Promoting effect of GA3 on primary bud necrosis and its underlying mechanism in grapevines

Abstract

This study aimed to investigate the mechanism underlying primary bud necrosis (PBN) in grapevines. PBN is a physiological disorder that significantly reduces grape yields. The four varieties, ‘Shine Muscat’, ‘Summer Black’, ‘Ruby Seedless’, and ‘Hutai 8’, were investigated and found to exhibit differences in PBN, which was positively correlated with the speed and extent of inflorescence differentiation. Among them, ‘Summer Black’ was most susceptible to PBN. Treatment with gibberellin acid 3 (GA3) notably accelerated and exacerbated PBN in ‘Summer Black’, whereas the endogenous gibberellin (GA) inhibitor chlorocholine chloride (CCC) delayed or prevented PBN onset. Histological observations of dormant bud tissues revealed PBN progression in stages, starting with the expansion of cells in the necrosis zone (NZ), followed by cell wall irregularities and collapse, buckling cell layer formation, and subsequent cell separation. In the water control group, NZ mainly occurred in the bud scale layer. However, by the second week after GA3 treatment, primary buds visibly elongated, and NZ was formed at multiple locations along the primary buds. Transcriptomic analyses revealed significant regulation of stress-related genes, including reactive oxygen species (ROS) and heat-shock proteins (HSPs), following GA3 treatment. Genes related to jasmonic acid (JA) biosynthesis and signaling pathways were upregulated after week 2, whereas CCC treatment led to the downregulation of these genes. Furthermore, genes associated with cations such as calcium, iron, and copper showed significant changes across all transcriptome samples. Genes associated with the degradation of cell membranes and cell walls were upregulated in samples treated with GA3 and water control. Overall, these findings suggested that GA3 promoted PBN by enhancing JA synthesis and modulating the cell necrosis pathway via JA signaling. This process involved ROS accumulation and activation of cation pathways, leading to endomembrane and cell wall degradation, cell rupture, and, ultimately, PBN development.