GABA-TaGAD6 Signaling Mediates Salt Tolerance in Wheat via Regulation of Antioxidant Defense, Ion Transport, and...

Soil salinity adversely impacts crop yields by inhibiting plant growth. Although it is known that autophagy regulates plant response to salt stress, γ-aminobutyric acid (GABA) mitigates salt-induced damage, and glutamate decarboxylases (GADs) are key GABA biosynthetic enzymes, the interaction among GABA metabolism, GAD isoforms, and autophagy in underlying plant adaptation to salt stress remains unclear. Here, we found exogenous application of 0.05 mM GABA optimally alleviated NaCl stress in wheat seedlings, improving growth parameters including plant height, leaf length, leaf width, and root length, chlorophyll content, and chlorophyll fluorescence parameters (F_v/F_m, Y(II), qP, NPQ, and ETR_max). GABA supplementation enhanced ROS scavenging (reduced H₂O₂, O^2•-, MDA), improved ionic homeostasis, and upregulated initiating autophagy activity. Genome-wide analysis identified seven salt-responsive TaGADs encoding cytoplasmic PLP-dependent decarboxylases (448-528 aa) with conserved catalytic domains (Lys277, HVDAASGG motif) and calmodulin (CaM)-binding regions. Exogenous GABA significantly upregulated the expression levels of TaGAD2/5/6/7 in wheat seedling leaves under NaCl treatment. Further functional experiments showed that silencing TaGAD6 significantly decreased salt tolerance by reducing GABA content, weakening antioxidant capacity, and amplifying oxidative damage in wheat seedling leaves. This led to aberrant autophagy activation, resulting in autophagic cell death. The salt-sensitive phenotypes induced by TaGAD6 silencing are rescued through GABA supplementation. Protein interaction assays demonstrated isoform-specific associations: TaGAD1/3/4 interact with TaATG8, and TaGAD1/4 interact with TaATG12, while TaGAD6 interacted with calmodulin TaCa1. These findings establish that GABA-TaGAD6 signaling regulates wheat salt tolerance via modulating autophagy activity; this provides mechanistic insights into metabolic-autophagic crosstalk during abiotic stress adaptation.