Improving disease resistance in plants by editing the epigenome

Pathogens rely on expression of host susceptibility (S) genes to promote infection and disease. DNA methylation is an epigenetic modification that affects gene expression. Theoretically, blocking access to S genes through targeted methylation could increase disease resistance. Xanthomonas axonopodis pv. manihotis, the causal agent of cassava bacterial blight (CBB), uses transcription activator-like20 (TAL20) to induce expression of the S gene MeSWEET10a. We directed methylation to the TAL20 effector binding element within the MeSWEET10a promoter using a synthetic zinc-finger DNA binding domain fused to a component of the RNA-directed DNA methylation pathway. We demonstrate that this methylation prevents TAL20 binding, blocks transcriptional activation of MeSWEET10a and that these plants display increased resistance to CBB. This work establishes epigenome editing as a new strategy for crop improvement. This dataset includes WGBS data to understand target DNA methylation in cassava.

病原菌依赖寄主感病基因（host susceptibility genes, S）的表达以促进侵染与病害发生。DNA甲基化（DNA methylation）是一类影响基因表达的表观遗传修饰（epigenetic modification）。理论上，通过靶向甲基化阻断病原菌对感病基因的可及性，可提升作物抗病性。引发木薯细菌性枯萎病（cassava bacterial blight, CBB）的地毯草黄单胞菌木薯萎蔫致病型（Xanthomonas axonopodis pv. manihotis），可借助转录激活类20（transcription activator-like20, TAL20）效应蛋白诱导感病基因MeSWEET10a的表达。本研究通过将融合了RNA指导的DNA甲基化途径（RNA-directed DNA methylation pathway）组分的合成锌指DNA结合结构域，靶向结合MeSWEET10a启动子内的TAL20效应蛋白结合元件并实施甲基化修饰。实验证实，该甲基化修饰可阻断TAL20的结合，抑制MeSWEET10a的转录激活，且此类植株对木薯细菌性枯萎病的抗性显著提升。本研究确立了表观基因组编辑作为作物改良的全新策略。本数据集包含全基因组亚硫酸氢盐测序（whole-genome bisulfite sequencing, WGBS）数据，用于解析木薯中的靶向DNA甲基化调控机制。