Nucleic Acids Research Advance Access originally published online on September 16, 2009
Nucleic Acids Research 2009 37(20):6655-6664; doi:10.1093/nar/gkp676
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Nucleic Acids Research, 2009, Vol. 37, No. 20 6655-6664
© The Author(s) 2009. Published by Oxford University Press.
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.5/uk/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
Gene Regulation, Chromatin and Epigenetics |
Transcription from bacteriophage 
pR promoter is regulated independently and antagonistically by DksA and ppGpp
y
e
grzyn
asz*
Department of Molecular Biology, University of Gdask, Kadki 24, 80-822 Gdask, Poland
*To whom correspondence should be addressed. Tel: +48 58 523 6376; Fax: +48 58 523 6424; Email: szalewsk{at}biotech.ug.gda.pl
Received March 27, 2009. Revised July 31, 2009. Accepted July 31, 2009.
The stringent response effector, guanosine tetraphosphate (ppGpp), adjust gene expression and physiology in bacteria, by affecting the activity of various promoters. RNA polymerase-interacting protein, DksA, was proposed to be the co-factor of ppGpp effects; however, there are reports suggesting independent roles of these regulators. Bacteriophage 
major lytic promoter, pR, is down-regulated by the stringent response and ppGpp. Here, we present evidence that DksA significantly stimulates pR-initiated transcription in vitro in the reconstituted system. DksA is also indispensable for pR activity in vivo. DksA-mediated activation of pR-initiated transcription is predominant over ppGpp effects in the presence of both regulators in vitro. The possible role of the opposite regulation by ppGpp and DksA in phage development is discussed. The major mechanism of DksA-mediated activation of transcription from pR involves facilitating of RNA polymerase binding to the promoter region, which results in more productive transcription initiation. Thus, our results provide evidence for the first promoter inhibited by ppGpp that can be stimulated by the DksA protein both in vivo and in vitro. Therefore, DksA role could be not only independent but antagonistic to ppGpp in transcription regulation.