Abstract Pear (Pyrus) stone cells, a major determinant of fruit quality, form via cell wall lignification. The plant hormone jasmonic acid (JA) plays a pivotal role in regulating secondary cell wall formation, although the underlying molecular mechanisms remain unclear. Here, we demonstrated that JA positively regulates stone cell lignification via respiratory burst oxidase homolog F (PuRBOHF)-dependent reactive oxygen species (ROS) production. The NAC transcription factor PuNAC43 acts as a central mediator, enhancing JA-induced ROS accumulation and lignin deposition. PuNAC43 directly binds to promoters of the PuRBOHF and lignin biosynthesis genes (cinnamoyl-CoA reductase 1, PuCCR1; cinnamyl alcohol dehydrogenase 2, PuCAD2), thereby enhancing their transcription. Additionally, PuMYC2, a central MYC transcription factor in the JA signaling pathway, mediates JA-induced upregulation of PuNAC43 function. PuMYC2 binds directly to the PuNAC43 promoter, activating its expression. Furthermore, PuMYC2 recruits the bHLH transcription factor PubHLH93 through promoter binding and protein–protein interaction, forming a heterodimeric complex that synergistically enhances the activation of PuNAC43. Notably, PuMYC2-mediated transcriptional activation depends on JA levels. Our findings reveal a JA-responsive transcriptional complex, PuMYC2-PubHLH93-PuNAC43, that elevates the transcription of PuRBOHF and lignin-related genes to drive stone cell formation, thereby revealing pivotal mechanisms underlying JA-induced lignification in pear fruit.
Sun et al. (Tue,) studied this question.