bea
New Member
Posts: 16 
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Post by bea on Nov 14, 2015 16:54:48 GMT -6
The virus group that I discuss in this topic is Carmovirus, focusing basically in the Turnip Crinkle Virus (TCV). The model applied to this genus of virus is RNA-RNA recombination. Actually the main proposal for RNA viruses is that they evolved from correcting high error rates through an ability to recombine mutant genomes with wild-type genomes, but still maintaining functional integrity. Also, enzymes mediating the replication and expression of virus genomes contain arrays of conserved sequence motifs. Proteins with such motifs include RNA-dependent RNA polymerase, putative RNA helicase, chymotrypsin-like and papain-like proteases, and methyltransferases. The genes for these proteins form partially conserved modules in large subsets of viruses. A concept of the virus genome as a relatively evolutionarily stable “core” of housekeeping genes accompanied by a much more flexible “shell” consisting mostly of genes coding for virion components and various accessory proteins is discussed. Shuffling of the “shell” genes including genome reorganization and recombination between remote groups of viruses is considered to be one of the major factors of virus evolution. TCV is naturally associated with a number of sub viral RNAs that require the TCV genomic RNA for accumulation in turnip plants and protoplasts. RNA recombination in plant virus were only infectious if they were able to recombine with sat-RNA D in a plant. Single-base changes proximal to the crossover site did not affect recombination. However, other single-base alterations both within and downstream from the motif I sequence eliminated recombination. RNA recombination was found to mediate the rearrangement of viral genes, the repair of deleterious mutations, and the acquisition of nonself sequences influencing the phylogenetics of viral taxa. The evidence for recombination, not only between related viruses but also among distantly related viruses, and even with host RNAs, suggests that plant viruses unabashedly test recombination with any genetic material at hand. The frequency of RNA recombination greatly depends on mechanistic and ecological factors. To support intraspecies, intragenus, and inter-genus RNA recombination, multiple virus strains must co-infect the same host cell. Co-infections may be rare, especially when the virus strains are ecologically or geographically isolated, or if the immune response limits superinfection. Even if co-infection is successful, mechanistic restraints, such as the level of sequence dissimilarity, or the specificity of viral RdRp may prevent the formation of viable hybrids. Finally, most recombinants are likely to be deleterious and thus purified from the population.
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Post by gabriela on Nov 16, 2015 21:03:26 GMT -6
The virus group that I discuss in this topic is Carmovirus, focusing basically in the Turnip Crinkle Virus (TCV). The model applied to this genus of virus is RNA-RNA recombination. Actually the main proposal for RNA viruses is that they evolved from correcting high error rates through an ability to recombine mutant genomes with wild-type genomes, but still maintaining functional integrity. Also, enzymes mediating the replication and expression of virus genomes contain arrays of conserved sequence motifs. Proteins with such motifs include RNA-dependent RNA polymerase, putative RNA helicase, chymotrypsin-like and papain-like proteases, and methyltransferases. The genes for these proteins form partially conserved modules in large subsets of viruses. A concept of the virus genome as a relatively evolutionarily stable “core” of housekeeping genes accompanied by a much more flexible “shell” consisting mostly of genes coding for virion components and various accessory proteins is discussed. Shuffling of the “shell” genes including genome reorganization and recombination between remote groups of viruses is considered to be one of the major factors of virus evolution. TCV is naturally associated with a number of sub viral RNAs that require the TCV genomic RNA for accumulation in turnip plants and protoplasts. RNA recombination in plant virus were only infectious if they were able to recombine with sat-RNA D in a plant. Single-base changes proximal to the crossover site did not affect recombination. However, other single-base alterations both within and downstream from the motif I sequence eliminated recombination. RNA recombination was found to mediate the rearrangement of viral genes, the repair of deleterious mutations, and the acquisition of nonself sequences influencing the phylogenetics of viral taxa. The evidence for recombination, not only between related viruses but also among distantly related viruses, and even with host RNAs, suggests that plant viruses unabashedly test recombination with any genetic material at hand. The frequency of RNA recombination greatly depends on mechanistic and ecological factors. To support intraspecies, intragenus, and inter-genus RNA recombination, multiple virus strains must co-infect the same host cell. Co-infections may be rare, especially when the virus strains are ecologically or geographically isolated, or if the immune response limits superinfection. Even if co-infection is successful, mechanistic restraints, such as the level of sequence dissimilarity, or the specificity of viral RdRp may prevent the formation of viable hybrids. Finally, most recombinants are likely to be deleterious and thus purified from the population. Bea, thanks so much for your information.. I have some questions related with your information: 1) "Shuffling of the “shell” genes including genome reorganization": this reorganization means in the order of the genes in the virus? or in the expression of these genes? and if is in the order how does it occurs? 2) " recombination between remote groups of viruses:" which are the major groups that recombinate with carmovirus? |
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Post by dulanjani on Nov 18, 2015 20:24:08 GMT -6
The virus group that I discuss in this topic is Carmovirus, focusing basically in the Turnip Crinkle Virus (TCV). The model applied to this genus of virus is RNA-RNA recombination. Actually the main proposal for RNA viruses is that they evolved from correcting high error rates through an ability to recombine mutant genomes with wild-type genomes, but still maintaining functional integrity. Also, enzymes mediating the replication and expression of virus genomes contain arrays of conserved sequence motifs. Proteins with such motifs include RNA-dependent RNA polymerase, putative RNA helicase, chymotrypsin-like and papain-like proteases, and methyltransferases. The genes for these proteins form partially conserved modules in large subsets of viruses. A concept of the virus genome as a relatively evolutionarily stable “core” of housekeeping genes accompanied by a much more flexible “shell” consisting mostly of genes coding for virion components and various accessory proteins is discussed. Shuffling of the “shell” genes including genome reorganization and recombination between remote groups of viruses is considered to be one of the major factors of virus evolution. TCV is naturally associated with a number of sub viral RNAs that require the TCV genomic RNA for accumulation in turnip plants and protoplasts. RNA recombination in plant virus were only infectious if they were able to recombine with sat-RNA D in a plant. Single-base changes proximal to the crossover site did not affect recombination. However, other single-base alterations both within and downstream from the motif I sequence eliminated recombination. RNA recombination was found to mediate the rearrangement of viral genes, the repair of deleterious mutations, and the acquisition of nonself sequences influencing the phylogenetics of viral taxa. The evidence for recombination, not only between related viruses but also among distantly related viruses, and even with host RNAs, suggests that plant viruses unabashedly test recombination with any genetic material at hand. The frequency of RNA recombination greatly depends on mechanistic and ecological factors. To support intraspecies, intragenus, and inter-genus RNA recombination, multiple virus strains must co-infect the same host cell. Co-infections may be rare, especially when the virus strains are ecologically or geographically isolated, or if the immune response limits superinfection. Even if co-infection is successful, mechanistic restraints, such as the level of sequence dissimilarity, or the specificity of viral RdRp may prevent the formation of viable hybrids. Finally, most recombinants are likely to be deleterious and thus purified from the population. Dear Bea What do you mean by RNA recombination in plant virus were only infectious if they were able to recombine with sat-RNA D in a plant? Dose that mean recombination between TCV and Sat-RNA D is only infectious? Can you explain more about it? Further more is it possible recombination between Sat RNAs? Such as sat-RNA D and sat-RNA C? |
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Post by omararias on Nov 21, 2015 0:07:31 GMT -6
The virus group that I discuss in this topic is Carmovirus, focusing basically in the Turnip Crinkle Virus (TCV). The model applied to this genus of virus is RNA-RNA recombination. Actually the main proposal for RNA viruses is that they evolved from correcting high error rates through an ability to recombine mutant genomes with wild-type genomes, but still maintaining functional integrity. Also, enzymes mediating the replication and expression of virus genomes contain arrays of conserved sequence motifs. Proteins with such motifs include RNA-dependent RNA polymerase, putative RNA helicase, chymotrypsin-like and papain-like proteases, and methyltransferases. The genes for these proteins form partially conserved modules in large subsets of viruses. A concept of the virus genome as a relatively evolutionarily stable “core” of housekeeping genes accompanied by a much more flexible “shell” consisting mostly of genes coding for virion components and various accessory proteins is discussed. Shuffling of the “shell” genes including genome reorganization and recombination between remote groups of viruses is considered to be one of the major factors of virus evolution. TCV is naturally associated with a number of sub viral RNAs that require the TCV genomic RNA for accumulation in turnip plants and protoplasts. RNA recombination in plant virus were only infectious if they were able to recombine with sat-RNA D in a plant. Single-base changes proximal to the crossover site did not affect recombination. However, other single-base alterations both within and downstream from the motif I sequence eliminated recombination. RNA recombination was found to mediate the rearrangement of viral genes, the repair of deleterious mutations, and the acquisition of nonself sequences influencing the phylogenetics of viral taxa. The evidence for recombination, not only between related viruses but also among distantly related viruses, and even with host RNAs, suggests that plant viruses unabashedly test recombination with any genetic material at hand. The frequency of RNA recombination greatly depends on mechanistic and ecological factors. To support intraspecies, intragenus, and inter-genus RNA recombination, multiple virus strains must co-infect the same host cell. Co-infections may be rare, especially when the virus strains are ecologically or geographically isolated, or if the immune response limits superinfection. Even if co-infection is successful, mechanistic restraints, such as the level of sequence dissimilarity, or the specificity of viral RdRp may prevent the formation of viable hybrids. Finally, most recombinants are likely to be deleterious and thus purified from the population. Nice information, could you please help me with somes questions... You mentioned that such motifs are present in RdRp, helicases and other enzymes, do you know if there is any differentiation in the recombination level among these proteins, if so, wich one is more and less efficient?. Also, do they differ in the mechanism of crossing over? Thanks. |
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Post by ravendra on Nov 21, 2015 14:04:39 GMT -6
The virus group that I discuss in this topic is Carmovirus, focusing basically in the Turnip Crinkle Virus (TCV). The model applied to this genus of virus is RNA-RNA recombination. Actually the main proposal for RNA viruses is that they evolved from correcting high error rates through an ability to recombine mutant genomes with wild-type genomes, but still maintaining functional integrity. Also, enzymes mediating the replication and expression of virus genomes contain arrays of conserved sequence motifs. Proteins with such motifs include RNA-dependent RNA polymerase, putative RNA helicase, chymotrypsin-like and papain-like proteases, and methyltransferases. The genes for these proteins form partially conserved modules in large subsets of viruses. A concept of the virus genome as a relatively evolutionarily stable “core” of housekeeping genes accompanied by a much more flexible “shell” consisting mostly of genes coding for virion components and various accessory proteins is discussed. Shuffling of the “shell” genes including genome reorganization and recombination between remote groups of viruses is considered to be one of the major factors of virus evolution. TCV is naturally associated with a number of sub viral RNAs that require the TCV genomic RNA for accumulation in turnip plants and protoplasts. RNA recombination in plant virus were only infectious if they were able to recombine with sat-RNA D in a plant. Single-base changes proximal to the crossover site did not affect recombination. However, other single-base alterations both within and downstream from the motif I sequence eliminated recombination. RNA recombination was found to mediate the rearrangement of viral genes, the repair of deleterious mutations, and the acquisition of nonself sequences influencing the phylogenetics of viral taxa. The evidence for recombination, not only between related viruses but also among distantly related viruses, and even with host RNAs, suggests that plant viruses unabashedly test recombination with any genetic material at hand. The frequency of RNA recombination greatly depends on mechanistic and ecological factors. To support intraspecies, intragenus, and inter-genus RNA recombination, multiple virus strains must co-infect the same host cell. Co-infections may be rare, especially when the virus strains are ecologically or geographically isolated, or if the immune response limits superinfection. Even if co-infection is successful, mechanistic restraints, such as the level of sequence dissimilarity, or the specificity of viral RdRp may prevent the formation of viable hybrids. Finally, most recombinants are likely to be deleterious and thus purified from the population. Thank you, Beatriz. I wanted to know what are the current major investigations going on to understand the biology of Carmoviruses around the world? Where do we stand in our understanding of carmoviruses? Thank you. Ravendra
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