AUTHOR=Yang Xiao , Luo Xiangwen , Zhang Yu , Zhang Zhanhong , OuYang Xian , Shi Xiaobin , Lv Xiaoyuan , Li Fan , Zhang Songbai , Liu Yong , Zhang Deyong TITLE=Tomato chlorosis virus CPm protein is a pathogenicity determinant and suppresses host local RNA silencing induced by single-stranded RNA JOURNAL=Frontiers in Microbiology VOLUME=14 YEAR=2023 URL=https://www.frontiersin.org/journals/microbiology/articles/10.3389/fmicb.2023.1151747 DOI=10.3389/fmicb.2023.1151747 ISSN=1664-302X ABSTRACT=Introduction

Tomato chlorosis virus (ToCV) is a typical member of the genus Crinivirus, which severely threatens Solanaceae crops worldwide. The CPm protein encoded by ToCV has been reported to be associated with virus transmission by vectors and is involved in RNA silencing suppression, while the mechanisms remain ambiguous.

Methods

Here, ToCV CPm was ectopically expressed by a Potato virus X (PVX) vector and infiltrated into Nicotiana benthamiana wild-type and GFP-transgenic16c plants.

Results

The phylogenetic analysis showed that the CPm proteins encoded by criniviruses were distinctly divergent in amino acid sequences and predicted conserved domains, and the ToCV CPm protein possesses a conserved domain homologous to the TIGR02569 family protein, which does not occur in other criniviruses. Ectopic expression of ToCV CPm using a PVX vector resulted in severe mosaic symptoms followed by a hypersensitive-like response in N. benthamiana. Furthermore, agroinfiltration assays in N. benthamiana wilt type or GFP-transgenic 16c indicated that ToCV CPm protein effectively suppressed local RNA silencing induced by single-stranded but not double-stranded RNA, which probably resulted from the activity of binding double-stranded but not single-stranded RNA by ToCV CPm protein.

Conclusion

Taken together, the results of this study suggest that the ToCV CPm protein possesses the dual activities of pathogenicity and RNA silencing, which might inhibit host post-transcriptional gene silencing (PTGS)-mediated resistance and is pivotal in the primary process of ToCV infecting hosts.