Gal4 turnover and transcription activation

Galen A. Collins (), J. Russell Lipford, Raymond J. Deshaies and William P. Tansey ()
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Galen A. Collins: Watson School of Biological Sciences, 1 Bungtown Road
J. Russell Lipford: ‡ Caltech, 1200 East California Boulevard, Pasadena, California 91125, USA
Raymond J. Deshaies: ‡ Caltech, 1200 East California Boulevard, Pasadena, California 91125, USA
William P. Tansey: Cold Spring Harbor Laboratory, 1 Bungtown Road

Nature, 2009, vol. 461, issue 7265, E7-E7

Abstract: Abstract Arising from: K. Nalley, S. A. Johnston & T. Kodadek Nature 442, 1054–1057 (2006)10.1038/nature05067 ; Nalley et al. reply Growing evidence supports the notion that proteasome-mediated destruction of transcriptional activators can be intimately coupled to their function1,2. Recently, Nalley et al.3 challenged this view by reporting that the prototypical yeast activator Gal4 does not dynamically associate with chromatin, but rather ‘locks in’ to stable promoter complexes that are resistant to competition. Here we present evidence that the assay used to reach this conclusion is unsuitable, and that promoter-bound, active Gal4 is indeed susceptible to competition in vivo. Our data challenge the key evidence that Nalley et al.3 used to reach their conclusion, and indicate that Gal4 functions in vivo within the context of dynamic promoter complexes.

Date: 2009
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DOI: 10.1038/nature08406

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