Abstract
The potato virus Y (PVY) is a plant virus that causes massive crop losses globally, especially in Solanaceae crops. A strain of the plant growth-promoting rhizobacterium (PGPR), Serratia marcescens-S3 was found to inhibit PVY replication in Nicotiana benthamiana. However, there have been no in-depth studies demonstrating the underlying mechanism. In the current study, we found that ubiquitination of NbHsc70-2 is an important way for Serratia marcescens-S3 to trigger induced systemic resistance (ISR). After the treatment with S. marcescens-S3, the protein level of NbHsc70-2 reduced significantly. Inhibiting of ubiquitination increased the accumulation of NbHsc70-2 in plants and reduced S. marcescens-S3-mediated resistance to PVY. Furthermore, transgenic engineered Nicotiana benthamiana NbHsc70-2KO and NbHsc70-2USM were constructed using CRISPR-Cas9-mediated NbHsc70-2 knock-out and ubiquitination respectively. S. marcescens-S3 significantly reduced the inhibition of NbHsc70-2 protein accumulation in NbHsc70-2KO and NbHsc70-2USM . The virulence of PVY was stronger in NbHsc70-2USM than the wild-type plants. These results showed that S. marcescens-S3 increases the ubiquitination of NbHsc70-2 to inhibit the recruitment of molecular chaperone NbHsc70-2 to reduce its replication and infection of PVY.