Unveiling the power of PavGID1s: the critical player in sweet cherry flower bud dormancy release.

Abstract

Exogenous hormones can regulate bud dormancy release, particularly in cases where inadequate winter chill accumulation due to global warming affects perennial plants. Gibberellin (GA) is recognized as a critical signal for dormancy release in woody perennials. This study explores the influence of GA and its signaling components on the dormancy release in sweet cherry. The external application of GA_4 + 7 significantly promoted the bud break rate and dormancy release. Notably, there was a substantial accumulation of GA₃, GA₄, and GA₇ in the buds, accompanied by a reduced concentration of abscisic acid (ABA) following GA treatment. RNA-Seq identified 8,610 differentially expressed transcripts in GA-treated buds compared to the Mock group. Transcriptome sequencing revealed differential expressions of PavGID1s, the GA receptor GID1, in sweet cherry flower buds after GA treatment. These findings were further verified across different seasons in sweet cherry. In both PavGID1b and PavGID1c, the open reading frame (ORF) is 1,032 bases long and encodes 344 amino acids. Overexpression of PavGID1b and PavGID1c resulted in early flowering and higher plants in Arabidopsis. However, these genes have opposing roles in seed germination in Arabidopsis. Furthermore, PavWRKY31 may regulate the stabilization and release of dormancy by modulating the transcriptional level of PavGID1c. PavGA20ox-2 and PavGID2 may also influence sweet cherry dormancy release by interacting with GID1s and affecting DELLA protein stability. These results provide a theoretical basis for understanding the regulatory effect of gibberellin on the bud dormancy of plants.