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A spontaneous genomic deletion in Listeria ivanovii identifies LIPI-2, a species-specific pathogenicity island encoding sphingomyelinase and numerous internalins

Molecular Microbiology publish this investigation article

January 1st, 2006

Listeria ivanovii differs from the human pathogen Listeria monocytogenes in that it specifically affects ruminants, causing septicaemia and abortion but not meningo-encephalitis. The genetic characterization of spontaneous L. ivanovii mutants lacking the virulence factor SmcL (sphingomyelinase) led us to identify LIPI-2, the first species-specific pathogenicity island from Listeria. Besides SmcL, this 22 kb chromosomal locus encodes 10 internalin (Inl) proteins: i-InlB1 and -B2 are large/surface-associated Inls similar to L. monocytogenes InlB; i-InlE to -L are small/excreted (SE)-Inls, i-InlG being a tandem fusion of two SE-Inls. Except i-inlB1, all LIPI-2 inl genes are controlled by the virulence regulator, PrfA. LIPI-2 is inserted into a tRNA locus and is unstable - half of it deleting at approximately 10(-4) frequency with a portion of contiguous DNA. The spontaneous mutants were attenuated in vivo in mice and lambs and showed impaired intracellular growth and apoptosis induction in bovine MDBK cells. Targeted knock-out mutations associated the virulence defect with LIPI-2 genes. The region between the core genome loci ysnB-tRNA(arg) and ydeI flanking LIPI-2 contained different gene complements in the different Listeria spp. and even serovars of L. monocytogenes, including remnants of the PSA bacteriophage int gene in serovar 4b, indicating it is a hot spot for horizontal genome diversification. LIPI-2 is conserved in L. ivanovii ssp. ivanovii and londoniensis, suggesting an early acquisition during the species` evolution. LIPI-2 is likely to play an important role in the pathogenic and host tropism of L. ivanovii




Dominguez-Bernal G., Muller-Altrock S., Gonzalez-Zorn B., Scortti M., Herrmann P., Monzo HJ., Lacharme L., Kreft J. and Vazquez-Boland JA.




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A spontaneous genomic deletion in Listeria ivanovii identifies LIPI-2, a species-specific pathogenicity island encoding sphingomyelinase and numerous internalins

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A spontaneous genomic deletion in Listeria ivanovii identifies LIPI-2, a species-specific pathogenicity island encoding sphingomyelinase and numerous internalins



Participants:

Universidad ComplutenseDepartamento de Sanidad Animal. Facultad de Veterinaria. Universidad Complutense (UCM).

Universidad ComplutenseServicio de Zoonosis de Transmisión Alimentaria y Resistencia a Antimicrobianos (ZTA). Centro de Vigilancia Sanitaria Veterinaria (VISAVET). Universidad Complutense (UCM).

Universidad ComplutenseInfectología Bacteriana Veterinaria (INBAVET). Facultad de Veterinaria. Universidad Complutense (UCM).

Lehrstuhl für Mikrobiologie, Biozentrum. Universität Würzburg.

Universidad de LeónGrupo de Patogénesis Molecular Bacteriana. Facultad de Veterinaria. Universidad de León.

Bacterial Molecular Pathogenesis Group. Faculty of Medical and Veterinary Sciences. University of Bristol.







Molecular Microbiology
FACTOR YEAR Q
5.634 2006

NLMID: 8712028

PMID: 16390439

ISSN: 0950-382X



TITLE: A spontaneous genomic deletion in Listeria ivanovii identifies LIPI-2, a species-specific pathogenicity island encoding sphingomyelinase and numerous internalins


JOURNAL: Mol. Microbiol.


NUMERACIÓN: 59(2):415-32


AÑO: 2006


PUBLISHER: Blackwell Scientific Publications


AUTHORS: Dominguez-Bernal G., Muller-Altrock S., Gonzalez-Zorn B., Scortti M., Herrmann P., Monzo HJ., Lacharme L., Kreft J. and Vazquez-Boland JA.


VISAVET PARTICIPANTS


Bruno González Zorn

DOI: https://doi.org/ 10.1111/j.1365-2958.2005.04955.x


CITE THIS PUBLICATION:

Dominguez-Bernal G., Muller-Altrock S., Gonzalez-Zorn B., Scortti M., Herrmann P., Monzo HJ., Lacharme L., Kreft J. and Vazquez-Boland JA. A spontaneous genomic deletion in Listeria ivanovii identifies LIPI-2, a species-specific pathogenicity island encoding sphingomyelinase and numerous internalins. Molecular Microbiology. 59(2):415-32. 2006. (A). ISSN: 0950-382X. DOI: 10.1111/j.1365-2958.2005.04955.x


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