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Insertional mutagenesis in the zoonotic pathogen Chlamydia caviae
University of Maryland, Department of Microbial Pathogenesis.
Umeå universitet, Medicinska fakulteten, Institutionen för molekylärbiologi (Medicinska fakulteten). Umeå universitet, Medicinska fakulteten, Umeå Centre for Microbial Research (UCMR). Umeå universitet, Medicinska fakulteten, Molekylär Infektionsmedicin, Sverige (MIMS).
Umeå universitet, Medicinska fakulteten, Institutionen för molekylärbiologi (Medicinska fakulteten). Umeå universitet, Medicinska fakulteten, Molekylär Infektionsmedicin, Sverige (MIMS). Umeå universitet, Medicinska fakulteten, Umeå Centre for Microbial Research (UCMR).
Umeå universitet, Medicinska fakulteten, Institutionen för molekylärbiologi (Medicinska fakulteten). Umeå universitet, Medicinska fakulteten, Molekylär Infektionsmedicin, Sverige (MIMS). Umeå universitet, Medicinska fakulteten, Umeå Centre for Microbial Research (UCMR).ORCID-id: 0000-0002-7745-2844
Vise andre og tillknytning
2019 (engelsk)Inngår i: PLOS ONE, E-ISSN 1932-6203, Vol. 14, nr 11, artikkel-id e0224324Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

The ability to introduce targeted genetic modifications in microbial genomes has revolutionized our ability to study the role and mode of action of individual bacterial virulence factors. Although the fastidious lifestyle of obligate intracellular bacterial pathogens poses a technical challenge to such manipulations, the last decade has produced significant advances in our ability to conduct molecular genetic analysis in Chlamydia trachomatis, a major bacterial agent of infertility and blindness. Similar approaches have not been established for the closely related veterinary Chlamydia spp., which cause significant economic damage, as well as rare but potentially life-threatening infections in humans. Here we demonstrate the feasibility of conducting site-specific mutagenesis for disrupting virulence genes in Ccaviae, an agent of guinea pig inclusion conjunctivitis that was recently identified as a zoonotic agent in cases of severe community-acquired pneumonia. Using this approach, we generated Ccaviae mutants deficient for the secreted effector proteins IncA and SinC. We demonstrate that Ccaviae IncA plays a role in mediating fusion of the bacteria-containing vacuoles inhabited by Ccaviae. Moreover, using a chicken embryo infection model, we provide first evidence for a role of SinC in Ccaviae virulence in vivo.

sted, utgiver, år, opplag, sider
Public Library of Science , 2019. Vol. 14, nr 11, artikkel-id e0224324
HSV kategori
Forskningsprogram
mikrobiologi
Identifikatorer
URN: urn:nbn:se:umu:diva-169550DOI: 10.1371/journal.pone.0224324ISI: 000532694400023PubMedID: 31697687Scopus ID: 2-s2.0-85074644319OAI: oai:DiVA.org:umu-169550DiVA, id: diva2:1421797
Tilgjengelig fra: 2020-04-06 Laget: 2020-04-06 Sist oppdatert: 2023-04-24bibliografisk kontrollert

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Vielfort, KatarinaMuraleedharan, SamadaHenriksson, JohanSixt, Barbara Susanne

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