Co-Authors:
Ayllón, M.A., Inst. Valenciano Invest. Agrarias, Apdo. Oficial, Moncada, Valencia, Spain
Löpez, C., Inst. Biol. Molec. Cel. Plantas, Univ. Politécnica de Valencia, Camino de Vera 14, 46022 Valencia, Spain
Navas-Castillo, J., Inst. Valenciano Invest. Agrarias, Apdo. Oficial, Moncada, Valencia, Spain, Estac. Experimental La Mayora, CSIC, Algarrobo-Costa, Málaga, Spain
Mawassi, M., Citrus Research and Education Center, IFAS, University of Florida, 700 Experiment Station Road, Lake Alfred, FL 33850, United States
Dawson, W.O., Citrus Research and Education Center, IFAS, University of Florida, 700 Experiment Station Road, Lake Alfred, FL 33850, United States
Guerri, J., Inst. Valenciano Invest. Agrarias, Apdo. Oficial, Moncada, Valencia, Spain
Flores, R., Inst. Biol. Molec. Cel. Plantas, Univ. Politécnica de Valencia, Camino de Vera 14, 46022 Valencia, Spain
Moreno, P., Inst. Valenciano Invest. Agrarias, Apdo. Oficial, Moncada, Valencia, Spain
Abstract:
Defective RNAs (D-RNAs) ranging in size from 1968 to 2759 nt were detected in four citrus tristeza virus (CTV) isolates by hybridization of electroblotted dsRNAs with two probes specific for the 5'- and 3'-terminal genomic regions. The RNAs that hybridized with both probes were eluted, cloned and sequenced. Comparison with the sequences of the corresponding genomic regions of the helper virus showed, in all cases, over 99% nucleotide identity and direct repeats of 4-5 nt flanking or in the vicinity of the junction sites. The presence of the repeats from two separate genome locations suggests a replicase-driven template switching mechanism for the generation of these CTV D-RNAs. Two of the CTV isolates that differed greatly in their pathogenicity contained an identical D-RNA, suggesting that it is unlikely that this D-RNA is involved in symptom modulation, which may be caused by another factor.
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