Embryonic Stem Cells, Retroviruses, and You

        The human cell contains roughly 25,000 genes, so it is natural to believe
that the majority of the human genome contains protein-coding genes. On the contrary, protein-coding genes only make up about 2% of our genomes. If protein-coding genes constitute a small percentage of the human genome, what is the function of the other subset of genes occupying our cells? Ninety-eight percent of our genomes contain non-coding DNA, which includes DNA sequences that regulate the expression of coding genes, pseudogenes (genes that no longer encode protein due to the acquisition of mutations over time), and transposons (DNA sequences that migrate through the genome). Scientists hypothesize that these non-coding sequences

Embryonic stem cells in the process of generating multiple cell types.
Courtesy: University of California, Merced 

  

originated from retroviruses. Retroviruses are a unique class of virus that convert their RNA sequences into DNA with the aid of an enzyme called reverse transcriptase. They also possess enzymes that facilitate the incorporation of their newly converted DNA into the genome of their host, ensuring that their genetic material will be replicated during the lifetime of the host cell. Retroviruses have received much negative attention due to the devastation caused by HIV, the most infamous retrovirus of all.

         However, retroviruses may have contributed to our evolution. A new study published in Nature Structural and Molecular Biology suggests that a retroviral infection may have bestowed pluripotency (the ability of a cell to generate multiple cell types) on primate embryonic stem cells. This study, led by Huck-Hui Ng's group in Singapore, discovered that sequences belonging to the human endogenous retrovirus H, or HERVH, could be detected in human embryonic stem cells. When mutations were introduced into these sequences, human embryonic stem cells no longer had the capacity to generate multiple cell populations, leading Ng and colleagues to conclude that HERVH infection played an important role in the origins of cell pluripotency.

       Interestingly, these scientists suggested that stem cells from non-primates do not rely on HERVH for pluripotency. This idea implies that primate and non-primate stem cells rely on different evolutionary sources for their pluripotency, and the next logical question concerns how this phenomenon occurred. These studies highlight a crucial role that environmental agents play in our evolution, and it will be fascinating to learn of other important cellular functions that may be dependent on virus-host interactions.