|Yokomi, Raymond - Ray|
Submitted to: Journal of Plant Pathology
Publication Type: Abstract only
Publication Acceptance Date: 10/22/2010
Publication Date: 4/10/2011
Citation: Saponari, M., Doddapaneni, H., Loconsole, G., Giampetruzzi, A., Saldarelli, P., Yokomi, R.K. 2011. Profiling of the small RNA populations derived from sour orange seedlings cross-protected against seedling yellows strains of Citrus tristeza virus. Journal of Plant Pathology. 92(4):S4.71-105. Interpretive Summary:
Technical Abstract: Control of Citrus tristeza virus (CTV) in central California changed in 2009 from removal of all CTV-infected trees to only those which react positive in tests with selective probes for potentially severe CTV strains. Therefore, new strategies for CTV control are needed. Greenhouse tests have shown amelioration of severe symptoms of CTV when mixed with a mild strain of the virus. Small RNA profiling using high-throughput sequencing was used to examine the basis of mild-strain cross protection. Small RNA fractions from a symptomless sour orange seedling (SO) infected with a mixture of T3, VT and non-standard genotypes of CTV (Treatment S2) vs. SO infected the VT genotype which induced severe seedling yellows (Treatment S1), were sequenced by Illumina Genome Analyzer II. The 21-24 nucleotide size classes dominated both libraries. BLASTN search and a de novo assembly in the S2 treatment showed presence of the three different CTV genotypes as well as Citrus tatterleaf virus and citrus viroids. The S1 treatment, derived from a VT3 genotype CTV strain, yielded sequences of only the CTV-VT component. Both libraries contained predominant small RNAs associated with three gene silencing suppressors of CTV; significant accumulation of P20 and P23 was observed. The most abundant host-derived small RNA was from the Ctv resistance gene locus and derived from the Gipsy-like retrotransposone C. Comparative bioinformatics analyses are being conducted to correlate small RNA profiles with disease phenotypes. The outcome of this research will lead to identification of host genes involved in CTV disease expression. Once known, these genes can be targets of new therapeutics to control CTV.