ZmNAC17 Integrates Transcriptional and Protein Interaction Networks to Regulate Maize Stalk Architecture

Maize plant height and stalk mechanical strength are critical traits that influence planting density, yield, and lodging resistance. Although numerous dwarf mutants have been characterized in maize, most cannot be directly utilized in breeding programs due to associated developmental and reproductive deficiencies. In a previous study, we demonstrated that ZmNAC17 regulates mesocotyl elongation by mediating auxin and reactive oxygen species (ROS) biosynthetic pathways. Here, we characterize the role of ZmNAC17 in maize stalk development using both zmnac17 mutants and ZmNAC17-overexpressing (OE) lines. Plant height, stalk diameter, and internode length were reduced in both the zmnac17-1 EMS mutant and the zmnac17-3 CRISPR mutant. Internode cell length and cell area were decreased, whereas cell number was increased in zmnac17-1. Cellulose and lignin contents were elevated in zmnac17-1. Stalk bending force was diminished in zmnac17-3 but enhanced in the OE lines. The ratio of syringyl to guaiacyl (S/G), a key lignin monomer composition, was increased in zmnac17-3 while reduced in the OE lines. ZmNAC17 functions as a transcription factor, with its downstream targets implicated in phytohormone biosynthesis, phytohormone signaling, and lignin biosynthesis. CUT&Tag binding profile, EMSA, and dual-luciferase reporter assay demonstrate that ZmNAC17 promotes the expression of caffeoyl-CoA O-methyltransferase (CCoAOMT). IP-MS, Co-IP, and GST pull-down assays reveal that ZmNAC17 interacts with Beta glucosidase aggregating factor1 (BGAF1). Collectively, our findings indicate that ZmNAC17 regulates maize stalk development through transcriptional activation and protein-protein interactions, thereby providing new genetic resources for modifying plant architecture and mechanical strength in maize.