Auxin and Jasmonic Acid Signalling Crosstalk Mediates Plant Growth Regulator-Stimulated Epigallocatechin Gallate Accumulation in Tea Plants (Camellia sinensis)

Abstract

Epigallocatechin gallate (EGCG) imparts distinctive health benefits and flavor to tea, and its accumulation is modulated by plant growth regulators (PGRs). However, the regulatory mechanisms of Paclobutrazol (PAC) and Lovastatin (LS) underlying EGCG biosynthesis remain uncharacterized. We integrated quantitative analysis, transcriptomics, and metabolomics to investigate the regulatory effects of exogenous PAC and LS on EGCG accumulation in tea plants and systematically elucidate the underlying molecular mechanism governing EGCG biosynthesis. The results demonstrated that exogenous PAC and LS treatments significantly elevated the accumulation of EGCG, as well as endogenous auxin and jasmonic acid (JA) contents. The variation trend of these key metabolites was highly consistent with the accumulation patterns of upstream flavonoid components, including eriodictyol, delphinidin, and epigallocatechin. Transcriptomic profiling further verified the critical involvement of auxin and JA signal transduction pathways in PGR-induced EGCG differential accumulation, and we screened a total of 14 auxin-related and 8 JA-related core signal regulatory factors. Furthermore, integrated bioinformatic analyses and antisense oligonucleotide (AsODN) functional validation experiments revealed that the core hormone signaling genes CsARF2 and CsMYC2 regulate the expression of CsSCPL16 through the transcription factor CsMYB80, and ultimately promote the conversion of epigallocatechin to EGCG and promote the accumulation of EGCG in tea plants. Collectively, the PGRs boost EGCG biosynthesis by mediating endogenous auxin and JA signal transduction. These results support the development of targeted agronomic practices to improve tea quality and lay a theoretical basis for expanding the industrial exploitation of tea bioactive constituents.