木材形成过程中木质素生物合成的表观遗传调控

Lignin,a major wood component,is the key limiting factor for wood conversion efficiency.Its biosynthesis is controlled by transcriptional regulatory networks involving transcription factor(TF)-DNA interactions.However,the epigenetic mechanisms underlying these interactions in lignin biosynthesis remain largely unknown.Understanding these functions in wood formation regulation can offer crucial insights into the molecular mechanisms of wood formation and facilitate the creation of new wood species with superior material properties.In this study,Populus trichocarpa served as the model organism.Using yeast one-hybrid,chromatin immunoprecipitation,and electrophoretic mobility shift assays,we identified that PtrbZIP44-A1,a key wood-forming TF,directly interacts with the promoters of PtrCCoAOMT2 and PtrCCR2,genes involved in the monolignol biosynthetic pathway.We employed yeast two-hybrid,bimolecular fluorescence complementation,biochemical analyses,transient and CRISPR-mediated transgenesis in P.trichocarpa to analyze how PtrHDA15 interacts with PtrbZIP44-A1 and alters chromatin histone modifications at the promoters of PtrCCoAOMT2 and PtrCCR2.(1)PtrbZIP44-A1 directly binds and represses PtrCCoAOMT2 and PtrCCR2.(2)PtrHDA15,a histone deacetylase,acts as an epigenetic inhibitor and is recruited by PtrbZIP44-A1 for chromatin histone modifications to repress PtrCCoAOMT2 and PtrCCR2,leading to reduced lignin deposition.(3)In transgenic plants overexpressing PtrbZIP44-A1 or PtrHDA15,histone acetylation at the promoters of PtrCCoAOMT2 and PtrCCR2 decreased,resulting in reduced gene expression and lignin content.Conversely,in loss-of-function ptrbzip44-a1 and ptrhda15 mutants,increased histone acetylation at PtrCCoAOMT2 and PtrCCR2 promoters enhanced target gene expression and lignin content.This study uncovered an epigenetic mechanism that suppresses lignin biosynthesis.This finding may help fill a knowledge gap between epigenetic regulation and lignin biosynthesis during wood formation in Populus.