JB
Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
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 HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Mhlanga-Mutangadura, T.
Right arrow Articles by Golomb, M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Mhlanga-Mutangadura, T.
Right arrow Articles by Golomb, M.

 Previous Article  |  Next Article 

Journal of Bacteriology, September 1998, p. 4693-4703, Vol. 180, No. 17
0021-9193/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.

Evolution of the Major Pilus Gene Cluster of Haemophilus influenzae

Tendai Mhlanga-Mutangadura,1,2 Gregory Morlin,3 Arnold L. Smith,3 Abraham Eisenstark,1,4 and Miriam Golomb1,*

Division of Biological Sciences, University of Missouri, Columbia, Missouri 652111; Department of Biological Sciences, University of Zimbabwe, Harare, Zimbabwe2; Department of Molecular Microbiology and Immunology, University of Missouri, Columbia, Missouri 652123; and Cancer Research Center, Columbia, Missouri 652014

Received 23 February 1998/Accepted 10 June 1998

Haemophilus influenzae is a ubiquitous colonizer of the human respiratory tract and causes diseases ranging from otitis media to meningitis. Many H. influenzae isolates express pili (fimbriae), which mediate adherence to epithelial cells and facilitate colonization. The pilus gene (hif) cluster of H. influenzae type b maps between purE and pepN and resembles a pathogenicity island: it is present in invasive strains, absent from the nonpathogenic Rd strain, and flanked by direct repeats of sequence at the insertion site. To investigate the evolution and role in pathogenesis of the hif cluster, we compared the purE-pepN regions of various H. influenzae laboratory strains and clinical isolates. Unlike Rd, most strains had an insert at this site, which usually was the only chromosomal locus of hif DNA. The inserts are diverse in length and organization: among 20 strains, nine different arrangements were found. Several nontypeable isolates lack hif genes but have two conserved open reading frames (hicA and hicB) upstream of purE; their inferred products are small proteins with no data bank homologs. Other isolates have hif genes but lack hic DNA or have combinations of hif and hic genes. By comparing these arrangements, we have reconstructed a hypothetical ancestral genotype, the extended hif cluster. The hif region of INT1, an invasive nontypeable isolate, resembles the hypothetical ancestor. We propose that a progenitor strain acquired the extended cluster by horizontal transfer and that other variants arose as deletions. The structure of the hif cluster may correlate with colonization site or pathogenicity.

* Corresponding author. Mailing address: Division of Biological Sciences, 110 Tucker Hall, University of Missouri, Columbia, MO 65211. Phone: (573) 882-9628. Fax: (573) 882-0123. E-mail: golomb{at}biosci.mbp.missouri.edu.

Journal of Bacteriology, September 1998, p. 4693-4703, Vol. 180, No. 17
0021-9193/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.


This article has been cited by other articles:



Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
Appl. Environ. Microbiol. Infect. Immun. Eukaryot. Cell
Mol. Cell. Biol. J. Virol. Microbiol. Mol. Biol. Rev.
ALL ASM JOURNALS

Copyright © 1998 by the American Society for Microbiology. All rights reserved.