miR319-Regulated TCP3 Modulates Silique Development Associated with Seed Shattering in Brassicaceae

Seed shattering is an undesirable trait that leads to crop yield loss. Improving silique resistance to shattering is critical for grain and oil crops. In this study, we found that miR319-targeted TEOSINTE BRANCHED 1, CYCLOIDEA, and PROLIFERATING CELL NUCLEAR ANTIGEN BINDING FACTOR (TCPs) inhibited the process of post-fertilized fruits (silique) elongation and dehiscence via regulation of FRUITFULL (FUL) expression in Arabidopsis thaliana and Brassica napus. AtMIR319a activation resulted in a longer silique with thickened and lignified replum, whereas overexpression of an miR319a-resistant version of AtTCP3 (mTCP3) led to a short silique with narrow and less lignified replum. Further genetic and expressional analysis suggested that FUL acted downstream of TCP3 to negatively regulate silique development. Moreover, hyper-activation of BnTCP3.A8, a B. napus homolog of AtTCP3, in rapeseed resulted in an enhanced silique resistance to shattering due to attenuated replum development. Taken together, our findings advance our knowledge of TCP-regulated silique development and provide a potential target for genetic manipulation to reduce silique shattering in Brassica crops.

Automated summary

Seed shattering is an undesirable trait that leads to crop yield loss. This study found that miR319-targeted TCPs inhibit the elongation and dehiscence of post-fertilized fruits (silique) by regulating FUL expression. FUL acts downstream of TCP3 to negatively regulate silique development, and over-activation of TCP3 enhances silique resistance to shattering. These findings provide a potential target for reducing seed shattering in Brassica crops.