Tomato Yellow Leaf Curl Virus C4 Suppresses Antiviral Immunity by Targeting the 14‐3‐3 Protein SlTFT2
TL;DR
It is established that the C4–SlTFT2 interaction is indispensable for TYLCV‐mediated immunosuppression, and C4 promotes successful TYLCV infection by reducing the nuclear accumulation of SlTFT2 through this interaction, revealing a novel mechanism by which the virus subverts host defence by targeting a 14‐3‐3 protein.
Abstract
Geminiviruses severely threaten global crop production. Tomato yellow leaf curl virus (TYLCV) encodes multifunctional effector C4, which participates in diverse biological processes and interacts with host proteins to facilitate infection. Despite extensive studies on geminiviral C4, how TYLCV C4 suppresses tomato immunity remains poorly characterized. In this study, we identified the tomato 14‐3‐3 protein SlTFT2 as a specific interaction partner of the TYLCV C4 protein. We demonstrated that SlTFT2 functions as a positive regulator of antiviral defence, as its silencing enhanced systemic viral infection, whereas its overexpression restricted infection. A critical serine residue at position 86 in C4 was essential for this interaction, and mutation of this residue (S86A or S86L) in TYLCV infectious clones significantly attenuated viral infectivity. Furthermore, C4, but not the S86A or S86L mutants, reduced the nuclear accumulation of SlTFT2. Collectively, our findings establish that the C4–SlTFT2 interaction is indispensable for TYLCV‐mediated immunosuppression. Moreover, C4 promotes successful TYLCV infection by reducing the nuclear accumulation of SlTFT2 through this interaction, revealing a novel mechanism by which the virus subverts host defence by targeting a 14‐3‐3 protein.