Lili Hou, Baoxin Li, Yueying Liu, Qingzhu Zhang, Zhimin Zheng
Optimization of tree architecture is essential for advancing sustainable forestry, as appropriate canopy structure can contribute to growth and development. However, the molecular mechanisms that control tree architecture have not been fully characterized. While the putative NAD-dependent histone deacetylase HST1 was shown to regulate branching architecture in multiple crop species, whether epigenetic mechanism also influence tree architecture is unknown. Here, we investigated the genetic regulation of branching angle in white birch (Betula platyphylla Suk.), a pioneer tree of the temperate and boreal forests. Using bphst1 mutants generated via gene editing, we demonstrate that BpHST1 is involved in tree architecture by modulating branching angles. We provide evidence that BpHST1 is a histone deacetylase associated with altered H3K27ac levels and that it affects the expression of the cellulase gene CELLULASE 1 (BpCEL1). Compared with the wild type, BpHST1 knockout and BpCEL1 overexpression both resulted in reduced branch angles, supporting BpCEL1 as a candidate downstream effector of BpHST1. Our study suggests that BpHST1 influences the birch architecture by altering H3K27 acetylation at the BpCEL1 locus, elucidating a previously unknown aspect of the epigenetic mechanisms that control tree architecture in white birch.