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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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5-Bromodeoxyuridine suppresses position effect variegation of transgenes in HeLa cells.

An ectopic gene integrated in the host genome is occasionally silenced due to a position effect of its adjacent chromatin structure. We found that 5-bromodeoxyuridine clearly activated such a transgene in HeLa cells. The transgene was also activated to various degrees by inhibitors of histone deacetylase, DNA topoisomerases, or DNA methyltransferase. The peptide antibiotic distamycin A potentiated markedly the effect of 5-bromodeoxyuridine. Transient expression of an artificial AT-hook protein termed MATH20 also potentiated its effect although significantly activated the transgene alone. Since distamycin A and MATH20 are able to displace histone H1 and other DNA-binding proteins bound to specific AT-rich sequences by a dominant, mutually exclusive fashion, these results suggest that 5-bromodeoxyuridine targets such an AT-rich sequence located adjacent to the silenced transgene, resulting in chromatin accessibility.[1]

References

  1. 5-Bromodeoxyuridine suppresses position effect variegation of transgenes in HeLa cells. Suzuki, T., Yaginuma, M., Oishi, T., Michishita, E., Ogino, H., Fujii, M., Ayusawa, D. Exp. Cell Res. (2001) [Pubmed]
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