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Infection and Immunity, August 2005, p. 4834-4845, Vol. 73, No. 8
0019-9567/05/$08.00+0     doi:10.1128/IAI.73.8.4834-4845.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Global Gene Expression and the Role of Sigma Factors in Neisseria gonorrhoeae in Interactions with Epithelial Cells

Ying Du, Jonathan Lenz, and Cindy Grove Arvidson*

Department of Microbiology and Molecular Genetics and Center for Microbial Pathogenesis, Michigan State University, East Lansing, Michigan 48824-1101

Received 12 November 2004/ Returned for modification 8 February 2005/ Accepted 23 March 2005

Like many bacterial pathogens, Neisseria gonorrhoeae must adapt to environmental changes in order to successfully colonize and proliferate in a new host. Modulation of gene expression in response to environmental signals is an efficient mechanism used by bacteria to achieve this goal. Using DNA microarrays and a tissue culture model for gonococcal infection, we examined global changes in gene expression in N. gonorrhoeae in response to adherence to host cells. Among those genes induced upon adherence to human epithelial cells in culture was rpoH, which encodes a homolog of the heat shock sigma factor, {sigma}32 (RpoH), as well as genes of the RpoH regulon, groEL and groES. Attempts to construct an rpoH null mutant in N. gonorrhoeae were unsuccessful, suggesting that RpoH is essential for viability of N. gonorrhoeae. The extracytoplasmic sigma factor, RpoE ({sigma}E), while known to regulate rpoH in other bacteria, was found not to be necessary for the up-regulation of rpoH in gonococci upon adherence to host cells. To examine the role of RpoH in host cell interactions, an N. gonorrhoeae strain conditionally expressing rpoH was constructed. The results of our experiments showed that while induction of rpoH expression is not necessary for adherence of gonococci to epithelial cells, it is important for the subsequent invasion step, as gonococci depleted for rpoH invade cells two- to threefold less efficiently than a wild-type strain. Taken together, these results indicate that {sigma}32, but not {sigma}E, is important for the response of gonococci in the initial steps of an infection.

* Corresponding author. Mailing address: Department of Microbiology and Molecular Genetics, Michigan State University, East Lansing, MI 48824-1101. Phone: (517) 355-6463, ext. 1573. Fax: (517) 353-8957. E-mail: arvidso3{at}msu.edu.

Editor: V. J. DiRita

Infection and Immunity, August 2005, p. 4834-4845, Vol. 73, No. 8
0019-9567/05/$08.00+0     doi:10.1128/IAI.73.8.4834-4845.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.



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