Downregulation of Light-Harvesting Complex II Induces ROS-Mediated Defense Against Turnip Mosaic Virus Infection in Nicotiana benthamiana

The light-harvesting chlorophyll a/b complex protein 3 (LHCB3) of photosystem II plays important roles distributing the excitation energy and modulating the rate of state transition and stomatal response to abscisic acid. However, the functions of LHCB3 in plant immunity have not been well investigated. Here, we show that the expression of LHCB3 in Nicotiana benthamiana (NbLHCB3) was down-regulated by turnip mosaic virus (TuMV) infection. When NbLHCB3 was silenced by tobacco rattle virus-induced gene silencing, systemic infection of TuMV was inhibited. H2O2 was over-accumulated in NbLHCB3-silenced plants. Chemical treatment to inhibit or eliminate reactive oxygen species (ROS) impaired the resistance of the NbLHCB3-silenced plants to TuMV infection. Co-silencing of NbLHCB3 with genes involved in ROS production compromised the resistance of plants to TuMV but co-silencing of NbLHCB3 with genes in the ROS scavenging pathway increased resistance to the virus. Transgenic plants overexpressing NbLHCB3 were more susceptible to TuMV. These results indicate that downregulation of NbLHCB3 is involved in defense against TuMV by inducing ROS production.

Automated summary

The LHCB3 protein in plants plays a crucial role in defense against TuMV infection by inducing the production of ROS, which enhances the resistance of plants to the virus.