【原】通过编辑表观基因组提高植物抗病能力

病原体依赖宿主易感性(S)基因的表达来促进感染和疾病。由于DNA甲基化是一种影响基因表达的表观遗传修饰，通过靶向甲基化阻断S基因的访问可以提高抗病能力。黄axonopodis pv。木薯细菌性疫病(CBB)的致病因子manihotis利用转录激活因子-like20 (TAL20)诱导S基因MeSWEET10a的表达。我们使用合成的锌指DNA结合域融合到rna定向DNA甲基化途径的一个组成部分，将甲基化指向MeSWEET10a启动子内的TAL20效应结合元件。他们证明，这种甲基化阻止了TAL20的结合，阻止了MeSWEET10a在体内的转录激活，这些植物在保持正常生长和发育的同时，对CBB表现出了更高的抗性。这项工作建立了表观基因组编辑作为一种新的作物改良策略。

Pathogens rely on expression of host susceptibility (S) genes to promote infection and disease. As DNA methylation is an epigenetic modification that affects gene expression, 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 in vivo and that these plants display increased resistance to CBB while maintaining normal growth and development. This work establishes epigenome editing as a new strategy for crop improvement.

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