zhangzhenluwenchao@163.com
Yu-Jin Hao, haoyujin@sdau.edu.cn
ยง the author has been passed away.
Abstract Apple necrotic mosiac virus (ApNMV) is a newly
identified causal agent that is highly associated with the occurrence of
apple mosaic disease in China. However, resistance gene against this
virus has not been identified yet. We reported here that nitrate
treatment destablized viral protein 1a via the ubiquitin-proteasome
pathways to restrain ApNMV genomic RNA accumulation. A
nitrate-responsive BTB/TAZ domain-containing protein MdBT2 was
identified in a yeast-two-hybrid screening of apple cDNA library using
viral protein 1a as bait, and 1a was confirmed to interact with MdBT2
both in vivo and in vitro. MdBT2 was further verified to promote the
ubiquitination and degradation of viral protein 1a through the
proteasome pathways in a MdCUL3A-scaffold protein in E3 ligase
complex-independent manner. Viral genomic RNA accumulation was decreased
in MdBT2 overexpression transgenic apple leaves but enhanced inMdBT2 antisense leaves compared to that in wild type. Moreover,
MdBT2 was found to interfere with the interactions between viral
replication proteins 1a and 2apol by competing with
the latter. Taken together, our work demonstrated that nitrate-inducible
MdBT2 functioned as a limiting factor in ApNMV viral RNA accumulation by
promoting the ubiquitination and degradation of viral protein 1a and
interfering with the interactions between viral replication proteins.
Keywords ApNMV, Malus domestica , MdBT2, ubiquitination,
viral genomic RNA replication, viral-host interactions