GABA-induced lipid transfer protein MaLTP60 orchestrates dual ROS-regulatory strategies to confer resistance against banana anthracnose

Anthracnose, caused by Colletotrichum musae, is the most devastating postharvest disease limiting the shelf life and marketability of banana fruit. While γ-aminobutyric acid (GABA) is known to mitigate abiotic stress, its role and mechanisms in controlling postharvest diseases remain elusive. Here, we report that exogenous GABA treatment significantly attenuates anthracnose severity in harvested banana fruit. Through integrative physiological and transcriptomic analyses, we identified a non-specific lipid transfer protein, MaLTP60, as a critical regulator robustly triggered by GABA signaling and C. musae challenge. Crucially, silencing of MaLTP60 attenuated GABA-induced disease resistance. Then, we demonstrate that MaLTP60 orchestrates a dual-mechanism antioxidant defense to maintain redox homeostasis. Mechanistically, MaLTP60 physically targets the mitochondrial voltage-dependent anion channel MaVDAC9. Structural modeling and functional assays reveal that MaLTP60 acts as a molecular plug to occlude the MaVDAC9 pore, thereby blocking ROS transport, inhibiting channel activity and antagonizing MaVDAC9-mediated susceptibility. Concurrently, MaLTP60 interacts with the peroxiredoxin MaPRDX1 and functions as an affinity helper, synergistically enhancing its stabilization and ROS-scavenging efficiency. Collectively, our findings uncover a novel regulatory network in which GABA-induced MaLTP60 functions as a redox brake that coordinates dual antioxidant strategies to confer basal immunity in banana fruit to C. musae.