Dominique.
If polyadenylation has a role in RNA degradation , would you expect RNA genomes to carry such a signal,?
Viruses apparently would do everything to stabilize their large genomes , yet potyviruses with 10KB ss positive RNA are polyadenylated / Assume you considered this
Moshe
1. Viruses are inactive outside host then how will they evolve ??
2. Based on ans 1: since viruses are dependent on host metabolism it may be possible that they have acquired this suicide signal from host????
3. Considering the above two arguments...it the host which is evolving not the virus..
4. It might be natures mechanism to eliminate them as they are unfit [dependent on host](principle of natural selection)
5. Some viruses might be eliminated with time through this mechanism.
First off, I'm not an expert on viruses. But coming from a molecular evolution background I can give a different view than the one above.
I agree with (1) above that viruses probably experience the most selective pressure when in their host so that's when the most evolutionary change will take place.
I also agree that the viral sequences probably got their polyA tails from their host. While the host will definitely co-evolve with the virus, I have to disagree that it is the host only and not the virus evolving, and that this is "natures" means of eliminating unfit viral species.
Mohit, can you clarify what you mean when you say polyA tails are "suicide signals? Obviously polyA signals don't lead to immediate degradation of an RNA molecule, otherwise mRNA transcripts would be so unstable that there wouldn't be time for translation to take place. Just because polyA signals have a role in degradation doesn't mean that they render an RNA fragment useless. I believe they also have a role in protecting eukaryotic mRNAs. So why not have ssRNA viral genomes with polyA tails? Sure, they're probably quite a bit less stable than DNA genomes for long term storage, but when they're not in the host environment there probably aren't many enzymes around that degrade them. Also, it would make them more efficient/quick than DNA viruses at expressing their genes soon after host cell infection because there's no need for transcription.
Take a look at this paper about how molecular complexity can increase without benefits to survival/fitness that would be selected for:
http://www.uvm.edu/pdodds/files/papers/others/2010/gray2010a.pdf
The genomes of (+)ssRNA viruses such as the potyviruses are polyadenlyated because they also serve as mRNA for translation of the first viral proteins (usually the replicase peptides) upon entering the cytoplasm of the eukaryotic cell. Normal eukaryotic translation requires the poly(A) tail (there are exceptions, e.g. replication-dependent histone mRNAs).
Also most poly(A)+ mRNA in eukaryotes have a long half-life and are by no mean 'destabilized' per se. The average half-life of mRNA is in the same order of magnitude as the replication time for the genomic RNA for many pathogenic (+)ssRNA viruses in most hosts (3-12 hours).
However, there are of course also different adaptations in other (+)ssRNA viruses. The non-polyadenylated genomic RNAs of Tombusviridae have translation-enhancing CITE elements in the 3'-UTR that promote translation without the poly(A) tail.
Also many of the (+)ssRNA viruses require oligomeric end stretches such as oligo(A) and oligo(U) for the replication of dsRNA intermediates by the RNA-dependent RNA polymerases, e.g. alphaviruses.
I would say it is really an adaption to the host whether a (+)ssRNA virus carries a poly(A) tail and how the viral life cycle integrates into the host system.
Best
- Badges
- Science topic
- Similar topics
- Biological Science
- Molecular Biology
- Biomolecules
- Nucleic Acids
- RNA