美国密苏里大学Bing Yang、德国杜塞尔多夫大学Wolf B. Frommer以及菲律宾国际水稻研究所Ricardo Oliva等人员合作取得进展。他们利用基因组编辑技术产生了具有细菌性枯萎病广谱抗性的水稻。这一研究成果于10月28日在线发表于国际学术期刊《自然—生物技术》。

研究人员使用CRISPR–Cas9介导的基因组编辑在所有三个SWEET基因启动子中引入突变。通过对63个Xanthomonas oryzae pv. oryzae（简称为Xoo）菌株中转录激活物样效应蛋白（TALe）基因的序列分析进一步改进编辑，该分析揭示了SWEET13等位基因的多个TALe变体。研究人员在SWEET14中也创建了突变，这也是非洲Xoo品系两种TAL的靶标。研究人员将总共五个启动子突变同时引入到水稻系Kitaake和优秀超级品种IR64和Ciherang-Sub1中。稻田试验表明，基因组编辑的SWEET启动子赋予了水稻品系强大的广谱抗性。

据了解，水稻的细菌性疫病是存在于亚洲和非洲的重要疾病。病原体Xoo分泌六种已知的TALe中的一种或多种，这些效应蛋白结合特定的启动子序列并至少诱导三种宿主蔗糖转运蛋白基因SWEET11、SWEET13和SWEET14中的一种，其表达是疾病易感性所必需的。

附：英文原文

Title: Broad-spectrum resistance to bacterial blight in rice using genome editing

Author: Ricardo Oliva, Chonghui Ji, Genelou Atienza-Grande, Jos C. Huguet-Tapia, Alvaro Perez-Quintero, Ting Li, Joon-Seob Eom, Chenhao Li, Hanna Nguyen, Bo Liu, Florence Auguy, Coline Sciallano, Van T. Luu, Gerbert S. Dossa, Sbastien Cunnac, Sarah M. Schmidt, Inez H. Slamet-Loedin, Casiana Vera Cruz, Boris Szurek, Wolf B. Frommer, Frank F. White, Bing Yang

Issue&Volume: 2019-10-28

Abstract: Bacterial blight of rice is an important disease in Asia and Africa. The pathogen, Xanthomonas oryzae pv. oryzae (Xoo), secretes one or more of six known transcription-activator-like effectors (TALes) that bind specific promoter sequences and induce, at minimum, one of the three host sucrose transporter genes SWEET11, SWEET13 and SWEET14, the expression of which is required for disease susceptibility. We used CRISPR–Cas9-mediated genome editing to introduce mutations in all three SWEET gene promoters. Editing was further informed by sequence analyses of TALe genes in 63 Xoo strains, which revealed multiple TALe variants for SWEET13 alleles. Mutations were also created in SWEET14, which is also targeted by two TALes from an African Xoo lineage. A total of five promoter mutations were simultaneously introduced into the rice line Kitaake and the elite mega varieties IR64 and Ciherang-Sub1. Paddy trials showed that genome-edited SWEET promoters endow rice lines with robust, broad-spectrum resistance.

DOI: 10.1038/s41587-019-0267-z

Source: https://www.nature.com/articles/s41587-019-0267-z