RKP, a RING finger E3 ligase induced by BSCTV C4 protein, affects geminivirus infection by regulation of the plant cell cycle

Abstract

SummaryThe C4 protein from Curtovirus is 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 the C4 gene from Beet severe curly top virus (BSCTV) into Arabidopsis under a conditional expression promoter; the resulting overexpression of BSCTV C4 led 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 of RKP reduced the susceptibility to BSCTV in Arabidopsis and impaired BSCTV replication in plant cells. Callus formation is impaired in rkp mutants, 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 proteins in vitro. Accumulation of the protein ICK2/KRP2 was found increased in the rkp mutant. 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 of ICK1/KRP1 in Arabidopsis could reduce the 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.

Ubiquitin and Plant Viruses, Let’s Play Together!

“…In the geminivirus Beet severe curly top virus (BSCTV), expression of the C4 protein, a major determinant of pathogenesis affecting cell division, was found to promote expression of the RING-type E3 ligase RKP (for related to KPC1; Lai et al, 2009). Interestingly, RKP regulates the cell cycle through degradation of the cell cycle inhibitors ICK/KRPs (for interactors/inhibitors of Cdc2 kinases/Kip-related proteins; Ren et al, 2008), and modification of the accumulation level of these protein substrates was also observed in BSCTV-infected plants.…”

Ubiquitination during Plant Immune Signaling

“…Therefore, induction of RKP expression by the virus may account for the observed C4-induced abnormal cell division in Arabidopsis. It is hypothesized that this modification of the cell cycle may provide a more suitable environment for viral replication (Lai et al, 2009). …”

WRKY8 transcription factor functions in the TMV-cg defense response by mediating both abscisic acid and ethylene signaling in Arabidopsis

“…Although plant viruses are among the least genetically complex pathogens, they use a variety of strategies to suppress or bypass host defense and then promote their infection of susceptible hosts. In plants, these strategies involve enhancing infection by manipulating host resources, such as the formation of replication complexes (1), enlargement of the plasmodesma size-exclusion limit (2, 3), evolution of viral suppressors of RNA silencing to counteract antiviral silencing (4), interference with regulation of the plant cell cycle (5,6), and using host components for its own replication (7).…”