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Background  R2R3-MYB transcription factors (TFs) play important roles in plant growth and development, and response to biotic and abiotic stresses. However, their regulatory mechanisms in wound-induced anthocyanin biosynthesis in woody plants are largely unknown.    Results  In this work, we report that expression of anthocyanin biosynthesis genes ( ABGs ) were activated by PdMYB118, a MYB TF encoding gene from  Populus deltoids , and the activation of PdMYB118 was significantly enhanced by PdTT8, a bHLH protein, through its direct interaction with PdMYB118.  PdMYB118  and some  ABGs  were evidently induced by wound induction and methyl jasmonate (MeJA) treatment. Overexpression of  PdMYB118  promoted anthocyanin accumulation in transgenic poplar upon wound induction. Furthermore, a poplar JASMONATE ZIM-domain (JAZ) protein, PtrJAZ1, repressed the transcriptional function of PdMYB118/PdTT8 complex by binding to PdTT8, and wound stimulated the biosynthesis of jasmonic acid (JA) and the degradation of PtrJAZ1.    Conclusions  Based on these observations, we proposed that PtrJAZ1 degradation triggered the expression of  ABGs , leading to increased biosynthesis of anthocyanins in the wounded leaves of transgenic poplar. Therefore, our findings not only illustrate the crucial role of PdMYB118 in wound-induced anthocyanin biosynthesis in poplar, but also provide a molecular basis for the genetic engineering of colorful tree species.

MYB transcription factor PdMYB118 directly interacts with bHLH transcription factor PdTT8 to regulate wound-induced anthocyanin biosynthesis in poplar