Resumen:
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[EN] Despite being composed by a single-stranded, circular, non-protein-coding RNA of just 246-401 nucleotides (nt), viroids can incite in their host plants symptoms similar to those caused by DNA and RNA viruses, which ...[+]
[EN] Despite being composed by a single-stranded, circular, non-protein-coding RNA of just 246-401 nucleotides (nt), viroids can incite in their host plants symptoms similar to those caused by DNA and RNA viruses, which have genomes at least 20-fold bigger and encode proteins. On the other hand, certain non-protein-coding plant satellite RNAs display structural similarities with viroids but for replication and transmission they need to parasitize specific helper viruses (modifying concomitantly the symptoms they induce). While phenotypic alterations accompanying infection by viruses may partly result from expressing the proteins they code for, how the non-protein-coding viroids (and satellite RNAs) cause disease remains a conundrum. Initial ideas on viroid pathogenesis focused on a direct interaction of the genomic RNA with host proteins resulting in their malfunction. With the advent of RNA silencing, it was alternatively proposed that symptoms could be produced by viroid-derived small RNAs (vd-sRNAs)-generated by the host defensive machinery-targeting specific host mRNA or DNA sequences for post-transcriptional or transcriptional gene silencing, respectively, a hypothesis that could also explain pathogenesis of non-protein-coding satellite RNAs. Evidence sustaining this view has been circumstantial, but recent data provide support for it in two cases: i) the yellow symptoms associated with a specific satellite RNA result from a 22-nt small RNA (derived from the 24-nt fragment of the satellite genome harboring the pathogenic determinant), which is complementary to a segment of the mRNA of the chlorophyll biosynthetic gene CHL1 and targets it for cleavage by the RNA silencing machinery, and ii) two 21-nt vd-sRNAS containing the pathogenic determinant of the albino phenotype induced by a chloroplast-replicating viroid target for cleavage the mRNA coding for the chloroplastic heat-shock protein 90 via RNA silencing too. This evidence, which is compelling for the satellite RNA, does not exclude alternative mechanisms.
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Código del Proyecto:
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info:eu-repo/grantAgreement/MEF//191%2F2009/
info:eu-repo/grantAgreement/EC/FP6/512092/EU/A European model for bioinformatics research and community education/EMBRACE/
info:eu-repo/grantAgreement/MICINN//BFU2011-28443/ES/VIROIDES: DOMINIOS ESTRUCTURALES, INICIACION DE LA TRANSCRIPCION, INTERACCION CON PROTEINAS ARGONAUTAS DEL HUESPED, Y TASAS DE MUTACION/
info:eu-repo/grantAgreement/MICINN//BFU2008-03154/ES/INTERACCIONES VIROIDE-HUESPED: PAPEL DE LAS RIBOZIMAS, DEL SILENCIAMIENTO MEDIADO POR RNA, Y DE LA RECOMBINACION DE RNA/
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Agradecimientos:
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Work in B.N. and F.D.S. laboratory has been supported by the Dipartimento Agroalimentare of the CNR of Italy (A. Leone and D. Mariotti 2008 award for advanced research in Agriculture) and a dedicated grant of the Ministero ...[+]
Work in B.N. and F.D.S. laboratory has been supported by the Dipartimento Agroalimentare of the CNR of Italy (A. Leone and D. Mariotti 2008 award for advanced research in Agriculture) and a dedicated grant of the Ministero dell'Economia e Finanze Italiano to the CNR (Legge n. 191/2009), in A.G laboratory by the project EMBRACE (European Union FP6 Programme, thematic area 'Life Sciences, Genomics and Biotechnology for Health', contract No. LUNG-CT-2004-512092), and in R.F. laboratory by the Ministerio de Ciencia e Innovacion of Spain (grants BFU2008-03154 and BFU2011-28443).
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