Artículo
Viral silencing suppressors and cellular proteins partner with plant RRP6-like exoribonucleases
Fecha de publicación:
10/2020
Editorial:
Springer
Revista:
Virus Genes
ISSN:
0920-8569
e-ISSN:
1572-994X
Idioma:
Inglés
Tipo de recurso:
Artículo publicado
Clasificación temática:
Resumen
RNA silencing and RNA decay are functionally interlaced, regulate gene expression and play a pivotal role in antiviral responses. As a counter defensive strategy, many plant and mammalian viruses encode suppressors which interfere with both mechanisms. However, the protein interactions that connect these pathways remain elusive. Previous work reported that RNA silencing suppressors from different potyviruses, together with translation initiation factors EIF(iso)4E, interacted with the C-terminal region of the tobacco exoribonuclease RRP6-Like 2, a component of the RNA decay exosome complex. Here, we investigate whether other viral silencing suppressors and cellular proteins might also bind RRP6-Like exoribonucleases. A candidate search approach based on yeast-two hybrid protein interaction assays showed that three other unrelated viral suppressors, two from plant viruses and one from a mammalian virus, bound the C-terminus of the tobacco RRP6-Like 2, the full-length of the Arabidopsis RRP6L1 protein and its C-terminal region. In addition, RRP6-Like proteins were found to interact with members of the cellular double-stranded RNA binding protein (DRB) family involved in RNA silencing. The C-terminal regions of RRP6L proteins are engaged in homotypic and heterotypic interactions and were predicted to be disordered. Collectively, these results suggest a protein interaction network that connects components of RNA decay and RNA silencing that is targeted by viral silencing suppressors.
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Articulos(IMBIV)
Articulos de INST.MULTIDISCIPL.DE BIOLOGIA VEGETAL (P)
Articulos de INST.MULTIDISCIPL.DE BIOLOGIA VEGETAL (P)
Citación
Freire, Miguel Angel; Viral silencing suppressors and cellular proteins partner with plant RRP6-like exoribonucleases; Springer; Virus Genes; 56; 5; 10-2020; 621-631
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