作者: | Jianbin Lai,Hao Chen,Kunling Teng,Qingzhen Zhao,Zhonghui Zhang,Yin Li,Liming Liang,Ran Xia,Yaorong Wu,Huishan Guo and Qi Xie. |
---|---|
刊物名称: | The Plant Journal |
DOI: | |
联系作者: | |
英文联系作者: | |
卷: | |
摘要: | C4 protein from Curtovirus was known as a major symptom determinant, but the action model of C4 protein remains unclear. To understand the mechanism of C4 protein in virus-plant interaction, we introduced the C4 gene from Beet severe curly top virus (BSCTV) into Arabidopsis under a conditional expression promoter; as a result, overexpression of BSCTV-C4 led to abnormal host cell division. RKP, a RING finger protein, which is a homologue of a human cell cycle regulator KPC1, was discovered to be induced by BSCTV C4 protein. Mutation of RKP reduced susceptibility to BSCTV in Arabidopsis and impaired BSCTV replication in plant cells. Callus formation is impaired in rkp mutants that indicated the role of RKP in plant cell cycle. RKP was demonstrated to be a functional ubiquitin E3 ligase and be able to interact with the cell cycle inhibitor ICK/KRP proteins in vitro. The accumulation of the protein level of ICK2/KRP2 was found to be increased in rkp mutant. The above results strengthen that RKP might regulate the degradation of ICK/KRP proteins. In addition, the protein level of ICK2/KRP2 was decreased in BSCTV infection. Overexpression of ICK1/KRP1 in Arabidopsis could reduce susceptibility to BSCTV. In conclusion, we found that RKP is induced by BSCTV C4 and may affect BSCTV infection by regulating the host cell cycle. |