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Project PHC SAKURA with UR GAFL

Summary

Pathogens have evolved various strategies to bypass the defense systems of their host cells, including the delivery of effector proteins that suppress these systems and facilitate infection. The 2b protein of cucumber mosaic virus (CMV) is a well-studied viral effector that can inhibit plant defense mechanisms including RNA silencing, salicylic acid, and jasmonic acid signaling. We previously discovered that host calmodulin-like proteins act as antagonists to 2b by binding to and directing its degradation through autophagy. More recently, we identified a mutant eIF4E1 protein as another counteracting factor to 2b in tomato plants. Using CRISPR/Cas9 gene editing, we generated mutant tomato plants with eIF4E1 alleles: one with a single nucleotide insertion (1INS), resulting in a knockout mutant that exhibits resistance to potato virus Y, which depends on eIF4E1 for infection, but not to CMV; and another with a nine nucleotide deletion (9DEL), which shows partial resistance to CMV. Our findings suggest that the 9DEL mutation produces a mutant eIF4E1 protein that binds to 2b and promotes its degradation via autophagy. Since CMV requires 2b to infect tomato plants systemically, the resistance to CMV in 9DEL plants is likely due to the inhibitory effect on 2b.

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