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Journal of Bacteriology, January 2005, p. 434-442, Vol. 187, No. 2
0021-9193/05/$08.00+0     doi:10.1128/JB.187.2.434-442.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Starvation for Different Nutrients in Escherichia coli Results in Differential Modulation of RpoS Levels and Stability

Mark J. Mandel and Thomas J. Silhavy*

Department of Molecular Biology, Princeton University, Princeton, New Jersey

Received 14 September 2004/ Accepted 13 October 2004

Levels of RpoS increase upon glucose starvation in Escherichia coli, which leads to the transcription of genes whose products combat a variety of stresses. RpoS stability is a key level of control in this process, as SprE (RssB)-mediated degradation is inhibited under glucose starvation. Starvation for ammonia or phosphate also results in increased stress resistance and induction of RpoS-dependent genes. However, we demonstrate that RpoS levels following ammonia starvation are only slightly increased compared to growing cells and are 10-fold below the levels observed under glucose or phosphate limitation. This difference is largely due to regulated proteolysis of RpoS, as its stability in ammonia-starved cells is intermediate between that in logarithmic-phase cells and glucose-starved cells. Use of an rpoS construct that is devoid of the gene's native transcriptional and translational control regions reveals that stability differences are sufficient to explain the different levels of RpoS observed in logarithmic phase, ammonia starvation, and glucose starvation. Under phosphate starvation, however, rpoS translation is increased. The cellular response to nutrient limitation is much more complex than previously appreciated, as there is not simply one response that is activated by starvation for any essential nutrient. Our data support the hypothesis that SprE activity is the key level at which ammonia and glucose starvation signals are transmitted to RpoS, and they suggest that carbon source and/or energy limitation are necessary for full inactivation of the SprE pathway.

* Corresponding author. Mailing address: Department of Molecular Biology, 310 Lewis Thomas Laboratory, Princeton University, Princeton, NJ 08544. Phone: (609) 258-5899. Fax: (609) 258-2957. E-mail: tsilhavy{at}molbio.princeton.edu.

Journal of Bacteriology, January 2005, p. 434-442, Vol. 187, No. 2
0021-9193/05/$08.00+0     doi:10.1128/JB.187.2.434-442.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.



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