Journal of Plant Pathology & Microbiology

Abstract

Mutation in Arabidopsis CSN5A partially complements the lack of Beet curly top virus pathogenicity factor L2

Rosa Lozano-Durán and Eduardo R. Bejarano

Ubiquitination, a post-translational modification that controls multiple cellular processes, has proven to be a common target for viruses. Recently, geminivirus C2/L2 protein has been shown to interact with the plant CSN5, catalytic subunit of the CSN complex, and possibly disrupt the activity of this complex over CULLIN1, thus interfering with the function of the CULLIN1-based SCF ubiquitin E3 ligases. With the aim of shedding light on the genetic interaction between geminivirus C2/L2 and the plant CSN5, we designed an infection experiment using a combination of mutant plant and virus. Our results indicate that the geminivirus Beet curly top virus (BCTV) infects the Arabidopsis CSN5a mutant less efficiently; moreover, mutation in BCTV L2 can be partially complemented by mutation in Arabidopsis CSN5a. These results suggest that the inhibition of the CSN5 activity might be an important role of geminivirus C2/L2 during the establishment of the infection, and raises the possibility that geminiviral infection might require CSN activity.