Barley Yellow Dwarf Virus‐GAV 17K Manipulates HvSRC2 to Dampen Plant Defence to Promote Viral Infection

SRC2 is a C2 domain-containing protein that responds to attack from the host and non-host pathogens as well as abiotic stresses. The role of SRC2 in regulating viral infection is largely unknown. We employed the BYDV-barley pathosystem to characterize the involvement of HvSRC2 in viral infection. Here, we report that 17K protein encoded by barley yellow dwarf virus-GAV (BYDV-GAV) interacted with Hordeum vulgare SRC2 (HvSRC2) and promoted its accumulation. Silencing of HvSRC2 expression blocked BYDV-GAV accumulation. Transcriptome sequencing indicated that HvSRC2 regulated plant defence-related pathways like plant hormone signal transduction, plant-pathogen interaction and other disease resistance pathways. Genes involved in plant immunity including HvRBOHC, HvRGA1, HvB-2b, HvNPR2, HvBSK3, HvRPP13L3, HvMYC2 and HvMkk4 were upregulated upon HvSRC2 silencing. We further found that HvRBOHC interacted with HvSRC2. HvRBOHC silencing increased BYDV-GAV accumulation, coinciding with upregulated expression of other HvRBOHs and elevated H₂O₂ and O₂ ^- levels. Furthermore, we also found that MaYMV MP and TuMV viral genome-linked protein (VPg), can both interact with HvSRC2, indicating the relative conservation between viral proteins and HvSRC2. Silencing of NbSRC2 inhibited the accumulation of TuMV and MaYMV. Taken together, our findings suggest that viral proteins utilize HvSRC2 to regulate plant defence pathways to aid viral infection.