Tomato Chlorotic Virus Minor Coat Protein Interferes With the Host Proteasome Function by Competitive Disruption of <scp>SlPAD1</scp> – <scp>SlPA4</scp> Interaction to Enhance Viral Infection

The tomato chlorosis virus (ToCV) is one of the most destructive plant viruses affecting tomato crops, leading to significant agricultural losses. As an obligate parasite, ToCV depends on the macromolecular machinery of host cells for replication. The ubiquitin 26S proteasome system maintains the intracellular protein homeostasis, which is essential for plant growth and development. Our study found that the CPm protein of ToCV interacted with SlPAD1, a component of the 26S proteasome, to enhance viral infection. This interaction disrupts the binding between SlPAD1 and SlPA4, thereby impairing the 26S proteasome function. In addition, SlPAD1 and SlPA4 positively regulate plant resistance to ToCV. Our findings reveal a mechanism by which ToCV proteins facilitate infection by interfering with 26S proteasome function.