2020 journal article

Engineering Cercospora disease resistance via expression of Cercospora nicotianae cercosporin-resistance genes and silencing of cercosporin production in tobacco

PLOS ONE, 15(3).

By: E. Thomas n‚ÄČ, S. Herrero n, H. Eng n, N. Gomaa n, J. Gillikin n, R. Noar n, A. Beseli n, M. Daub n

MeSH headings : Ascomycota / drug effects; Ascomycota / genetics; Disease Resistance / drug effects; Disease Resistance / genetics; Drug Resistance, Fungal / drug effects; Drug Resistance, Fungal / genetics; Gene Expression Regulation, Fungal / drug effects; Gene Silencing / drug effects; Genes, Fungal; Genetic Engineering; Perylene / analogs & derivatives; Perylene / pharmacology; Plants, Genetically Modified; Tobacco / microbiology; Transformation, Genetic; Transgenes
TL;DR: It is concluded that expression of fungal cercosporin autoresistance genes as well as silencing of the cercsporin pathway are both effective strategies for engineering resistance to Cercospora diseases where cercOSporin plays a critical role. (via Semantic Scholar)
Source: Web Of Science
Added: June 8, 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.