Mostrar el registro sencillo del ítem
dc.contributor.author | Lalic, Jasna | es_ES |
dc.contributor.author | Elena Fito, Santiago Fco | es_ES |
dc.date.accessioned | 2016-10-31T12:38:33Z | |
dc.date.available | 2016-10-31T12:38:33Z | |
dc.date.issued | 2012-08 | |
dc.identifier.issn | 0018-067X | |
dc.identifier.uri | http://hdl.handle.net/10251/72998 | |
dc.description.abstract | How epistatic interactions between mutations determine the genetic architecture of fitness is of central importance in evolution. The study of epistasis is particularly interesting for RNA viruses because of their genomic compactness, lack of genetic redundancy, and apparent low complexity. Moreover, interactions between mutations in viral genomes determine traits such as resistance to antiviral drugs, virulence and host range. In this study we generated 53 Tobacco etch potyvirus genotypes carrying pairs of single-nucleotide substitutions and measured their separated and combined deleterious fitness effects. We found that up to 38% of pairs had significant epistasis for fitness, including both positive and negative deviations from the null hypothesis of multiplicative effects. Interestingly, the sign of epistasis was correlated with viral protein-protein interactions in a model network, being predominantly positive between linked pairs of proteins and negative between unlinked ones. Furthermore, 55% of significant interactions were cases of reciprocal sign epistasis (RSE), indicating that adaptive landscapes for RNA viruses maybe highly rugged. Finally, we found that the magnitude of epistasis correlated negatively with the average effect of mutations. Overall, our results are in good agreement to those previously reported for other viruses and further consolidate the view that positive epistasis is the norm for small and compact genomes that lack genetic robustness. Heredity (2012) 109, 71-77; doi: 10.1038/hdy.2012.15; published online 11 April 2012 | es_ES |
dc.description.sponsorship | We thank Francisca de la Iglesia and Angels Prosper for their excellent technical assistance, Stephanie Bedhomme and Mark P Zwart for the discussion and Mario A Fares for statistical advice. Jose A Daros generously gifted us the pMTEV plasmid. This research was supported by the Spanish Ministry of Science and Innovation grant BFU2009-06993 to SFE. JL was supported by the JAE program from CSIC. | en_EN |
dc.language | Inglés | es_ES |
dc.publisher | Nature Publishing Group | es_ES |
dc.relation.ispartof | Heredity | es_ES |
dc.rights | Reserva de todos los derechos | es_ES |
dc.subject | Epistasis | es_ES |
dc.subject | Fitness landscapes | es_ES |
dc.subject | Genome architecture | es_ES |
dc.subject | Virus evolution | es_ES |
dc.title | Magnitude and sign epistasis among deleterious mutations in a positive-sense plant RNA virus | es_ES |
dc.type | Artículo | es_ES |
dc.identifier.doi | 10.1038/hdy.2012.15 | |
dc.relation.projectID | info:eu-repo/grantAgreement/MICINN//BFU2009-06993/ES/Biologia Evolutiva Y De Sistemas De La Emergencia De Fitovirus De Rna/ | es_ES |
dc.rights.accessRights | Cerrado | es_ES |
dc.contributor.affiliation | Universitat Politècnica de València. Instituto Universitario Mixto de Biología Molecular y Celular de Plantas - Institut Universitari Mixt de Biologia Molecular i Cel·lular de Plantes | es_ES |
dc.description.bibliographicCitation | Lalic, J.; Elena Fito, SF. (2012). Magnitude and sign epistasis among deleterious mutations in a positive-sense plant RNA virus. Heredity. 109(2):71-77. https://doi.org/10.1038/hdy.2012.15 | es_ES |
dc.description.accrualMethod | S | es_ES |
dc.relation.publisherversion | http://dx.doi.org/10.1038/hdy.2012.15 | es_ES |
dc.description.upvformatpinicio | 71 | es_ES |
dc.description.upvformatpfin | 77 | es_ES |
dc.type.version | info:eu-repo/semantics/publishedVersion | es_ES |
dc.description.volume | 109 | es_ES |
dc.description.issue | 2 | es_ES |
dc.relation.senia | 232201 | es_ES |
dc.contributor.funder | Ministerio de Ciencia e Innovación | es_ES |
dc.contributor.funder | Consejo Superior de Investigaciones Científicas | es_ES |
dc.description.references | Bagheri HC, Wagner GP (2004). Evolution of dominance in metabolic pathways. Genetics 168: 1716–1735. | es_ES |
dc.description.references | Bedoya LC, Daròs JA (2010). Stability of Tobacco etch virus infectious clones in plasmid vectors. Virus Res 149: 234–240. | es_ES |
dc.description.references | Bershtein S, Segal M, Bekerman R, Tokuriki N, Tawfik DS (2006). Robustness-epistasis link shapes the fitness landscape of a randomly drifting protein. Nature 444: 929–932. | es_ES |
dc.description.references | Betancourt AJ (2010). Lack of evidence for sign epistasis between beneficial mutations in an RNA bacteriophage. J Mol Evol 71: 437–443. | es_ES |
dc.description.references | Bonhoeffer S, Chappey C, Parkin NT, Whitcomb JM, Petropoulos CJ (2004). Evidence for positive epistasis in HIV-1. Science 306: 1547–1550. | es_ES |
dc.description.references | Burch CL, Chao L (2004). Epistasis and its relationship to canalization in the RNA virus φ6. Genetics 167: 559–567. | es_ES |
dc.description.references | Carrasco P, Daròs JA, Agudelo-Romero P, Elena SF (2007a). A real-time RT-PCR assay for quantifying the fitness of Tobacco etch virus in competition experiments. J Virol Meth 139: 181–188. | es_ES |
dc.description.references | Carrasco P, de la Iglesia F, Elena SF (2007b). Distribution of fitness and virulence effects caused by single-nucleotide substitutions in Tobacco etch virus. J Virol 81: 12979–12984. | es_ES |
dc.description.references | Cong M, Heneine W, García-Lerma JG (2007). The fitness cost of mutations associated with Human immunodeficiency virus type 1 drug resistance is modulated by mutational interactions. J Virol 81: 3037–3041. | es_ES |
dc.description.references | Coyne JA (1992). Genetics and speciation. Nature 355: 511–515. | es_ES |
dc.description.references | Crow JF, Kimura M (1970) An Introduction to Population Genetics Theory. Harper and Row New York. | es_ES |
dc.description.references | Da Silva J, Coetzer M, Nedellec R, Pastore C, Mosier DE (2010). Fitness epistasis and constraints on adaptation in a Human immunodeficiency virus type 1 protein region. Genetics 185: 293–303. | es_ES |
dc.description.references | Desai MM, Weissman D, Feldman MW (2007). Evolution can favor antagonistic epistasis. Genetics 177: 1001–1010. | es_ES |
dc.description.references | De la Iglesia F, Elena SF (2007). Fitness declines in Tobacco etch virus upon serial bottleneck transfers. J Virol 81: 4941–4947. | es_ES |
dc.description.references | De Visser JAGM, Elena SF (2007). The evolution of sex: empirical insights into the roles of epistasis and drift. Nat Rev Genet 8: 139–149. | es_ES |
dc.description.references | De Visser JAGM, Hermisson J, Wagner GP, Ancel-Meyers L, Bagheri-Chaichian H, Blanchard JL et al. (2003). Perspective: Evolution and detection of genetic robustness. Evolution 57: 1959–1972. | es_ES |
dc.description.references | De Visser JAGM, Cooper TF, Elena SF (2011). The causes of epistasis. Proc R Soc B 10: 3617–3624. | es_ES |
dc.description.references | Edlund JA, Adami C (2004). Evolution of robustness in digital organisms. Artif Life 10: 167–179. | es_ES |
dc.description.references | Elena SF (1999). Little evidence for synergism among deleterious mutations in a nonsegmented RNA virus. J Mol Evol 49: 703–707. | es_ES |
dc.description.references | Elena SF, Solé RV, Sardanyés J (2010). Simple genomes, complex interactions: epistasis in RNA virus. Chaos 20: 026106. | es_ES |
dc.description.references | Franke J, Klözer A, de Visser JAGM, Krug J (2011). Evolutionary accessibility of mutational pathways. PLoS Comp Biol 7: e1002134. | es_ES |
dc.description.references | Killcoyne S, Carter GW, Smith J, Boyle J (2009). Cytoscape: a community-based framework for network modeling. Meth Mol Biol 563: 219–239. | es_ES |
dc.description.references | Kondrashov AS (1994). Muller’s ratchet under epistatic selection. Genetics 136: 1469–1473. | es_ES |
dc.description.references | Kondrashov AS, Crow JF (1991). Haploidy or diploidy: which is better. Nature 351: 314–315. | es_ES |
dc.description.references | Kondrashov FA, Kondrashov AS (2001). Multidimensional epistasis and the disadvantage of sex. Proc Natl Acad Sci USA 98: 12089–12092. | es_ES |
dc.description.references | Kouyos RD, Silander OK, Bonhoeffer S (2007). Epistasis between deleterious mutations and the evolution of recombination. Trends Ecol Evol 6: 308–315. | es_ES |
dc.description.references | Kvitek DJ, Sherlock G (2011). Reciprocal sign epistasis between frequently experimentally evolved adaptive mutations causes a rugged fitness landscape. PLoS Genet 7: e1002056. | es_ES |
dc.description.references | Macía J, Solé RV, Elena SF (2012). The causes of epistasis in genetic networks. Evolution 66: 586–596. | es_ES |
dc.description.references | Maisnier-Patin S, Berg OG, Lijas L, Andersson DI (2002). Compensatory adaptation to the deleterious effect of antibiotic resistance in Salmonella typhimurium. Mol Microbiol 46: 355–366. | es_ES |
dc.description.references | Martínez JP, Bocharov G, Ignatovich A, Reiter J, Dittmar MT, Wain-Hobson S et al. (2011). Fitness ranking of individual mutants drives patterns of epistatic interactions in HIV-1. PLoS ONE 6: e18375. | es_ES |
dc.description.references | Martínez-Picado J, Martínez MA (2009). HIV-1 reverse transcriptase inhibitor resistance mutations and fitness: a view from the clinic and ex vivo. Virus Res 134: 104–123. | es_ES |
dc.description.references | Molla A, Korneyeve M, Gao Q, Vasavanonda S, Schipper PJ, Mo HM et al. (1996). Ordered accumulation of mutations in HIV protease confers resistance to ritonavir. Nat Med 2: 760–766. | es_ES |
dc.description.references | Parera M, Pérez-Álvarez N, Clotet B, Martínez MA (2009). Epistasis among deleterious mutations in the HIV-1 protease. J Mol Biol 392: 243–250. | es_ES |
dc.description.references | Pepin KM, Wichman HA (2007). Variable epistatic effects between mutations at host recognition sites in φX174. Evolution 67: 1710–1724. | es_ES |
dc.description.references | Pfaffl MV (2004). Quantification strategies in real-time PCR. In Bustin SA ed A-Z of Quantitative PCR, International University Line. La Jolla USA. pp 87–112. | es_ES |
dc.description.references | Phillips PC (2008). Epistasis – the essential role of gene interactions in the structure and evolution of genetic systems. Nat Rev Genet 9: 855–867. | es_ES |
dc.description.references | Poelwijk FJ, Kiviet DJ, Weinreich DM, Tans SJ (2007). Empirical fitness landscapes reveal accessible evolutionary paths. Nature 445: 383–386. | es_ES |
dc.description.references | Poelwijk FJ, Tanase-Nicola S, Kiviet DJ, Tans SJ (2011). Reciprocal sign epistasis is a necessary condition for multi-peaked fitness landscapes. J Theor Biol 272: 141–144. | es_ES |
dc.description.references | Poon AFY, Chao L (2006). Functional origins of fitness effect-sizes of compensatory mutations in the DNA bacteriophage φX174. Evolution 60: 2032–2043. | es_ES |
dc.description.references | Proulx SR, Phillips PC (2005). The opportunity for canalization and the evolution of genetic networks. Am Nat 165: 147–162. | es_ES |
dc.description.references | Remold SK, Lenski RE (2004). Pervasive joint influence of epistasis and plasticity on mutational effects in Escherichia coli. Nat Genet 36: 423 426. | es_ES |
dc.description.references | Rice WR (1989). Analyzing tables of statistical tests. Evolution 43: 223–225. | es_ES |
dc.description.references | Rodrigo G, Carrera J, Ruiz-Ferrer V, Del Toro FJ, Llave C, Voinnet O et al. (2011). Characterization of the Arabidopsis thaliana interactome targeted by viruses. Santa Fe Institute Working Paper 11-10-049. | es_ES |
dc.description.references | Rokyta DR, Joyce P, Caudle B, Miller C, Beisel CJ, Wichman HA (2011). Epistasis between beneficial mutations and the phenotype-to-fitness map for a ssDNA virus. PLoS Genet 7: e1002075. | es_ES |
dc.description.references | Salverda MLM, Dellus E, Gorter FA, Debets AJM, Van der Oost J, Hoekstra RF et al. (2011). Initial mutations direct alternative pathways of protein evolution. PLoS Genet 7: e1001321. | es_ES |
dc.description.references | Sanjuán R (2006). Quantifying antagonistic epistasis in a multifunctional RNA secondary structure of the Rous sarcoma virus. J Gen Virol 87: 1595–1602. | es_ES |
dc.description.references | Sanjuán R, Elena SF (2006). Epistasis correlates to genomic complexity. Proc Natl Acad Sci USA 103: 14402–14405. | es_ES |
dc.description.references | Sanjuán R, Forment J, Elena SF (2006). In silico predicted robustness of viroids RNA secondary structure. II. Interaction between mutation pairs. Mol Biol Evol 23: 2123–2130. | es_ES |
dc.description.references | Sanjuán R, Moya A, Elena SF (2004). The contribution of epistasis to the architecture of fitness in an RNA virus. Proc Natl Acad Sci USA 101: 15376–15379. | es_ES |
dc.description.references | Sanjuán R, Nebot MR (2008). A network model for the correlation between epistasis and genomic complexity. PLoS ONE 3: e2663. | es_ES |
dc.description.references | Schrag SJ, Perrot V, Levin BR (1997). Adaptation to the fitness cost of antibiotic resistance in E. coli. Proc R Soc B 264: 1287–1291. | es_ES |
dc.description.references | Van Opijnen T, Boerlijst MC, Berkhout B (2006). Effects of random mutations in the Human immunodeficiency virus type 1 transcriptional promoter on viral fitness in different host cell environments. J Virol 80: 6678–6685. | es_ES |
dc.description.references | Weinreich DM (2005). The rank ordering of genotypic fitness values predicts genetic constraints on natural selection on landscapes lacking sign epistasis. Genetics 171: 1397–1405. | es_ES |
dc.description.references | Weinreich DM, Delaney NF, DePristo MA, Hartl DL (2006). Darwinian evolution can follow only very few mutational paths to fitter proteins. Science 312: 111–114. | es_ES |
dc.description.references | Weinreich DM, Watson RA, Chao L (2005). Perspective: sign epistasis and genetic constraint on evolutionary trajectories. Evolution 59: 1165–1174. | es_ES |
dc.description.references | Welch JJ, Waxman D (2005). The nk model and population genetics. J Theor Biol 234: 329–340. | es_ES |
dc.description.references | Wilke CO, Adami C (2001). Interaction between directional epistasis and average mutational effects. Proc R Soc B 298: 1469–1474. | es_ES |
dc.description.references | Wilke CO, Lenski RE, Adami C (2003). Compensatory mutations cause excess of antagonistic epistasis in RNA secondary structure folding. BMC Evol Biol 3: 1–14. | es_ES |
dc.description.references | Withlock MC, Phillips PC, Moore FBG, Tonsor SJ (1995). Multiple fitness peaks and epistasis. Annu Rev Ecol Evol Syst 26: 601–629. | es_ES |
dc.description.references | You L, Yin J (2002). Dependence of epistasis on environment and mutation severity as revealed by in silico mutagenesis of phage T7. Genetics 160: 1273–1281. | es_ES |