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Infection and Immunity, October 1999, p. 5265-5274, Vol. 67, No. 10
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.
Common and Specific Characteristics of the
High-Pathogenicity Island of Yersinia
enterocolitica
A.
Rakin,*
C.
Noelting,
S.
Schubert, and
J.
Heesemann
Max-von-Pettenkofer-Institüt für Hygiene
und Medizinische Mikrobiologie, Ludwig Maximilians Universität
München, 80336 Munich, Germany
Received 24 May 1999/Returned for modification 22 June
1999/Accepted 6 July 1999
Yersinia pestis, Y. pseudotuberculosis O:1,
and Y. enterocolitica biogroup 1B strains carry a
high-pathogenicity island (HPI), which mediates biosynthesis and uptake
of the siderophore yersiniabactin and a mouse-lethal phenotype. The HPI
of Y. pestis and Y. pseudotuberculosis (Yps
HPI) are highly conserved in sequence and organization, while the HPI
of Y. enterocolitica (Yen HPI) differs significantly. The
43,393-bp Yen HPI sequence of Y. enterocolitica WA-C,
serotype O:8, was completed and compared to that of the Yps HPI of
Y. pseudotuberculosis PB1, serotype O:1A. A common
GC-rich region (G+C content, 57.5 mol%) of 30.5 kb is conserved
between yersinia strains. This region carries genes for yersiniabactin
biosynthesis, regulation, and uptake and thus can be considered the
functional "core" of the HPI. In contrast, the second part of the
HPI is AT rich and completely different in two evolutionary lineages of
the HPI, being 12.8 kb in the Yen HPI and 5.6 kb in the Yps HPI. The
variable part acquired one IS100 element in the Yps HPI and
accumulated four insertion elements, IS1328,
IS1329, IS1400, and IS1222, in the Yen HPI. The insertion of a 125-bp ERIC sequence modifies the structure
of the promoter of the ybtA yersiniabactin regulator in the
Yen HPI. In contrast to the precise excision of the Yps HPI in Y. pseudotuberculosis, the Yen HPI suffers imprecise deletions. The
Yen HPI is stably integrated in one of the three asn tRNA copies in Y. enterocolitica biogroup 1B (serotypes O:8,
O:13, O:20, and O:21), probably due to inactivation of the putative integrase. The 17-bp duplications of the 3' end of the asnT
RNA are present in both Yersinia spp. The HPI attachment
site is unoccupied in nonpathogenic Y. enterocolitica NF-O,
biogroup 1A, serotype O:5. The HPI of Yersinia is a
composite and widely spread genomic element with a highly conserved
yersiniabactin functional "core" and a divergently evolved variable part.
*
Corresponding author. Mailing address: Max von
Pettenkofer-Institut für Hygiene und Medizinische Mikrobiologie,
Pettenkofer Str.9a, 80336 Munich, Germany. Phone: 49-0-89-5160-5261. Fax: 49-0-89-51605223. E-mail:
rakin{at}m3401.mpk.med.uni-muenchen.de.
Infection and Immunity, October 1999, p. 5265-5274, Vol. 67, No. 10
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.
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