Work

The interaction between autophagy-related gene FtATG8a and FtE2FB is involved in the drought resistance of Tartary buckwheat

Year: 2025

Type: article

Abstract: Drought remains a significant abiotic stressor restricting global crop yields, with the autophagy pathway critically influencing plant responses to such conditions. Evidence suggests that drought stress triggers the accumulation of autophagosomes and the upregulation of FtATG8a expression in Tartary buckwheat. However, the regulatory mechanisms governing FtATG8a remain unclear. Our findings indicate that FtATG8a enhances drought resistance in transgenic Tartary buckwheat and Arabidopsis by amplifying autophagy, increasing the activities of antioxidant enzymes (SOD, POD, and CAT), and promoting proline accumulation. This study identifies FtE2FB as a FtATG8a-interacting protein through yeast two-hybrid library screening. The interaction between FtATG8a and FtE2FB was validated through yeast two-hybrid, bimolecular fluorescence complementation, and firefly luciferase fragment complementation assays. Remarkably, FtATG8a co-localizes with FtE2FB in the nucleus, with this interaction contingent on the ATG8-interacting motif (EKFEDI) on FtE2FB. Moreover, FtE2FB expression was elevated in FtATG8a-overexpressing plants and further induced by drought stress (P < 0.01). Further analysis indicated that the overexpression of FtE2FB enhances drought stress tolerance by altering the activities of antioxidant enzymes and promoting proline accumulation in transgenic Arabidopsis. Besides, co-expression of FtATG8a-FtE2FB resulted in a more pronounced increase in antioxidant enzyme activity and proline content compared to FtE2FB or FtATG8a overexpression alone under 20%PEG6000 treatment. This study suggests that FtATG8a interacts with FtE2FB to bolster drought tolerance by modulating autophagy, the antioxidant system, and downstream target genes, providing new insights into the drought response mechanisms in Tartary buckwheat.

Source: Plant Stress

DOI: 10.1016/j.stress.2025.100821