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Post by dulanjani on Nov 16, 2015 1:42:13 GMT -6
Model- Recombination driven evolution of Tombusvirus DI RNAs
TBSV is a plant RNA virus with a monopartite positive sense single strand 4.8 kb genomic RNA component. In infected cells genomic RNA is translated by host ribosomes producing 2 replication proteins and g RNA is also involved in production of sub genomic RNA for the expression of 3 viral proteins. Via Yeast model system many details about TBSV replication and recombination is revealed. So for this virus group best fitting genome evolution model is Recombination driven evolution. It is indicated that TBSV RNA frequently participates in RNA recombination in experimental plants. In addition TBSV rep RNA also recombines in Yeast cells. This frequent recombination of TBSV G RNA would lead to production of new recombine viruses. TBSV Cis acting replication element affects the selection of the recombination sites. These Cis acting replicating element found to bind to TBSV RNA dependent RNA polymerase more efficient than non-viral elements. Furthermore in the case of TBSV its ability to naturally develop small replicating deletion mutants of their genomes during infection is another method of RNA recombination. These are called Defective interfering RNA. Defective interfering RNA was first described in 1987. These are 396 nt long and is derived from TBSV G RNA with 6 internal deletions.
What this model inform us about the host range and genetic drift?
As we all know natural selection is the process by which best fitting variants in a specific environment increase their frequency in population. Recombination of TBSV and creation of DI RNA creates new variants where best fitted variants is going to be selected to survive. Less fitted variants decrease in their population which end of creating less divers environment. This is an environment where genetic drift can occur when limited number of individuals are passed though. Any ideas about how Genetic drift affect virus titer? If genetic drift occurs what does it inform about the host range?
Control strategy
It is important to consider about Defective interfering RNAs as a controlling strategy for the disease. It is reported that accumulating of DI RNAs in TBSV infected plants has dramatically reduced the virus accumulation. It is important to discuss about how this DI RNA interfere in TBSV accumulation and possibilities of controlling the disease via DI RNAs.
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Post by gabriela on Nov 16, 2015 21:26:18 GMT -6
Model- Recombination driven evolution of Tombusvirus DI RNAs TBSV is a plant RNA virus with a monopartite positive sense single strand 4.8 kb genomic RNA component. In infected cells genomic RNA is translated by host ribosomes producing 2 replication proteins and g RNA is also involved in production of sub genomic RNA for the expression of 3 viral proteins. Via Yeast model system many details about TBSV replication and recombination is revealed. So for this virus group best fitting genome evolution model is Recombination driven evolution. It is indicated that TBSV RNA frequently participates in RNA recombination in experimental plants. In addition TBSV rep RNA also recombines in Yeast cells. This frequent recombination of TBSV G RNA would lead to production of new recombine viruses. TBSV Cis acting replication element affects the selection of the recombination sites. These Cis acting replicating element found to bind to TBSV RNA dependent RNA polymerase more efficient than non-viral elements. Furthermore in the case of TBSV its ability to naturally develop small replicating deletion mutants of their genomes during infection is another method of RNA recombination. These are called Defective interfering RNA. Defective interfering RNA was first described in 1987. These are 396 nt long and is derived from TBSV G RNA with 6 internal deletions. What this model inform us about the host range and genetic drift? As we all know natural selection is the process by which best fitting variants in a specific environment increase their frequency in population. Recombination of TBSV and creation of DI RNA creates new variants where best fitted variants is going to be selected to survive. Less fitted variants decrease in their population which end of creating less divers environment. This is an environment where genetic drift can occur when limited number of individuals are passed though. Any ideas about how Genetic drift affect virus titer? If genetic drift occurs what does it inform about the host range? Control strategy It is important to consider about Defective interfering RNAs as a controlling strategy for the disease. It is reported that accumulating of DI RNAs in TBSV infected plants has dramatically reduced the virus accumulation. It is important to discuss about how this DI RNA interfere in TBSV accumulation and possibilities of controlling the disease via DI RNAs. Thanks so much Dulanjani for this information  I have read that symptom attenuation of TBSV was once mainly attributed to simple competition between the subviral RNA and helper virus for limited quantities of replication factors. However, recent evidence from several systems suggests that subviral RNA-mediated enhancement of host resistance might be of equal or greater importance. Concepts delineating the evolutionary relationship between subviral RNA and helper virus have been evolving. In the beginning the relationship between subviral RNA and helper virus was viewed as purely parasitic, other studies suggested that their relationship is more complex, including mutualistic, benefiting both participants. Which relationship do you think is actually occurring? Personalty I think that natural selection can be actually occurring like your mentioned before but why not mutualistic? I think it might be possible, maybe in some point during evolution plants were getting benefits from this mutualistic relationship and then virus got advantage of that and then they use it as a mechanism to create more virulent progeny? ... do you think is possible... Is just a thought... |
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Post by omararias on Nov 18, 2015 17:29:31 GMT -6
Model- Recombination driven evolution of Tombusvirus DI RNAs TBSV is a plant RNA virus with a monopartite positive sense single strand 4.8 kb genomic RNA component. In infected cells genomic RNA is translated by host ribosomes producing 2 replication proteins and g RNA is also involved in production of sub genomic RNA for the expression of 3 viral proteins. Via Yeast model system many details about TBSV replication and recombination is revealed. So for this virus group best fitting genome evolution model is Recombination driven evolution. It is indicated that TBSV RNA frequently participates in RNA recombination in experimental plants. In addition TBSV rep RNA also recombines in Yeast cells. This frequent recombination of TBSV G RNA would lead to production of new recombine viruses. TBSV Cis acting replication element affects the selection of the recombination sites. These Cis acting replicating element found to bind to TBSV RNA dependent RNA polymerase more efficient than non-viral elements. Furthermore in the case of TBSV its ability to naturally develop small replicating deletion mutants of their genomes during infection is another method of RNA recombination. These are called Defective interfering RNA. Defective interfering RNA was first described in 1987. These are 396 nt long and is derived from TBSV G RNA with 6 internal deletions. What this model inform us about the host range and genetic drift? As we all know natural selection is the process by which best fitting variants in a specific environment increase their frequency in population. Recombination of TBSV and creation of DI RNA creates new variants where best fitted variants is going to be selected to survive. Less fitted variants decrease in their population which end of creating less divers environment. This is an environment where genetic drift can occur when limited number of individuals are passed though. Any ideas about how Genetic drift affect virus titer? If genetic drift occurs what does it inform about the host range? Control strategy It is important to consider about Defective interfering RNAs as a controlling strategy for the disease. It is reported that accumulating of DI RNAs in TBSV infected plants has dramatically reduced the virus accumulation. It is important to discuss about how this DI RNA interfere in TBSV accumulation and possibilities of controlling the disease via DI RNAs. Hi Dulanjani, thanks for the information. Please I have some questions. First of all, from what you've read, besides of the TBSV, which other Tombusviruses have shown a reduction in the accumulation?, in which hosts is it more common to find a higher reduction of viral accumulation? Secondly, besides of the yeast model for evaluating the evolution mechanism, have you found any other information regarding additional models? Thanks. |
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Post by dulanjani on Nov 18, 2015 19:31:46 GMT -6
Model- Recombination driven evolution of Tombusvirus DI RNAs TBSV is a plant RNA virus with a monopartite positive sense single strand 4.8 kb genomic RNA component. In infected cells genomic RNA is translated by host ribosomes producing 2 replication proteins and g RNA is also involved in production of sub genomic RNA for the expression of 3 viral proteins. Via Yeast model system many details about TBSV replication and recombination is revealed. So for this virus group best fitting genome evolution model is Recombination driven evolution. It is indicated that TBSV RNA frequently participates in RNA recombination in experimental plants. In addition TBSV rep RNA also recombines in Yeast cells. This frequent recombination of TBSV G RNA would lead to production of new recombine viruses. TBSV Cis acting replication element affects the selection of the recombination sites. These Cis acting replicating element found to bind to TBSV RNA dependent RNA polymerase more efficient than non-viral elements. Furthermore in the case of TBSV its ability to naturally develop small replicating deletion mutants of their genomes during infection is another method of RNA recombination. These are called Defective interfering RNA. Defective interfering RNA was first described in 1987. These are 396 nt long and is derived from TBSV G RNA with 6 internal deletions. What this model inform us about the host range and genetic drift? As we all know natural selection is the process by which best fitting variants in a specific environment increase their frequency in population. Recombination of TBSV and creation of DI RNA creates new variants where best fitted variants is going to be selected to survive. Less fitted variants decrease in their population which end of creating less divers environment. This is an environment where genetic drift can occur when limited number of individuals are passed though. Any ideas about how Genetic drift affect virus titer? If genetic drift occurs what does it inform about the host range? Control strategy It is important to consider about Defective interfering RNAs as a controlling strategy for the disease. It is reported that accumulating of DI RNAs in TBSV infected plants has dramatically reduced the virus accumulation. It is important to discuss about how this DI RNA interfere in TBSV accumulation and possibilities of controlling the disease via DI RNAs. Thanks so much Dulanjani for this information I have read that symptom attenuation of TBSV was once mainly attributed to simple competition between the subviral RNA and helper virus for limited quantities of replication factors. However, recent evidence from several systems suggests that subviral RNA-mediated enhancement of host resistance might be of equal or greater importance. Concepts delineating the evolutionary relationship between subviral RNA and helper virus have been evolving. In the beginning the relationship between subviral RNA and helper virus was viewed as purely parasitic, other studies suggested that their relationship is more complex, including mutualistic, benefiting both participants. Which relationship do you think is actually occurring? Personalty I think that natural selection can be actually occurring like your mentioned before but why not mutualistic? I think it might be possible, maybe in some point during evolution plants were getting benefits from this mutualistic relationship and then virus got advantage of that and then they use it as a mechanism to create more virulent progeny? ... do you think is possible... Is just a thought... Part about the Sub viral RNA is correct, As you mentioned subviral RNAs, many of which are noncoding, can cause profound alterations to the normal disease progression induced by their helper virus. Subviral RNA replication is completely dependent on enzymes encoded by their helper virus and thus amplification is limited to co infected cells. Several DI RNAs have been described in tombusvirus infections and all possess common structural features that maintain non contiguous elements of the parental genome corresponding to terminal regions and an internal segment while losing all coding capacity. New models for DI RNA-mediated reduction in helper virus levels and symptom attenuation include DI RNA enhancement of post transcriptional gene silencing (PTGS), which is an antiviral defense mechanism in plants which i think what causes helper viral suppression. According to what i read in one paper suggest that it is not necessarily have to be only parasitism between helper virus and sub genomic RNA, resent studies sugested that the relationship between helper and DI RNA can be mutualistic. |
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Post by dulanjani on Nov 18, 2015 19:42:34 GMT -6
Model- Recombination driven evolution of Tombusvirus DI RNAs TBSV is a plant RNA virus with a monopartite positive sense single strand 4.8 kb genomic RNA component. In infected cells genomic RNA is translated by host ribosomes producing 2 replication proteins and g RNA is also involved in production of sub genomic RNA for the expression of 3 viral proteins. Via Yeast model system many details about TBSV replication and recombination is revealed. So for this virus group best fitting genome evolution model is Recombination driven evolution. It is indicated that TBSV RNA frequently participates in RNA recombination in experimental plants. In addition TBSV rep RNA also recombines in Yeast cells. This frequent recombination of TBSV G RNA would lead to production of new recombine viruses. TBSV Cis acting replication element affects the selection of the recombination sites. These Cis acting replicating element found to bind to TBSV RNA dependent RNA polymerase more efficient than non-viral elements. Furthermore in the case of TBSV its ability to naturally develop small replicating deletion mutants of their genomes during infection is another method of RNA recombination. These are called Defective interfering RNA. Defective interfering RNA was first described in 1987. These are 396 nt long and is derived from TBSV G RNA with 6 internal deletions. What this model inform us about the host range and genetic drift? As we all know natural selection is the process by which best fitting variants in a specific environment increase their frequency in population. Recombination of TBSV and creation of DI RNA creates new variants where best fitted variants is going to be selected to survive. Less fitted variants decrease in their population which end of creating less divers environment. This is an environment where genetic drift can occur when limited number of individuals are passed though. Any ideas about how Genetic drift affect virus titer? If genetic drift occurs what does it inform about the host range? Control strategy It is important to consider about Defective interfering RNAs as a controlling strategy for the disease. It is reported that accumulating of DI RNAs in TBSV infected plants has dramatically reduced the virus accumulation. It is important to discuss about how this DI RNA interfere in TBSV accumulation and possibilities of controlling the disease via DI RNAs. Hi Dulanjani, thanks for the information. Please I have some questions. First of all, from what you've read, besides of the TBSV, which other Tombusviruses have shown a reduction in the accumulation?, in which hosts is it more common to find a higher reduction of viral accumulation? Secondly, besides of the yeast model for evaluating the evolution mechanism, have you found any other information regarding additional models? Thanks. One of other examples beside TBSV would be Cucumber Necrosis Virus (CNV). High levels of DI RNAs are found associated with persistent infections initiated with laboratory cultures of cucumber necrosis virus. Two synthetic CNV transcripts that were derived through site-directed mutagenesis of a highly infectious CNV cDNA clone and that do not express the CNV 20-kDa nonstructural protein were found to generate high levels of symptom-attenuating DI RNAs de novo without serial high-moi passage in transcript-inoculated plants. Also this study has shown that CNV can efficiently replicate TBSV defective interfering (DI) RNAs as well. |
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Post by ravendra on Nov 21, 2015 13:52:04 GMT -6
Model- Recombination driven evolution of Tombusvirus DI RNAs TBSV is a plant RNA virus with a monopartite positive sense single strand 4.8 kb genomic RNA component. In infected cells genomic RNA is translated by host ribosomes producing 2 replication proteins and g RNA is also involved in production of sub genomic RNA for the expression of 3 viral proteins. Via Yeast model system many details about TBSV replication and recombination is revealed. So for this virus group best fitting genome evolution model is Recombination driven evolution. It is indicated that TBSV RNA frequently participates in RNA recombination in experimental plants. In addition TBSV rep RNA also recombines in Yeast cells. This frequent recombination of TBSV G RNA would lead to production of new recombine viruses. TBSV Cis acting replication element affects the selection of the recombination sites. These Cis acting replicating element found to bind to TBSV RNA dependent RNA polymerase more efficient than non-viral elements. Furthermore in the case of TBSV its ability to naturally develop small replicating deletion mutants of their genomes during infection is another method of RNA recombination. These are called Defective interfering RNA. Defective interfering RNA was first described in 1987. These are 396 nt long and is derived from TBSV G RNA with 6 internal deletions. What this model inform us about the host range and genetic drift? As we all know natural selection is the process by which best fitting variants in a specific environment increase their frequency in population. Recombination of TBSV and creation of DI RNA creates new variants where best fitted variants is going to be selected to survive. Less fitted variants decrease in their population which end of creating less divers environment. This is an environment where genetic drift can occur when limited number of individuals are passed though. Any ideas about how Genetic drift affect virus titer? If genetic drift occurs what does it inform about the host range? Control strategy It is important to consider about Defective interfering RNAs as a controlling strategy for the disease. It is reported that accumulating of DI RNAs in TBSV infected plants has dramatically reduced the virus accumulation. It is important to discuss about how this DI RNA interfere in TBSV accumulation and possibilities of controlling the disease via DI RNAs. Thank you, Dulanjani for the posting. I was wondering if there is any information on the production of resistant tomato plants against TBSV infection given that tomato is an important edible produce. I know that there are GM tomatoes out there and certain labs in different countries are currently working on nutritional aspects of tomato which is more of the nutraceutical aspect than disease aspect. So, I am curious that if you have come across any information on a successful field trial of tombusvirus resistant tomatoes? Thank you!
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Post by gabriela on Nov 22, 2015 21:08:57 GMT -6
Thanks so much Dulanjani for this information I have read that symptom attenuation of TBSV was once mainly attributed to simple competition between the subviral RNA and helper virus for limited quantities of replication factors. However, recent evidence from several systems suggests that subviral RNA-mediated enhancement of host resistance might be of equal or greater importance. Concepts delineating the evolutionary relationship between subviral RNA and helper virus have been evolving. In the beginning the relationship between subviral RNA and helper virus was viewed as purely parasitic, other studies suggested that their relationship is more complex, including mutualistic, benefiting both participants. Which relationship do you think is actually occurring? Personalty I think that natural selection can be actually occurring like your mentioned before but why not mutualistic? I think it might be possible, maybe in some point during evolution plants were getting benefits from this mutualistic relationship and then virus got advantage of that and then they use it as a mechanism to create more virulent progeny? ... do you think is possible... Is just a thought... Part about the Sub viral RNA is correct, As you mentioned subviral RNAs, many of which are noncoding, can cause profound alterations to the normal disease progression induced by their helper virus. Subviral RNA replication is completely dependent on enzymes encoded by their helper virus and thus amplification is limited to co infected cells. Several DI RNAs have been described in tombusvirus infections and all possess common structural features that maintain non contiguous elements of the parental genome corresponding to terminal regions and an internal segment while losing all coding capacity. New models for DI RNA-mediated reduction in helper virus levels and symptom attenuation include DI RNA enhancement of post transcriptional gene silencing (PTGS), which is an antiviral defense mechanism in plants which i think what causes helper viral suppression. According to what i read in one paper suggest that it is not necessarily have to be only parasitism between helper virus and sub genomic RNA, resent studies sugested that the relationship between helper and DI RNA can be mutualistic. thanks so much it sounds great.. |
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Post by omararias on Nov 22, 2015 22:33:20 GMT -6
Hi Dulanjani, thanks for the information. Please I have some questions. First of all, from what you've read, besides of the TBSV, which other Tombusviruses have shown a reduction in the accumulation?, in which hosts is it more common to find a higher reduction of viral accumulation? Secondly, besides of the yeast model for evaluating the evolution mechanism, have you found any other information regarding additional models? Thanks. One of other examples beside TBSV would be Cucumber Necrosis Virus (CNV). High levels of DI RNAs are found associated with persistent infections initiated with laboratory cultures of cucumber necrosis virus. Two synthetic CNV transcripts that were derived through site-directed mutagenesis of a highly infectious CNV cDNA clone and that do not express the CNV 20-kDa nonstructural protein were found to generate high levels of symptom-attenuating DI RNAs de novo without serial high-moi passage in transcript-inoculated plants. Also this study has shown that CNV can efficiently replicate TBSV defective interfering (DI) RNAs as well. Thanks for the information was very usefull |
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