What are Viral Retroposons?

What are Viral Retroposons?

By Gillian D’Souza, MSc

Retroposons are repetitive DNA fragments that are inserted into a host chromosome after reverse transcription from an RNA molecule.

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Retroposons that share structural similarities with retroviruses, such as the HIV virus, are called ‘viral retroposons’. Viral retroposons are movable genetic elements that undergo reverse transcription and integrate into the host genome. The viral retroposon may be a viral element by itself or originated from an ancient viral element.

Viral retroposons have so far been identified in eukaryotic organisms such as yeast, Drosophila (a genus of flies) and humans. A number of spontaneous mutations in Drosophila are caused by insertion of a mobile DNA element into or near a transcription unit. In humans too, many genes found to be mutant show presence of these mobile DNA elements.

An example of viral retroposons in humans include the ‘THE1’ repetitive sequences. THE1 have a length of 2.3 kb and 350 base pair LTRs, which duplicate a 5 base pair sequence at the insertion site. The human genome contains about 10,000 THE1 sequences, that code for a poly(A)-RNA of 2 kb.

Viral retroposition at the cellular level

The enzyme reverse transcriptase replicates the viral genetic fragment, producing a double stranded DNA that is identical to the original single stranded viral fragment. The DNA fragment is then sliced and inserted randomly into another chromosome, with the help of the enzyme integrase. The enzyme produces staggered cuts at the target site which are about 4-6 base pairs in length. Integration of DNA into the host chromosome occurs through the linear form of DNA.

Such recombination often enables these ‘transformed’ cells to elude the host cell’s immune response – a discovery that has fueled greater understanding of virus-induced diseases and host-cell mutations. Though retroposition was initially believed to provide a replicative advantage over host DNA, evidence now suggests it may confer a selective survival advantage to organisms under varying conditions.

Viral retroposons and evolution

By now it is well acknowledged that viral retroposons play an important role in evolution by promoting rearrangement and restructuring of genomes. Viral retroposons are able to successfully change a host cell’s DNA throughout the genome and have this replicated in future generations, clearly acting as ‘genetic editors’ that enable the evolution of diversity.

The study of viral retroposons has led to a better understanding of viral replication and strategies for parasitism with prokaryotic and eukayotic cells. Researchers hypothesize that the acquiring of additional cellular genes by viral retroposition, explains the horizontal spread of viral particles across species barriers over the years.

Research into viral retroposons

Recombination between these mobile elements may have also played a role in the expression of specific genes in particular cell types and the amount of the encoded protein produced. However, only 2-10% of 10,000 gene-duplication events caused by retroposition in the human genome have been found to be functional.

Research into viral retroposons is ongoing, in a quest to determine their origin, mechanisms of action and the role they play in the evolution of life as we know it. What cannot be disputed is their unquestionable impact on the cell’s basic regulatory function by promoting ‘genetic creativity’ at the very heart of the cell.

Sources:

  • Extensive gene traffic on the mammalian X chromosome: Emerson JJ, Kaessmann H, Betrán E, Long M (January 2004), Science. 303 (5657): 537–40
  • The Dictionary of Genomics, Transcriptomics and Proteomics: Guenter Kahl, Science, 2015.
  • Molecular Cell Biology, 4th edition: Lodish H, Berk A, Zipursky SL, et al, New York: W. H. Freeman; 2000
  • Comparative Animal Biochemistry: Klaus Urich, 2013.
  • Noncoding RNAs: Persistent Viral Agents as Modular Tools for Cellular Needs: Gunther Witzany, Natural Genetic Engineering and Natural Genome Editing, Ann. N.Y. Acad. Sci. 1178: 244–267 (2009)

Further Reading

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Last Updated: Mar 21, 2018

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