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Post by omararias on Oct 17, 2015 10:21:49 GMT -6
General aspects about Pararetrovirus
Plant Pararetrovirus also known as Caulimoviruses represent a group of discontinuous double stranded circular DNA viruses (ds DNA), such discontinuities can be corrected by polymerases when entered the host nucleus. In general the replication is carried out by reverse transcription of a pregenomic RNA. It is highly important to mention that the genome of these kind of viruses contain several mechanisms of organization of their ORF, therefore the number of mRNA will vary between specie as well as the translation system.
Viral mechanism of translation
The pre genomic or leader 35S RNA present in Caulimoviruses like the CaMV (Cauliflower mosaic virus) has several short open reading frames sORF and its translation requires an special mechanisms know as shunt ribosome mechanism in which: first of all, the most 5’ proximal sORF will be translated, secondly a large region is skipped for translation and thirdly there is a re initiation process at the first long ORF that can be found.
Host translation machinery and interaction with viral mechanisms
One of the clearest examples regarding this topic is the CaMV (Cauliflower mosaic virus) its genome contains seven ORF, from which the majority of them are translated by polycistronic strategies that involve the production of a transactivator/ viroplasmin (TAV) that can potentially exert functions as a regularity unit at host nuclear and cytoplasm level, interacting specifically with a large number of plant cellular proteins which include eukaryotic initiation factors, 60S ribosomal subunits and re initiation supporting protein (RISP). About re initiation translation mechanisms one of the host factors that can trigger such process is the plant target of rapamycin (TOR) when interacting with TAV by a phosphorylation reaction. In this way, it is quite clear that there is a strong relation between host and viral factors. Finally, when it comes to replication the TAV might also play a crucial role in the formation of inclusion bodies that could eventually help in the production of structural proteins that are essential for virus assembly.
Please if there is any question about this brief discription about Pararetroviruses, I will be more than happy to answer them.
Thanks.
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Post by gabriela on Oct 19, 2015 14:25:14 GMT -6
General aspects about Pararetrovirus Plant Pararetrovirus also known as Caulimoviruses represent a group of discontinuous double stranded circular DNA viruses (ds DNA), such discontinuities can be corrected by polymerases when entered the host nucleus. In general the replication is carried out by reverse transcription of a pregenomic RNA. It is highly important to mention that the genome of these kind of viruses contain several mechanisms of organization of their ORF, therefore the number of mRNA will vary between specie as well as the translation system. Viral mechanism of translation The pre genomic or leader 35S RNA present in Caulimoviruses like the CaMV ( Cauliflower mosaic virus) has several short open reading frames sORF and its translation requires an special mechanisms know as shunt ribosome mechanism in which: first of all, the most 5’ proximal sORF will be translated, secondly a large region is skipped for translation and thirdly there is a re initiation process at the first long ORF that can be found. Host translation machinery and interaction with viral mechanisms One of the clearest examples regarding this topic is the CaMV ( Cauliflower mosaic virus) its genome contains seven ORF, from which the majority of them are translated by polycistronic strategies that involve the production of a transactivator/ viroplasmin (TAV) that can potentially exert functions as a regularity unit at host nuclear and cytoplasm level, interacting specifically with a large number of plant cellular proteins which include eukaryotic initiation factors, 60S ribosomal subunits and re initiation supporting protein (RISP). About re initiation translation mechanisms one of the host factors that can trigger such process is the plant target of rapamycin (TOR) when interacting with TAV by a phosphorylation reaction. In this way, it is quite clear that there is a strong relation between host and viral factors. Finally, when it comes to replication the TAV might also play a crucial role in the formation of inclusion bodies that could eventually help in the production of structural proteins that are essential for virus assembly. Please if there is any question about this brief discription about Pararetroviruses, I will be more than happy to answer them. Thanks. Is there a reason of why the transactivator/ viroplasmin (TAV) regulates at host nuclear and cytoplasm level? Is that a prevention of pre-genomic RNA degradation? |
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bea
New Member
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Post by bea on Oct 20, 2015 14:31:11 GMT -6
Thank you Omar! I have a simple question: why only some ORF are translated by polycistronic strategies? What happens to the others?
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Post by dulanjani on Oct 21, 2015 13:17:21 GMT -6
Dear Omar thank you for the information I have one question would you please explain more about the rapamycin (TOR)and re initiation of translation? Is this a common process? what does this host protein do would it attach to ribosomes or viral RNA?
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Post by omararias on Oct 21, 2015 16:21:56 GMT -6
General aspects about Pararetrovirus Plant Pararetrovirus also known as Caulimoviruses represent a group of discontinuous double stranded circular DNA viruses (ds DNA), such discontinuities can be corrected by polymerases when entered the host nucleus. In general the replication is carried out by reverse transcription of a pregenomic RNA. It is highly important to mention that the genome of these kind of viruses contain several mechanisms of organization of their ORF, therefore the number of mRNA will vary between specie as well as the translation system. Viral mechanism of translation The pre genomic or leader 35S RNA present in Caulimoviruses like the CaMV ( Cauliflower mosaic virus) has several short open reading frames sORF and its translation requires an special mechanisms know as shunt ribosome mechanism in which: first of all, the most 5’ proximal sORF will be translated, secondly a large region is skipped for translation and thirdly there is a re initiation process at the first long ORF that can be found. Host translation machinery and interaction with viral mechanisms One of the clearest examples regarding this topic is the CaMV ( Cauliflower mosaic virus) its genome contains seven ORF, from which the majority of them are translated by polycistronic strategies that involve the production of a transactivator/ viroplasmin (TAV) that can potentially exert functions as a regularity unit at host nuclear and cytoplasm level, interacting specifically with a large number of plant cellular proteins which include eukaryotic initiation factors, 60S ribosomal subunits and re initiation supporting protein (RISP). About re initiation translation mechanisms one of the host factors that can trigger such process is the plant target of rapamycin (TOR) when interacting with TAV by a phosphorylation reaction. In this way, it is quite clear that there is a strong relation between host and viral factors. Finally, when it comes to replication the TAV might also play a crucial role in the formation of inclusion bodies that could eventually help in the production of structural proteins that are essential for virus assembly. Please if there is any question about this brief discription about Pararetroviruses, I will be more than happy to answer them. Thanks. Is there a reason of why the transactivator/ viroplasmin (TAV) regulates at host nuclear and cytoplasm level? Is that a prevention of pre-genomic RNA degradation? Yes, TAV plays an important role in both nuclear and cytoplasm levels. In the nucleus acts as suppressor of RNA silencing, therefore regulating alternative splicing of the 35S RNA. In the cytoplasm has an equal importance when regulating the translation re initiation mechanism and also the activation of TOR in order to keep a high phosphorylation level that is quite necessary for keeping the reinitiation complex itself and furthermore is involved in the formation of inclusion bodies and virus assembly. Regarding the pre genomic RNA degradation, of what I have read the 35 S RNA can act as pre genomic and Polycistronic indeed, but I haven’t been able to find any prevention degradation mechanism, so far I have only seen silencing mechanism. |
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Post by omararias on Oct 21, 2015 16:22:33 GMT -6
Thank you Omar! I have a simple question: why only some ORF are translated by polycistronic strategies? What happens to the others? Pararetroviruses have two translation strategies known, the transactivator-mediated Polycistronic translation and the shunting. The shunting mechanism involves the small open reading frames sORF that actually can lead to the scanning of the first large ORF. On the other hand, the transactivator-mediated Polycistronic translation can be found in the second ORF that can be only be expressed thanks to the regulator TAV that was previously co expressed by ORF VI, by the way, this mechanism of meditation for translation of a second ORF has also been found Soymoviruses. |
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Post by omararias on Oct 21, 2015 16:22:53 GMT -6
Dear Omar thank you for the information I have one question would you please explain more about the rapamycin (TOR)and re initiation of translation? Is this a common process? what does this host protein do would it attach to ribosomes or viral RNA? Basically, this is indeed a common regulatory pathway for this type of viruses when reinitiating translation after the expression of a long ORF, specifically what happens is that the viral protein TAV recruits and activates the host protein TOR (target of rapamycin) which binds to eIF3 (host translation initiation factor), this interaction triggers a phosphorylation cascade reaction of S6K1 (reinitiation protein) and RISP (reinitiation supporter protein). Finally all this reactions lead to the reestablishment of competent ribosomal subunits, leading to the eventual activation of the translation reinitiation. Thanks. |
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Post by gabriela on Oct 23, 2015 15:30:01 GMT -6
Is there a reason of why the transactivator/ viroplasmin (TAV) regulates at host nuclear and cytoplasm level? Is that a prevention of pre-genomic RNA degradation? Yes, TAV plays an important role in both nuclear and cytoplasm levels. In the nucleus acts as suppressor of RNA silencing, therefore regulating alternative splicing of the 35S RNA. In the cytoplasm has an equal importance when regulating the translation re initiation mechanism and also the activation of TOR in order to keep a high phosphorylation level that is quite necessary for keeping the reinitiation complex itself and furthermore is involved in the formation of inclusion bodies and virus assembly. Regarding the pre genomic RNA degradation, of what I have read the 35 S RNA can act as pre genomic and Polycistronic indeed, but I haven’t been able to find any prevention degradation mechanism, so far I have only seen silencing mechanism. thanks so much Omar for your information |
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