Skip to main content

Thank you for visiting nature.com. You are using a browser version with limited support for CSS. To obtain the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles and JavaScript.

  • Brief Communication
  • Published:

SILENCE: a new forward genetic technology

Nature Methods volume 4, pages 51–53 (2007)Cite this article

Abstract

Silencing induced by long terminal repeat (LTR)–encoded cis-acting response element, termed SILENCE, is a forward genetic system that allows for conditional, epigenetic control of host-gene transcription. This new research tool is independent of gene mutation or disruption, does not require complementation, and conditional gene repression appears complete at the level of protein function. SILENCE functions in hypodiploid cells and is a platform technology with broad applications in gene discovery.

This is a preview of subscription content, access via your institution

Access options

Buy this article

  • Purchase on Springer Link
  • Instant access to full article PDF
Buy now

Prices may be subject to local taxes which are calculated during checkout

Figure 1: Schematic representation of SILENCE and doxycycline-mediated transcriptional repression of neighboring host genes.
Figure 2: Toxin sensitivity, toxin binding and anthrax toxin receptor transcript amounts are condition-dependent.
Figure 3: Retroviral integration occurs within approximately 2 kb of the ANTXR start site in toxin-resistant clones.

Similar content being viewed by others

References

  1. Bradley, K.A., Mogridge, J., Mourez, M., Collier, R.J. & Young, J.A. Nature 414, 225–229 (2001).

    Article  CAS  PubMed  Google Scholar 

  2. Liu, S. & Leppla, S.H. Mol. Cell 12, 603–613 (2003).

    Article  CAS  PubMed  Google Scholar 

  3. Vanhecke, D. & Janitz, M. Drug Discov. Today 10, 205–212 (2005).

    Article  CAS  PubMed  Google Scholar 

  4. Dupuy, A.J., Akagi, K., Largaespada, D.A., Copeland, N.G. & Jenkins, N.A. Nature 436, 221–226 (2005).

    Article  CAS  PubMed  Google Scholar 

  5. Hobbie, L., Fisher, A.S., Lee, S., Flint, A. & Krieger, M. J. Biol. Chem. 269, 20958–20970 (1994).

    CAS  PubMed  Google Scholar 

  6. Deuschle, U., Meyer, W.K. & Thiesen, H.J. Mol. Cell. Biol. 15, 1907–1914 (1995).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  7. Gossen, M. & Bujard, H. Proc. Natl. Acad. Sci. USA 89, 5547–5551 (1992).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  8. Wu, X., Li, Y., Crise, B. & Burgess, S.M. Science 300, 1749–1751 (2003).

    Article  CAS  PubMed  Google Scholar 

  9. Wiznerowicz, M. & Trono, D. J. Virol. 77, 8957–8961 (2003).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  10. Boerger, A.L., Snitkovsky, S. & Young, J.A. Proc. Natl. Acad. Sci. USA 96, 9867–9872 (1999).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  11. Milne, J.C., Blanke, S.R., Hanna, P.C. & Collier, R.J. Mol. Microbiol. 15, 661–666 (1995).

    Article  CAS  PubMed  Google Scholar 

  12. Scobie, H.M., Rainey, G.J., Bradley, K.A. & Young, J.A. Proc. Natl. Acad. Sci. USA 100, 5170–5174 (2003).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  13. Livak, K.J. & Schmittgen, T.D. Methods 25, 402–408 (2001).

    Article  CAS  PubMed  Google Scholar 

  14. Jin, Y.F., Ishibashi, T., Nomoto, A. & Masuda, M. J. Virol. 76, 5540–5547 (2002).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  15. Bulliard, Y., Wiznerowicz, M., Barde, I. & Trono, D. J. Biol. Chem. 281, 35742–35746 (2006).

    Article  CAS  PubMed  Google Scholar 

  16. Forrai, A. & Robb, L. Exp. Hematol. 33, 845–856 (2005).

    Article  CAS  PubMed  Google Scholar 

  17. Guo, G., Wang, W. & Bradley, A. Nature 429, 891–895 (2004).

    Article  CAS  PubMed  Google Scholar 

  18. Suzuki, T., Minehata, K., Akagi, K., Jenkins, N.A. & Copeland, N.G. EMBO J. 25, 3422–3431 (2006).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

Download references

Acknowledgements

This work was supported by US National Institutes of Health awards AI-057870 and AI-59095. D.J.B. was supported by National Institutes of Health Microbial Pathogenesis Training Grant 2-T32-AI-07323. Flow cytometry was performed in the UCLA Jonsson Comprehensive Cancer Center (JCCC) and Center for AIDS Research Flow Cytometry Core Facility, which is supported by National Institutes of Health awards CA-16042 and AI-28697, and by the JCCC, the UCLA AIDS Institute and the David Geffen School of Medicine at UCLA. We thank P.J. Bradley for helpful suggestions and insight.

Author information

Authors and Affiliations

  1. Department of Microbiology, Immunology and Molecular Genetics, 609 Charles E. Young Dr. East, Molecular Sciences Building, University of California at Los Angeles (UCLA), Los Angeles, 90095, California, USA

    David J Banks & Kenneth A Bradley

Authors
  1. David J Banks
    View author publications

    You can also search for this author in PubMed Google Scholar

  2. Kenneth A Bradley
    View author publications

    You can also search for this author in PubMed Google Scholar

Corresponding author

Correspondence to Kenneth A Bradley.

Ethics declarations

Competing interests

The authors declare no competing financial interests.

Supplementary information

Rights and permissions

Reprints and permissions

About this article

Cite this article

Banks, D., Bradley, K. SILENCE: a new forward genetic technology. Nat Methods 4, 51–53 (2007). https://doi.org/10.1038/nmeth991

Download citation

  • Received:

  • Accepted:

  • Published:

  • Issue Date:

  • DOI: https://doi.org/10.1038/nmeth991

This article is cited by

Search

Advanced search

Quick links

Nature Briefing

Sign up for the Nature Briefing newsletter — what matters in science, free to your inbox daily.

Get the most important science stories of the day, free in your inbox. Sign up for Nature Briefing