Salicylic Acid-Induced MdTGA9-MdERF138-MdHCT Module Is Associated with Lignin Deposition and Improved Anthracnose Resistance in Autotetraploid Apple.

Apple anthracnose, caused by Colletotrichum gloeosporioides, severely threatens global apple production. Autotetraploid 'Hanfu' apples show stronger anthracnose resistance than diploids, but the underlying molecular mechanism remains unclear. This study identified a novel salicylic acid (SA)-regulated lignin biosynthesis signaling pathway that is closely associated with the enhanced resistance in autotetraploid 'Hanfu' apples. Autotetraploid apples accumulated higher endogenous SA levels, and the SA-responsive transcription factor MdTGA9 was markedly induced by both SA treatment and C. gloeosporioides infection. Mechanistically, MdTGA9 acts as a nuclear transcriptional activator to directly bind to the MdERF138 promoter and activate its expression. MdERF138 then transactivates the lignin biosynthetic gene MdHCT, thereby promoting lignin accumulation. Functional verification showed that MdTGA9 overexpression in apple calli, fruits and leaves significantly enhanced anthracnose resistance, and MdERF138 and MdHCT were confirmed as positive regulators of this resistance. Collectively, this study reveals a previously uncharacterized MdTGA9-MdERF138-MdHCT regulatory cascade that integrates SA signaling and lignin-based physical defense, which accounts for the enhanced disease resistance of autotetraploid apple. These findings provide valuable gene resources and a new molecular mechanism for disease-resistance breeding in apple.