Nucleic Acids Research Advance Access originally published online on March 11, 2008
Nucleic Acids Research 2008 36(8):2570-2580; doi:10.1093/nar/gkn091
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Nucleic Acids Research, 2008, Vol. 36, No. 8 2570-2580
© 2008 The Author(s)
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.0/uk/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
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The small RNA GlmY acts upstream of the sRNA GlmZ in the activation of glmS expression and is subject to regulation by polyadenylation in Escherichia coli
1Department of General Microbiology, Institute of Microbiology and Genetics, Georg-August University, Grisebachstrasse 8, D-37077 Göttingen, Germany and 2Régulation de l'Expression Génétique chez les Microorganismes, Université Denis Diderot Paris 7; CNRS, UPR9073; Institut de Biologie Physico-Chimique, 13 rue Pierre et Marie Curie, 75005 Paris, France
*To whom correspondence should be addressed. Tel: +49 551 393796; Fax: +49 551 393808; Email: bgoerke{at}gwdg.de
Received January 3, 2008. Revised February 11, 2008. Accepted February 12, 2008.
In Escherichia coli the glmS gene encoding glucosamine 6-phosphate (GlcN-6-P) synthase GlmS is feedback regulated by GlcN-6-P in a pathway that involves the small RNA GlmZ. Expression of glmS is activated by the unprocessed form of GlmZ, which accumulates when the intracellular GlcN-6-P concentration decreases. GlmZ stabilizes a glmS transcript that derives from processing. Overexpression of a second sRNA, GlmY, also activates glmS expression in an unknown way. Furthermore, mutations in two genes, yhbJ and pcnB, cause accumulation of full-length GlmZ and thereby activate glmS expression. The function of yhbJ is unknown and pcnB encodes poly(A) polymerase PAP-I known to polyadenylate and destabilize RNAs. Here we show that GlmY acts indirectly in a way that depends on GlmZ. When the intracellular GlcN-6-P concentration decreases, GlmY accumulates and causes in turn accumulation of full-length GlmZ, which finally activates glmS expression. In glmZ mutants, GlmY has no effect on glmS, whereas artificially expressed GlmZ can activate glmS expression also in the absence of GlmY. Furthermore, we show that PAP-I acts at the top of this regulatory pathway by polyadenylating and destabilizing GlmY. In pcnB mutants, GlmY accumulates and induces glmS expression by stabilizing full-length GlmZ. Hence, the data reveal a regulatory cascade composed of two sRNAs, which responds to GlcN-6-P and is controlled by polyadenylation.