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Post by gabriela on Nov 16, 2015 12:07:12 GMT -6
1) Please discuss the critical genome evolutionary models:
The potyviruses evolved between 6,600 to 7,250 years ago. They appear to have evolved in southwest Eurasia or North Africa. The estimated mutation rate is about 1.15×10−4 nucleotide substitutions/site/year. The virion is non-enveloped with a flexuous and filamentous nucleocapsid. The genome is a linear positive sense ssRNA ranging in size from 9000–12000 bases/nucleotides. Most potyviruses have non-segmented genomes, however some species are bipartite. In the species with a single genome, at the 5' end Vg protein is present and it encodes a single ORF expressed as a polyprotein. This is processed into seven smaller proteins: P1, helper component (HC), P3, cylindrical inclusion (CI), nuclear inclusion A (NIa), nuclear inclusion B (NIb), capsid protein (CP) and two small putative proteins known as 6K1 and 6K2. The P3 cistron also encodes a second protein—P3N-PIPO—which is generated by a +2 frameshift.
CP gene has a variable N terminal part that is often repetitive and seems to have evolved by replicase slippage in salutatory way. The remainder of the CP (C- terminal regions) has no unusual sequences of this sort, and seems to have evolved coherently and only by: point mutations, indels and occasional homologous recombination. RNA- RNA recombination is one of the major factors responsible for the mergence, often dangerous viral strains or species. The process of joining two or more noncontiguous RNA fragments together can operate in the same viral RNA genome, among different viral RNAs, or even between viral and host RNAs. In RNA recombination, recombinants are formed during the replication of a viral genome. Virus- encoded RdRp initiates nascent strand synthesis at 3’ end of RNA donor. If RdRp is paused during the elongation, a replicase nascent complex can dissociate from the donor template and re-associate with another template, RNA acceptor. The replicase resumes nascent strand synthesis on the acceptor template. The frequency of this process to occur depends on mechanistic and/or ecological factors.
Potyviruses also have its own “hotspots” for recombination in CP. Studies have showed “crossovers” at the CP ORF and 3 UTR sequences in Potato virus Y (PVY), Bean common mosaic virus (BCMV), Sweet potato feathery mottle virus (SPFMV), bean yellow mosaic virus (BYMV) Plum pox virus (PPV).
2) How do these models inform us about host range, genetic drift?
This model is informing us that potyviruses have the ability of rapid evolution and adaptation. This RNA recombination model favors the potyvirus group in the creation of variants best adapted to withstand environmental selective pressure, leading in some instance to the establishment of a new taxa. This model is also telling us that the choice of the host system could affect their frequency of the detection of recombinants.
3) How can this information be used to develop control strategies for disease.
Some resistance, derived from various plant species (e.g. closely related to peppers), is currently available and efforts are under way to develop more resistant varieties. In general, sources of genetic resistance in bell types is greater for Potato Y potyvirus, followed by Tobacco etch potyvirus, followed by Pepper mottle potyvirus. As well, this information can be used for the development of detection methods, by the use of two different approaches, for example 1) searching for the recombinants in natural viral populations or new viral strains in vitro, and 2) computational tools using recombination footprints.
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Post by dulanjani on Nov 18, 2015 20:34:36 GMT -6
1) Please discuss the critical genome evolutionary models:The potyviruses evolved between 6,600 to 7,250 years ago. They appear to have evolved in southwest Eurasia or North Africa. The estimated mutation rate is about 1.15×10−4 nucleotide substitutions/site/year. The virion is non-enveloped with a flexuous and filamentous nucleocapsid. The genome is a linear positive sense ssRNA ranging in size from 9000–12000 bases/nucleotides. Most potyviruses have non-segmented genomes, however some species are bipartite. In the species with a single genome, at the 5' end Vg protein is present and it encodes a single ORF expressed as a polyprotein. This is processed into seven smaller proteins: P1, helper component (HC), P3, cylindrical inclusion (CI), nuclear inclusion A (NIa), nuclear inclusion B (NIb), capsid protein (CP) and two small putative proteins known as 6K1 and 6K2. The P3 cistron also encodes a second protein—P3N-PIPO—which is generated by a +2 frameshift. CP gene has a variable N terminal part that is often repetitive and seems to have evolved by replicase slippage in salutatory way. The remainder of the CP (C- terminal regions) has no unusual sequences of this sort, and seems to have evolved coherently and only by: point mutations, indels and occasional homologous recombination. RNA- RNA recombination is one of the major factors responsible for the mergence, often dangerous viral strains or species. The process of joining two or more noncontiguous RNA fragments together can operate in the same viral RNA genome, among different viral RNAs, or even between viral and host RNAs. In RNA recombination, recombinants are formed during the replication of a viral genome. Virus- encoded RdRp initiates nascent strand synthesis at 3’ end of RNA donor. If RdRp is paused during the elongation, a replicase nascent complex can dissociate from the donor template and re-associate with another template, RNA acceptor. The replicase resumes nascent strand synthesis on the acceptor template. The frequency of this process to occur depends on mechanistic and/or ecological factors. Potyviruses also have its own “hotspots” for recombination in CP. Studies have showed “crossovers” at the CP ORF and 3 UTR sequences in Potato virus Y (PVY), Bean common mosaic virus (BCMV), Sweet potato feathery mottle virus (SPFMV), bean yellow mosaic virus (BYMV) Plum pox virus (PPV).
2) How do these models inform us about host range, genetic drift? This model is informing us that potyviruses have the ability of rapid evolution and adaptation. This RNA recombination model favors the potyvirus group in the creation of variants best adapted to withstand environmental selective pressure, leading in some instance to the establishment of a new taxa. This model is also telling us that the choice of the host system could affect their frequency of the detection of recombinants.
3) How can this information be used to develop control strategies for disease. Some resistance, derived from various plant species (e.g. closely related to peppers), is currently available and efforts are under way to develop more resistant varieties. In general, sources of genetic resistance in bell types is greater for Potato Y potyvirus, followed by Tobacco etch potyvirus, followed by Pepper mottle potyvirus. As well, this information can be used for the development of detection methods, by the use of two different approaches, for example 1) searching for the recombinants in natural viral populations or new viral strains in vitro, and 2) computational tools using recombination footprints. Thank ypou for the infromation Gaby Do you know anything about evolutionary force between rapidly evolving potyviral populations? What makes them to have RNA recombination and develop heterogenic populations? Could it be due to environmental selective force or random genetic drift? |
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Post by ravendra on Nov 21, 2015 13:43:01 GMT -6
1) Please discuss the critical genome evolutionary models:The potyviruses evolved between 6,600 to 7,250 years ago. They appear to have evolved in southwest Eurasia or North Africa. The estimated mutation rate is about 1.15×10−4 nucleotide substitutions/site/year. The virion is non-enveloped with a flexuous and filamentous nucleocapsid. The genome is a linear positive sense ssRNA ranging in size from 9000–12000 bases/nucleotides. Most potyviruses have non-segmented genomes, however some species are bipartite. In the species with a single genome, at the 5' end Vg protein is present and it encodes a single ORF expressed as a polyprotein. This is processed into seven smaller proteins: P1, helper component (HC), P3, cylindrical inclusion (CI), nuclear inclusion A (NIa), nuclear inclusion B (NIb), capsid protein (CP) and two small putative proteins known as 6K1 and 6K2. The P3 cistron also encodes a second protein—P3N-PIPO—which is generated by a +2 frameshift. CP gene has a variable N terminal part that is often repetitive and seems to have evolved by replicase slippage in salutatory way. The remainder of the CP (C- terminal regions) has no unusual sequences of this sort, and seems to have evolved coherently and only by: point mutations, indels and occasional homologous recombination. RNA- RNA recombination is one of the major factors responsible for the mergence, often dangerous viral strains or species. The process of joining two or more noncontiguous RNA fragments together can operate in the same viral RNA genome, among different viral RNAs, or even between viral and host RNAs. In RNA recombination, recombinants are formed during the replication of a viral genome. Virus- encoded RdRp initiates nascent strand synthesis at 3’ end of RNA donor. If RdRp is paused during the elongation, a replicase nascent complex can dissociate from the donor template and re-associate with another template, RNA acceptor. The replicase resumes nascent strand synthesis on the acceptor template. The frequency of this process to occur depends on mechanistic and/or ecological factors. Potyviruses also have its own “hotspots” for recombination in CP. Studies have showed “crossovers” at the CP ORF and 3 UTR sequences in Potato virus Y (PVY), Bean common mosaic virus (BCMV), Sweet potato feathery mottle virus (SPFMV), bean yellow mosaic virus (BYMV) Plum pox virus (PPV).
2) How do these models inform us about host range, genetic drift? This model is informing us that potyviruses have the ability of rapid evolution and adaptation. This RNA recombination model favors the potyvirus group in the creation of variants best adapted to withstand environmental selective pressure, leading in some instance to the establishment of a new taxa. This model is also telling us that the choice of the host system could affect their frequency of the detection of recombinants.
3) How can this information be used to develop control strategies for disease. Some resistance, derived from various plant species (e.g. closely related to peppers), is currently available and efforts are under way to develop more resistant varieties. In general, sources of genetic resistance in bell types is greater for Potato Y potyvirus, followed by Tobacco etch potyvirus, followed by Pepper mottle potyvirus. As well, this information can be used for the development of detection methods, by the use of two different approaches, for example 1) searching for the recombinants in natural viral populations or new viral strains in vitro, and 2) computational tools using recombination footprints. Hi Gabriela, Thank you for the information on potyviruses. It interests me more because I work with potyviruses. I have two questions- 1. You mentioned about "searching for the recombinants in natural viral populations", my question is 'what would be the most appropriate and practical way to meet this goal? Any reports or publicatipns on this? 2. Which computational tools and methods do you think are the best to meet the objectives of developing disease control strategies against potyviruses (as you mentioned)? Thank you!
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Post by gabriela on Nov 22, 2015 20:10:12 GMT -6
1) Please discuss the critical genome evolutionary models:The potyviruses evolved between 6,600 to 7,250 years ago. They appear to have evolved in southwest Eurasia or North Africa. The estimated mutation rate is about 1.15×10−4 nucleotide substitutions/site/year. The virion is non-enveloped with a flexuous and filamentous nucleocapsid. The genome is a linear positive sense ssRNA ranging in size from 9000–12000 bases/nucleotides. Most potyviruses have non-segmented genomes, however some species are bipartite. In the species with a single genome, at the 5' end Vg protein is present and it encodes a single ORF expressed as a polyprotein. This is processed into seven smaller proteins: P1, helper component (HC), P3, cylindrical inclusion (CI), nuclear inclusion A (NIa), nuclear inclusion B (NIb), capsid protein (CP) and two small putative proteins known as 6K1 and 6K2. The P3 cistron also encodes a second protein—P3N-PIPO—which is generated by a +2 frameshift. CP gene has a variable N terminal part that is often repetitive and seems to have evolved by replicase slippage in salutatory way. The remainder of the CP (C- terminal regions) has no unusual sequences of this sort, and seems to have evolved coherently and only by: point mutations, indels and occasional homologous recombination. RNA- RNA recombination is one of the major factors responsible for the mergence, often dangerous viral strains or species. The process of joining two or more noncontiguous RNA fragments together can operate in the same viral RNA genome, among different viral RNAs, or even between viral and host RNAs. In RNA recombination, recombinants are formed during the replication of a viral genome. Virus- encoded RdRp initiates nascent strand synthesis at 3’ end of RNA donor. If RdRp is paused during the elongation, a replicase nascent complex can dissociate from the donor template and re-associate with another template, RNA acceptor. The replicase resumes nascent strand synthesis on the acceptor template. The frequency of this process to occur depends on mechanistic and/or ecological factors. Potyviruses also have its own “hotspots” for recombination in CP. Studies have showed “crossovers” at the CP ORF and 3 UTR sequences in Potato virus Y (PVY), Bean common mosaic virus (BCMV), Sweet potato feathery mottle virus (SPFMV), bean yellow mosaic virus (BYMV) Plum pox virus (PPV).
2) How do these models inform us about host range, genetic drift? This model is informing us that potyviruses have the ability of rapid evolution and adaptation. This RNA recombination model favors the potyvirus group in the creation of variants best adapted to withstand environmental selective pressure, leading in some instance to the establishment of a new taxa. This model is also telling us that the choice of the host system could affect their frequency of the detection of recombinants.
3) How can this information be used to develop control strategies for disease. Some resistance, derived from various plant species (e.g. closely related to peppers), is currently available and efforts are under way to develop more resistant varieties. In general, sources of genetic resistance in bell types is greater for Potato Y potyvirus, followed by Tobacco etch potyvirus, followed by Pepper mottle potyvirus. As well, this information can be used for the development of detection methods, by the use of two different approaches, for example 1) searching for the recombinants in natural viral populations or new viral strains in vitro, and 2) computational tools using recombination footprints. Thank ypou for the infromation Gaby Do you know anything about evolutionary force between rapidly evolving potyviral populations? What makes them to have RNA recombination and develop heterogenic populations? Could it be due to environmental selective force or random genetic drift? that is actually a really good point  Seems unlikely that recombination has evolved as a means by which RNA viruses can purge deleterious mutations. Rather, the population sizes of RNA viruses may be so large that sufficient viable progeny are produced every generation to guarantee survival. In addition, large population sizes mean that the accumulation of deleterious mutations can be offset by frequent back and compensatory mutations. RNA viruses may therefore possess a population-scale robustness that protects them from the accumulation of deleterious mutations. Is important to note that with recombination there is also evolutionary costs associated with recombination in RNA viruses, as it is likely to increase both the degree of competition within a host and the extent of complementation. |
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Post by gabriela on Nov 22, 2015 20:46:29 GMT -6
1) Please discuss the critical genome evolutionary models:The potyviruses evolved between 6,600 to 7,250 years ago. They appear to have evolved in southwest Eurasia or North Africa. The estimated mutation rate is about 1.15×10−4 nucleotide substitutions/site/year. The virion is non-enveloped with a flexuous and filamentous nucleocapsid. The genome is a linear positive sense ssRNA ranging in size from 9000–12000 bases/nucleotides. Most potyviruses have non-segmented genomes, however some species are bipartite. In the species with a single genome, at the 5' end Vg protein is present and it encodes a single ORF expressed as a polyprotein. This is processed into seven smaller proteins: P1, helper component (HC), P3, cylindrical inclusion (CI), nuclear inclusion A (NIa), nuclear inclusion B (NIb), capsid protein (CP) and two small putative proteins known as 6K1 and 6K2. The P3 cistron also encodes a second protein—P3N-PIPO—which is generated by a +2 frameshift. CP gene has a variable N terminal part that is often repetitive and seems to have evolved by replicase slippage in salutatory way. The remainder of the CP (C- terminal regions) has no unusual sequences of this sort, and seems to have evolved coherently and only by: point mutations, indels and occasional homologous recombination. RNA- RNA recombination is one of the major factors responsible for the mergence, often dangerous viral strains or species. The process of joining two or more noncontiguous RNA fragments together can operate in the same viral RNA genome, among different viral RNAs, or even between viral and host RNAs. In RNA recombination, recombinants are formed during the replication of a viral genome. Virus- encoded RdRp initiates nascent strand synthesis at 3’ end of RNA donor. If RdRp is paused during the elongation, a replicase nascent complex can dissociate from the donor template and re-associate with another template, RNA acceptor. The replicase resumes nascent strand synthesis on the acceptor template. The frequency of this process to occur depends on mechanistic and/or ecological factors. Potyviruses also have its own “hotspots” for recombination in CP. Studies have showed “crossovers” at the CP ORF and 3 UTR sequences in Potato virus Y (PVY), Bean common mosaic virus (BCMV), Sweet potato feathery mottle virus (SPFMV), bean yellow mosaic virus (BYMV) Plum pox virus (PPV).
2) How do these models inform us about host range, genetic drift? This model is informing us that potyviruses have the ability of rapid evolution and adaptation. This RNA recombination model favors the potyvirus group in the creation of variants best adapted to withstand environmental selective pressure, leading in some instance to the establishment of a new taxa. This model is also telling us that the choice of the host system could affect their frequency of the detection of recombinants.
3) How can this information be used to develop control strategies for disease. Some resistance, derived from various plant species (e.g. closely related to peppers), is currently available and efforts are under way to develop more resistant varieties. In general, sources of genetic resistance in bell types is greater for Potato Y potyvirus, followed by Tobacco etch potyvirus, followed by Pepper mottle potyvirus. As well, this information can be used for the development of detection methods, by the use of two different approaches, for example 1) searching for the recombinants in natural viral populations or new viral strains in vitro, and 2) computational tools using recombination footprints. Hi Gabriela, Thank you for the information on potyviruses. It interests me more because I work with potyviruses. I have two questions- 1. You mentioned about "searching for the recombinants in natural viral populations", my question is 'what would be the most appropriate and practical way to meet this goal? Any reports or publicatipns on this? 2. Which computational tools and methods do you think are the best to meet the objectives of developing disease control strategies against potyviruses (as you mentioned)? Thank you!
1. The detection of recombination is a challenging task that prompted the development of both in vitro and in vivo experimental systems. In the divided genome of Brome mosaic virus system, both inter- and intrasegmental crossovers are described. Other systems utilize satellite or defective interfering RNAs (DI-RNAs) of Turnip crinkle virus, Tomato bushy stunt virus, Cucumber necrosis virus, and Potato virus X. These assays identified the mechanistic details of the recombination process, revealing the role of RNA structure and proteins in the replicase-mediated copy-choice mechanism. In this paper they described methods applied to searching for the recombinants in natural viral populations, they also described some examples of detection methods of recombined viruses or new viral strains, as well some examples of computational tools for revealing the recombination footprints using in silico panel.I would like to share with you this paper.... maybe it would be useful for your reasearch... RNA-RNA Recombination in Plant Virus Replication and Evolution (PDF Download Available). Available from: www.researchgate.net/publication/51085653_RNA-RNA_Recombination_in_Plant_Virus_Replication_and_Evolution [accessed Nov 22, 2015]. 2. Next generation sequencing is quickly emerging as the go-to tool for plant virologists when sequencing whole virus genomes, and undertaking plant metagenomic studies for new virus discoveries. Next generation sequencing is quickly emerging as the go-to tool for plant virologists when sequencing whole virus genomes, and undertaking plant metagenomic studies for new virus discoveries. |
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Post by omararias on Nov 22, 2015 22:39:52 GMT -6
Nice information, I just have one question regarding the structure of the potyvirus hot spots. Do you know if there is any study showing any recombinationation efficiency when comparing the hot spots in CP ORF vs the 3' UTR sequence ?
Thanks.
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