SummaryThe C4 protein fromCurtovirusis known as a major symptom determinant, but the mode of action of the C4 protein remains unclear. To understand the mechanism of involvement of C4 protein in virus–plant interactions, we introduced theC4gene fromBeet severe curly top virus(BSCTV) into Arabidopsis under a conditional expression promoter; the resulting overexpression ofBSCTV C4led to abnormal host cell division. RKP, a RING finger protein, which is a homolog of the human cell cycle regulator KPC1, was discovered to be induced by BSCTV C4 protein. Mutation ofRKPreduced the susceptibility to BSCTV in Arabidopsis and impaired BSCTV replication in plant cells. Callus formation is impaired inrkpmutants, indicating a role of RKP in the plant cell cycle. RKP was demonstrated to be a functional ubiquitin E3 ligase and is able to interact with cell‐cycle inhibitor ICK/KRP proteinsin vitro. Accumulation of the protein ICK2/KRP2 was found increased in therkpmutant. The above results strengthen the possibility that RKP might regulate the degradation of ICK/KRP proteins. In addition, the protein level of ICK2/KRP2 was decreased upon BSCTV infection. Overexpression ofICK1/KRP1in Arabidopsis could reduce the susceptibility to BSCTV. In conclusion, we found thatRKPis induced by BSCTV C4 and may affect BSCTV infection by regulating the host cell cycle.