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Nalley et al. reply

Author

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  • Kip Nalley

    (UT Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, Texas 75390-9185, USA. kodadek@scripps.edu
    Present addresses: Laboratory of Receptor Biology and Gene Expression, National Cancer Institute, Building 41, Room B602, 41 Library Drive MSC 5055, Bethesda, Maryland 20892-5055, USA (K.N.); Center for Innovations in Medicine, Biodesign Institute, Arizona State University, Tempe, Arizona 85287-5001, USA (S.A.J.); Departments of Chemistry & Cancer Biology, Scripps Research Institute, Scripps Florida, 130 Scripps Way, Jupiter, Florida 33458, USA (T.K.))

  • Stephen Albert Johnston

    (UT Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, Texas 75390-9185, USA. kodadek@scripps.edu
    Present addresses: Laboratory of Receptor Biology and Gene Expression, National Cancer Institute, Building 41, Room B602, 41 Library Drive MSC 5055, Bethesda, Maryland 20892-5055, USA (K.N.); Center for Innovations in Medicine, Biodesign Institute, Arizona State University, Tempe, Arizona 85287-5001, USA (S.A.J.); Departments of Chemistry & Cancer Biology, Scripps Research Institute, Scripps Florida, 130 Scripps Way, Jupiter, Florida 33458, USA (T.K.))

  • Thomas Kodadek

    (UT Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, Texas 75390-9185, USA. kodadek@scripps.edu
    Present addresses: Laboratory of Receptor Biology and Gene Expression, National Cancer Institute, Building 41, Room B602, 41 Library Drive MSC 5055, Bethesda, Maryland 20892-5055, USA (K.N.); Center for Innovations in Medicine, Biodesign Institute, Arizona State University, Tempe, Arizona 85287-5001, USA (S.A.J.); Departments of Chemistry & Cancer Biology, Scripps Research Institute, Scripps Florida, 130 Scripps Way, Jupiter, Florida 33458, USA (T.K.))

Abstract

Replying to: G. A. Collins, J. R. Lipford, R. J. Deshaies & W. P. Tansey Nature 461, 10.1038/nature08406 (2009) Proteasome-mediated turnover of some1,2, but clearly not all3,4, transcriptional activators is important for their activity. To facilitate the analysis of activator–promoter complex lifetime in vivo, a parameter relevant to this issue, we developed a competition chromatin immunoprecipitation (ChIP) assay in which binding of a native transactivator to its cognate promoters is challenged by a ligand-activated competitor protein with the same DNA-binding specificity. We applied this technique to the yeast Gal4 system5 and concluded that under non-inducing conditions (raffinose media) Gal4–promoter complexes exchange rapidly, but under inducing conditions (galactose media) the activator–promoter complexes are long-lived. Collins et al.6 report that, surprisingly, the addition of oestradiol to yeast lacking Myc–G4–ER–VP16 increased the amount of DNA co-immunoprecipitated with native Gal4.

Suggested Citation

  • Kip Nalley & Stephen Albert Johnston & Thomas Kodadek, 2009. "Nalley et al. reply," Nature, Nature, vol. 461(7265), pages 8-8, October.
    • Handle: RePEc:nat:nature:v:461:y:2009:i:7265:d:10.1038_nature08407
    DOI: 10.1038/nature08407
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