A pathogenic long noncoding RNA redesigns the epigenetic landscape of the infected cells by subverting host Histone Deacetylase 6 activity
© 2016 The Authors. New Phytologist © 2016 New Phytologist Trust.
| Veröffentlicht in: | The New phytologist. - 1979. - 211(2016), 4 vom: 26. Sept., Seite 1311-22 |
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| Format: | Online-Aufsatz |
| Sprache: | English |
| Veröffentlicht: |
2016
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| Zugriff auf das übergeordnete Werk: | The New phytologist |
| Schlagworte: | Journal Article DNA methylation epigenetic plant response to infections viroid-host interaction viroid-induced pathogenesis viroid-protein interactions Nuclear Proteins RNA, Long Noncoding RNA, Ribosomal RNA, Viral mehr... |
| Zusammenfassung: | © 2016 The Authors. New Phytologist © 2016 New Phytologist Trust. Viroids - ancient plant-pathogenic long noncoding RNAs - have developed a singular evolutionary strategy based on reprogramming specific phases of host-metabolism to ensure that their infection cycle can be completed in infected cells. However, the molecular aspects governing this transregulatory phenomenon remain elusive. Here, we use immunoprecipitation assays and bisulfite sequencing of rDNA to shown that, in infected cucumber and Nicotiana benthamina plants, Hop stunt viroid (HSVd) recruits and functionally subverts Histone Deacetylase 6 (HDA6) to promote host-epigenetic alterations that trigger the transcriptional alterations observed during viroid pathogenesis. This notion is supported by the demonstration that, during infection, the HSVd-HDA6 complex occurs in vivo and that endogenous HDA6 expression is increased in HSVd-infected cells. Moreover, transient overexpression of recombinant HDA6 reverts the hypomethylation status of rDNA observed in HSVd-infected plants and reduces viroid accumulation. We hypothesize that the host-transcriptional alterations induced as a consequence of viroid-mediated HDA6 recruitment favor spurious recognition of HSVd-RNA as an RNA Pol II template, thereby improving viroid replication. Our results constitute the first description of a physical and functional interaction between a pathogenic RNA and a component of the host RNA silencing mechanism, providing novel evidence of the potential of these pathogenic lncRNAs to physically redesign the host-cell environment and reprogram their regulatory mechanisms |
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| Beschreibung: | Date Completed 26.01.2018 Date Revised 13.12.2023 published: Print-Electronic GENBANK: AJ311872, XM_004138046.2, XM_004147305.2, XM_004168847.1 Citation Status MEDLINE |
| ISSN: | 1469-8137 |
| DOI: | 10.1111/nph.14001 |