Department of Plant and Microbial Biology, North Carolina State University, Raleigh, NC, United States of America.
Botany Department, Faculty of Science, Fayoum University, Al Fayoum, Egypt.
PLoS One. 2020 Mar 16;15(3):e0230362. doi: 10.1371/journal.pone.0230362. eCollection 2020.
Fungi in the genus Cercospora cause crop losses world-wide on many crop species. The wide host range and success of these pathogens has been attributed to the production of a photoactivated toxin, cercosporin. We engineered tobacco for resistance to Cercospora nicotianae utilizing two strategies: 1) transformation with cercosporin autoresistance genes isolated from the fungus, and 2) transformation with constructs to silence the production of cercosporin during disease development. Three C. nicotianae cercosporin autoresistance genes were tested: ATR1 and CFP, encoding an ABC and an MFS transporter, respectively, and 71cR, which encodes a hypothetical protein. Resistance to the pathogen was identified in transgenic lines expressing ATR1 and 71cR, but not in lines transformed with CFP. Silencing of the CTB1 polyketide synthase and to a lesser extent the CTB8 pathway regulator in the cercosporin biosynthetic pathway also led to the recovery of resistant lines. All lines tested expressed the transgenes, and a direct correlation between the level of transgene expression and disease resistance was not identified in any line. Resistance was also not correlated with the degree of silencing in the CTB1 and CTB8 silenced lines. We conclude that expression of fungal cercosporin autoresistance genes as well as silencing of the cercosporin pathway are both effective strategies for engineering resistance to Cercospora diseases where cercosporin plays a critical role.
尾孢菌属中的真菌在许多作物物种上引起全球作物损失。这些病原体的广泛宿主范围和成功归因于光激活毒素尾孢菌素的产生。我们利用两种策略利用烟草进行对 Cercospora nicotianae 的抗性工程改造：1）利用从真菌中分离的尾孢菌素自抗性基因进行转化，2）利用构建物在疾病发展过程中沉默尾孢菌素的产生进行转化。我们测试了三个 C. nicotianae 尾孢菌素自抗性基因：ATR1 和 CFP，分别编码 ABC 和 MFS 转运蛋白，以及 71cR，它编码一个假定蛋白。在表达 ATR1 和 71cR 的转基因系中鉴定到对病原体的抗性，但在转化为 CFP 的系中未鉴定到。尾孢菌素生物合成途径中的 CTB1 聚酮合酶和在较小程度上 CTB8 途径调节剂的沉默也导致了抗性系的恢复。所有测试的系都表达了转基因，并且在任何系中都没有鉴定到转基因表达水平与疾病抗性之间的直接相关性。抗性也与 CTB1 和 CTB8 沉默系中的沉默程度无关。我们得出结论，表达真菌尾孢菌素自抗性基因以及沉默尾孢菌素途径都是对尾孢菌素起关键作用的 Cercospora 疾病进行工程抗性的有效策略。
