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Summary  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 NbHsc70‐2 KO   and  NbHsc70‐2 USM   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  NbHsc70‐2 KO   and  NbHsc70‐2 USM  . The virulence of PVY was stronger in  NbHsc70‐2 USM   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.

Serratia marcescens ‐S3 inhibits Potato virus Y by activating ubiquitination of molecular chaperone proteins NbHsc70‐2 in Nicotiana benthamiana