The ABI5-dependent downregulation of mitochondrial ATP synthase OSCP subunit facilitates apple necrotic mosaic virus infection.

Apple necrotic mosaic virus (ApNMV) is significantly associated with apple mosaic disease in China. However, the mechanisms of ApNMV infection, as well as host defense against the virus, are still poorly understood. Mitochondrial ATP synthase plays a fundamental role in the regulation of plant growth and development. However, the mechanism of mitochondrial ATP synthase in response to virus infection remains to be defined. In the present study, a yeast two-hybrid (Y2H) screening revealed that the apple mitochondrial ATP synthase OSCP subunit (MdATPO) interacts with ApNMV coat protein (CP). It was further verified that overexpression of MdATPO in Nicotiana benthamiana inhibited viral accumulation. In contrast, silencing of NbATPO facilitated viral accumulation, indicating that ATPO plays a defensive role during ApNMV infection. Further investigation demonstrated that ApNMV infection accelerated abscisic acid (ABA) accumulation, and ABA negatively regulated ATPO transcription, which was related to the capacity of ABA insensitive 5 (ABI5) to bind to the ABA-responsive elements (ABREs) of the ATPO promoter. Altogether, our results indicated that transcription factor ABI5 negatively regulated ATPO transcription by directly binding its promoter, leading to the sensitivity of apple and N. benthamiana to ApNMV infection. The current presentation facilitates our comprehensive understanding of the intricate responses of host to ApNMV.