CITRUS LEPROSIS VIRUS C INFECTS ARABIDOPSIS THALIANA THE MODEL FOR PLANTPATHOGEN INTERACTIONS

G.D. Arena, M.P. Bergamini, A.D. Tassi, E.W. Kitajima, K.S. Kubo, J. Freitas-Astúa
doi: 10.4454/JPP.V95I2.003
Abstract:
Caused by Citrus leprosis virus C (CiLV-C) (genus Cilevirus) and vectored by Brevipalpus phoenicis Geijskes, leprosis is one of the main diseases of the Brazilian citrus industry. Although this disease was reported decades ago, the mechanisms involved in plant- virus interaction are still largely unknown. Since Arabidopsis thaliana has emerged as the major experimental model for essentially all aspects of plant biology, we tested the ability of CiLV-C to infect this model plant, evaluating the response of 12 ecotypes: Bur-0, Kas-1, Van- 0, Bay-0, C-24, Col-0, Ts-1, Tsu-1, Bla-2, Kon, Sha and Nfa-8. Four-week-old plants grown under 16 h photoperiod and 22°C were infested with two viruliferous or non viruliferous mites, or were not exposed to mites. Each treatment had twelve replicates of each ecotype. Localized necrotic lesions in green and senescent leaves and localized green lesions in senescent leaves appeared after 5-10 days only in plants infested with viruliferous mites. Thin-sectioned symptomatic tissues contained short bacilliform particles and viroplasm similar to those found in citrus. RT-PCR assays using primers that amplify part of the CiLV- C movement protein gene (Locali et al., 2003) yielded amplicons from all symptomatic plants, which were sequenced, proving identical to those obtained from the naturally infected CiLV-C source. CiLV-C was able to infect all of the tested A. thaliana ecotypes with reactions that identified three resistance level groups: more susceptible (Bur-0, Kas-1, Van-0, Bay-0, and C-24), intermediate (Col-0, Ts-1, and Tsu-1) and more resistant (Bla-2, Kon, Sha, and Nfa-8). Besides extending the range of CiLV-C hosts to a member of the family Brassicaceae, the use of A. thaliana in further studies will provide the opportunity for uncovering mechanisms involved in host-virus interaction.
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