This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Supplemental material
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Yerushalmi, G.
Right arrow Articles by Rosenshine, I.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Yerushalmi, G.
Right arrow Articles by Rosenshine, I.

 Previous Article  |  Next Article 

Journal of Bacteriology, December 2008, p. 7808-7818, Vol. 190, No. 23
0021-9193/08/$08.00+0     doi:10.1128/JB.00663-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Mutational Analysis of the Locus of Enterocyte Effacement-Encoded Regulator (Ler) of Enteropathogenic Escherichia coli{triangledown} ,{dagger}

Gal Yerushalmi, Chen Nadler, Tatiana Berdichevski, and Ilan Rosenshine*

Department of Molecular Genetics and Biotechnology, The Hebrew University, Faculty of Medicine, POB 12272, Jerusalem 91120, Israel

Received 13 May 2008/ Accepted 25 September 2008

The locus of enterocyte effacement (LEE) pathogenicity island of enterohemorrhagic and enteropathogenic Escherichia coli (EHEC and EPEC, respectively) comprises a cluster of operons encoding a type III secretion system and related proteins, all of which are essential for bacterial colonization of the host intestines. The LEE1 operon encodes Ler, which positively regulates many EPEC and EHEC virulence genes located in the LEE region and elsewhere in the chromosome. In addition, Ler is a specific autorepressor of LEE1 transcription. To better understand the function of Ler, we screened for Ler mutants defective in autorepression. We isolated 18 different point mutations in Ler, rendering it defective in autorepression and in DNA binding. Among these mutants were those defective in positive regulation as well as in autorepression, dominant-negative mutants, and a mutant deficient in oligomerization. Importantly, a group of Ler autorepression mutants complemented an EPEC ler deletion mutant for transcription activation in a dosage-dependent manner, suggesting that Ler and possibly other autorepressors have an intrinsic compensatory mechanism that enables them to sustain mutations. In addition, the phenotypes of the different mutants identified by the screen define a novel domain in Ler that is required for oligomerization.


* Corresponding author. Mailing address: Dept. of Molecular Genetics and Biotechnology, The Hebrew University Faculty of Medicine, POB 12272, Jerusalem 91120, Israel. Phone: 972 2 6758754. Fax: 972 2 6757308. E-mail: ilanr{at}ekmd.huji.ac.il

{triangledown} Published ahead of print on 3 October 2008.

{dagger} Supplemental material for this article may be found at http://jb.asm.org/.


Journal of Bacteriology, December 2008, p. 7808-7818, Vol. 190, No. 23
0021-9193/08/$08.00+0     doi:10.1128/JB.00663-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.