptation to abiotic stress. However, the relation of autophagy and PCD is still under debate and the mechanism behind remains not fully understood. In this study, salt-tolerant wheat cultivar Jimai22 was used as the experimental material, and 150 mM NaCl was added to the hydroponic culture to test the effect of salt treatment. The results showed that NaCl stress enhances autophagic activity and induced occurrence of PCD in roots and leaves of wheat seedlings. Then, the barley stripe mosaic virus-induced silencing (BSMV-VIGS) method was used to inhibit autophagy by silencing the expression of ATG2 or ATG7. The results showed that silencing of ATG2 or ATG7 significantly inhibited autophagy and impaired the tolerance of wheat to NaCl stress. Moreover, silencing of ATG2 or ATG7 disrupted the absorption of Na, Cl, K and Ca elements and led to subsequent disequilibrium of Na+, Cl-, K+ and Ca2+, induced generation of excess reactive oxygen species (ROS), decreased the antioxidant activity, damaged photosynthesis apparatus, increased the level of PCD and led to differential expression of the genes, two metacaspase genes, cysteine-rich receptor-like kinase (CRK) 10, and CRK26 in leaves of wheat seedlings under NaCl stress. The effect of the inhibitor 3-methyladenine (3-MA) on roots and leaves of wheat seedlings was in accordance with that of ATG2 and ATG7 silencing. Our results suggest that autophagy negatively regulates salt-induced PCD, or limits the scale of salt-induced PCD to avoid severe tissue death in wheat seedlings.

Automated summary

Salt stress enhances autophagy and induces programmed cell death in wheat seedlings, potentially through disrupting the balance of cellular death and element elements. Silencing of ATG2 or ATG7 inhibits autophagy and impairs salt tolerance, leading to oxidative stress, decreased antioxidant activity, and altered gene expression.