Molecular signatures of silencing suppression degeneracy from a complex RNA virus.

As genomic architectures become more complex, they begin to accumulate degenerate and redundant elements. However, analyses of the molecular mechanisms underlying these genetic architecture features remain scarce, especially in compact but sufficiently complex genomes. In the present study, we follo...

Descripción completa

Guardado en:

Detalles Bibliográficos
Autores principales:	Silvia Ambrós, Neus Gómez-Muñoz, Silvia Giménez-Santamarina, Javier Sánchez-Vicente, Josep Navarro-López, Fernando Martínez, José-Antonio Daròs, Guillermo Rodrigo
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2021
Materias:	Biology (General) QH301-705.5
Acceso en línea:	https://doaj.org/article/9824296705be40929eb35a6f70215df5
Etiquetas:	Agregar Etiqueta Sin Etiquetas, Sea el primero en etiquetar este registro!

id	oai:doaj.org-article:9824296705be40929eb35a6f70215df5
record_format	dspace
spelling	oai:doaj.org-article:9824296705be40929eb35a6f70215df52021-11-25T05:40:34ZMolecular signatures of silencing suppression degeneracy from a complex RNA virus.1553-734X1553-735810.1371/journal.pcbi.1009166https://doaj.org/article/9824296705be40929eb35a6f70215df52021-06-01T00:00:00Zhttps://doi.org/10.1371/journal.pcbi.1009166https://doaj.org/toc/1553-734Xhttps://doaj.org/toc/1553-7358As genomic architectures become more complex, they begin to accumulate degenerate and redundant elements. However, analyses of the molecular mechanisms underlying these genetic architecture features remain scarce, especially in compact but sufficiently complex genomes. In the present study, we followed a proteomic approach together with a computational network analysis to reveal molecular signatures of protein function degeneracy from a plant virus (as virus-host protein-protein interactions). We employed affinity purification coupled to mass spectrometry to detect several host factors interacting with two proteins of Citrus tristeza virus (p20 and p25) that are known to function as RNA silencing suppressors, using an experimental system of transient expression in a model plant. The study was expanded by considering two different isolates of the virus, and some key interactions were confirmed by bimolecular fluorescence complementation assays. We found that p20 and p25 target a common set of plant proteins including chloroplastic proteins and translation factors. Moreover, we noted that even specific targets of each viral protein overlap in function. Notably, we identified argonaute proteins (key players in RNA silencing) as reliable targets of p20. Furthermore, we found that these viral proteins preferentially do not target hubs in the host protein interactome, but elements that can transfer information by bridging different parts of the interactome. Overall, our results demonstrate that two distinct proteins encoded in the same viral genome that overlap in function also overlap in their interactions with the cell proteome, thereby highlighting an overlooked connection from a degenerate viral system.Silvia AmbrósNeus Gómez-MuñozSilvia Giménez-SantamarinaJavier Sánchez-VicenteJosep Navarro-LópezFernando MartínezJosé-Antonio DaròsGuillermo RodrigoPublic Library of Science (PLoS)articleBiology (General)QH301-705.5ENPLoS Computational Biology, Vol 17, Iss 6, p e1009166 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Biology (General) QH301-705.5
spellingShingle	Biology (General) QH301-705.5 Silvia Ambrós Neus Gómez-Muñoz Silvia Giménez-Santamarina Javier Sánchez-Vicente Josep Navarro-López Fernando Martínez José-Antonio Daròs Guillermo Rodrigo Molecular signatures of silencing suppression degeneracy from a complex RNA virus.
description	As genomic architectures become more complex, they begin to accumulate degenerate and redundant elements. However, analyses of the molecular mechanisms underlying these genetic architecture features remain scarce, especially in compact but sufficiently complex genomes. In the present study, we followed a proteomic approach together with a computational network analysis to reveal molecular signatures of protein function degeneracy from a plant virus (as virus-host protein-protein interactions). We employed affinity purification coupled to mass spectrometry to detect several host factors interacting with two proteins of Citrus tristeza virus (p20 and p25) that are known to function as RNA silencing suppressors, using an experimental system of transient expression in a model plant. The study was expanded by considering two different isolates of the virus, and some key interactions were confirmed by bimolecular fluorescence complementation assays. We found that p20 and p25 target a common set of plant proteins including chloroplastic proteins and translation factors. Moreover, we noted that even specific targets of each viral protein overlap in function. Notably, we identified argonaute proteins (key players in RNA silencing) as reliable targets of p20. Furthermore, we found that these viral proteins preferentially do not target hubs in the host protein interactome, but elements that can transfer information by bridging different parts of the interactome. Overall, our results demonstrate that two distinct proteins encoded in the same viral genome that overlap in function also overlap in their interactions with the cell proteome, thereby highlighting an overlooked connection from a degenerate viral system.
format	article
author	Silvia Ambrós Neus Gómez-Muñoz Silvia Giménez-Santamarina Javier Sánchez-Vicente Josep Navarro-López Fernando Martínez José-Antonio Daròs Guillermo Rodrigo
author_facet	Silvia Ambrós Neus Gómez-Muñoz Silvia Giménez-Santamarina Javier Sánchez-Vicente Josep Navarro-López Fernando Martínez José-Antonio Daròs Guillermo Rodrigo
author_sort	Silvia Ambrós
title	Molecular signatures of silencing suppression degeneracy from a complex RNA virus.
title_short	Molecular signatures of silencing suppression degeneracy from a complex RNA virus.
title_full	Molecular signatures of silencing suppression degeneracy from a complex RNA virus.
title_fullStr	Molecular signatures of silencing suppression degeneracy from a complex RNA virus.
title_full_unstemmed	Molecular signatures of silencing suppression degeneracy from a complex RNA virus.
title_sort	molecular signatures of silencing suppression degeneracy from a complex rna virus.
publisher	Public Library of Science (PLoS)
publishDate	2021
url	https://doaj.org/article/9824296705be40929eb35a6f70215df5
work_keys_str_mv	AT silviaambros molecularsignaturesofsilencingsuppressiondegeneracyfromacomplexrnavirus AT neusgomezmunoz molecularsignaturesofsilencingsuppressiondegeneracyfromacomplexrnavirus AT silviagimenezsantamarina molecularsignaturesofsilencingsuppressiondegeneracyfromacomplexrnavirus AT javiersanchezvicente molecularsignaturesofsilencingsuppressiondegeneracyfromacomplexrnavirus AT josepnavarrolopez molecularsignaturesofsilencingsuppressiondegeneracyfromacomplexrnavirus AT fernandomartinez molecularsignaturesofsilencingsuppressiondegeneracyfromacomplexrnavirus AT joseantoniodaros molecularsignaturesofsilencingsuppressiondegeneracyfromacomplexrnavirus AT guillermorodrigo molecularsignaturesofsilencingsuppressiondegeneracyfromacomplexrnavirus
_version_	1718414532509958144

Molecular signatures of silencing suppression degeneracy from a complex RNA virus.

Ejemplares similares