Abstract
The oomycete pathogen, Phytophthora infestans, is the causal agent of potato late blight, which is one of the most destructive and economically important plant diseases. We previously showed that mature N. benthamiana is resistant to P. infestans. Screening with virus-induced gene silencing (VIGS) identified genes for calreticulin 3 (NbCRT3), a molecular chaperone for glycoproteins in ER, and N-acetyl glucosamine phosphotransferase (NbGPT), an enzyme for N-glycosylation, as essential genes for the resistance of N. benthamiana against P. infestans. In NbCRT- and NbGPT-silenced plants, production of reactive oxygen species (ROS) induced by the treatment of INF1 elicitor, a secretory protein derived from P. infestans, was significantly reduced. Similarly, silencing of UDP-glucose:glycoprotein glucosyltransferase (UGGT), another component of the ER quality control of glycoprotein folding, compromised ROS production and hypersensitive cell death in response to INF1 treatment. These results suggested that N. benthamiana have N-glycosylated extracellular receptor, which undergoes ERQC during their folding and maturation, for the recognition of elicitor from P. infestans.
