The ABA receptor NtPYL6 promotes flavonol biosynthesis to enhance tobacco resistance to UV-B.

ABA and flavonol accumulation protect plants against UV-B radiation damage. However, the molecular mechanism by which UV-B enhances ABA signaling to induce flavonol biosynthesis remains largely unknown. Here, we found that ABA receptor ntpyl6 (PYRABACTIN RESISTANCE 1-LIKE6) mutants are more sensitive to UV-B than the WT and that UV-B significantly induces ABA accumulation and NtPYL6 expression in tobacco (Nicotiana tabacum). The induction of UV-B on NtPYL6 expression was achieved by inactivating NtBES1 (BRI1-EMS-SUPPRESSOR1), which directly binds to the E-box present in the NtPYL6 promoter to inhibit its expression. Metabolome and transcriptome analyses demonstrated that NtPYL6 positively mediates flavonol accumulation and the expression of related genes induced by ABA signaling. We further showed that NtPYL6-NtABI1/NtHAB1-NtSnRK2.12 constitute the core ABA signaling pathway to activate NtABF3 (ABA-RESPONSIVE ELEMENT-BINDING FACTOR 3). NtABF3 directly binds to the ABRE cis-elements present in the promoters of NtCHS and NtFLS genes to induce their transcription, leading to the increased accumulation of flavonols and enhanced plant resistance to UV-B. Our results elucidate a mechanism by which enhanced ABA signaling promotes flavonol accumulation, thereby improving plant resistance to UV-B.