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Please use this identifier to cite or link to this item: http://hdl.handle.net/10261/38942
Title: The switch from early to late transcription in phage GA-1: characterization of the regulatory protein p4G
Authors: Horcajadas, José Antonio; Monsalve, María ; Rojo, Fernando; Salas, Margarita
Keywords: Transcription regulation
Protein-DNA interactions
Prokaryotic repressor
Issue Date: 30-Jul-1999
Publisher: Elsevier
Citation: Journal of Molecular Biology 290(5): 917-928 (1999)
Abstract: The transcription program of the Bacillus phage GA-1, a distant relative of phage Φ29, has been studied. Transcription of the GA-1 genome occurred in two stages, early and late. Early genes were expressed from two promoters equivalent to the Φ29 A2b and A2c promoters, whereas late transcription started at a site equivalent to the Φ29 late A3 promoter. The activity of the GA-1 early A2b and A2c promoters diminished 10 minutes after infection, a time at which expression of the late promoter increased significantly. The switch from early to late transcription required protein synthesis, suggesting the need for viral protein(s). An open reading frame was found in the GA-1 genome coding for a protein showing a 53 % similarity to Φ29 regulatory protein p4, and was named p4G. In Φ29, protein p4 represses the early A2b and A2c promoters and activates the late A3 promoter by recruiting RNA polymerase to it. A binding site for protein p4G was localized upstream from the GA-1 late A3 promoter, overlapping with the early A2b promoter. In vitro, protein p4G prevented the binding of RNA polymerase to the GA-1 early A2b promoter but, unlike in Φ29, had no effect on the expression of the late A3 promoter: RNA polymerase could efficiently bind and initiate transcription from the A3 promoter in the absence of protein p4G. Therefore, activation of late transcription occurs differently in GA-1 and Φ29. We propose that protein p4G is an anti-repressor which inhibits the binding to the late promoter of an unknown repressor factor present in the host strain.
Publisher version (URL): http://dx.doi.org/10.1006/jmbi.1999.2932
URI: http://hdl.handle.net/10261/38942
DOI: 10.1006/jmbi.1999.2932
ISSN: 0022-2836
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