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The Coxiella Burnetii Qph1 Plasmid Is a Virulence Factor for Colonizing

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The Coxiella Burnetii Qph1 Plasmid Is a Virulence Factor for Colonizing bioRxiv preprint doi: https://doi.org/10.1101/2020.03.22.001875; this version posted March 25, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY-NC-ND 4.0 International license. 1 The Coxiella burnetii QpH1 plasmid is a virulence factor for 2 colonizing bone marrow-derived murine macrophages 3 4 Shengdong Luo1,2¶, Zhihui Sun2¶, Huahao Fan1¶, Shanshan Lu1,3&, Yan Hu3&, 5 Ruisheng Li3&, Xiaoping An1&, Yigang Tong1*, Lihua Song1,2* 6 7 1 Beijing Advanced Innovation Center for Soft Matter Science and Engineering, 8 College of Life Science and Technology, Beijing University of Chemical Technology, 9 Beijing, China 10 11 2 State Key Laboratory of Pathogen and Biosecurity, Beijing Institute of Microbiology 12 and Epidemiology, Beijing, China 13 14 3 Research Center for Clinical Medicine, The Fifth Medical Center of PLA General 15 Hospital, Beijing, China 16 17 * Corresponding author 18 Email: [email protected] (LS); [email protected] (YT). 19 20 ¶ These authors contributed equally to this work. 21 & These authors also contributed equally to this work. 22 bioRxiv preprint doi: https://doi.org/10.1101/2020.03.22.001875; this version posted March 25, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY-NC-ND 4.0 International license. 23 Abstract 24 Coxiella burnetii carries a large conserved plasmid or plasmid-like chromosomally 25 integrated sequence of unknown function. Here we report the curing of QpH1 plasmid 26 from C. burnetii Nine Mile phase II, the characterization of QpH1-deficient C. 27 burnetii in in vitro and in vivo infection models, and the characterization of plasmid 28 biology. A shuttle vector pQGK, which is composed of the CBUA0036-0039a region 29 (predicted for QpH1 maintenance), an E. coli plasmid ori, eGFP and kanamycin 30 resistance genes was constructed. The pQGK vector can be stably transformed into 31 Nine Mile II and maintained at a similar low copy like QpH1. Importantly, 32 transformation with pQGK cured the endogenous QpH1 due to plasmid 33 incompatibility. Compared to a Nine Mile II transformant of a RSF1010-based vector, 34 the pQGK transformant shows an identical one-step growth curve in axenic media, a 35 similar growth curve in Buffalo green monkey kidney cells, an evident growth defect 36 in macrophage-like THP-1 cells, and dramatically reduced ability of colonizing bone 37 marrow-derived murine macrophages. In the SCID mouse infection model, the pQGK 38 transformants caused a lesser extent of splenomegaly. Moreover, the plasmid biology 39 was investigated by mutagenesis. We found CBUA0037-0039 are essential for 40 plasmid maintenance, and CBUA0037-0038 account for plasmid compatibility. Taken 41 together, our data suggest that QpH1 encodes factor(s) essential for colonizing murine 42 macrophages, and to a lesser extent for colonizing human macrophages. This study 43 highlights a critical role of QpH1 for C. burnetii persistence in rodents, and expands 44 the toolkit for genetic studies in C. burnetii. 45 46 Author summary bioRxiv preprint doi: https://doi.org/10.1101/2020.03.22.001875; this version posted March 25, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY-NC-ND 4.0 International license. 47 It is postulated that C. burnetii recently evolved from an inherited symbiont of ticks 48 by the acquisition of novel virulence factors. All C. burnetii isolates carry a large 49 plasmid or have a chromosomally integrated plasmid-like sequence. The plasmid is a 50 candidate virulence factor that contributes to C. burnetii evolution. Here we describe 51 the construction of novel shuttle vectors that allow to make plasmid-deficient C. 52 burnetii mutants. With this plasmid-curing approach, we characterized the role of the 53 QpH1 plasmid in in vitro and in vivo C. burnetii infection models. We found that the 54 plasmid plays a critical role for C. burnetii growth in macrophages, especially in 55 murine macrophages, but not in axenic media and BGMK cells. Our work highlights 56 an essential role of the plasmid for the acquisition of colonizing capability in rodents 57 by C. burnetii. This study represents a major step toward unravelling the mystery of 58 the C. burnetii cryptic plasmids. 59 60 Introduction 61 C. burnetii is a Gram-negative intracellular bacterium that causes Q fever, a world 62 widely distributed zoonosis [1]. It is highly infectious and is classified as a potential 63 biowarfare agent [2]. Its infections in humans are mostly asymptomatic but may 64 manifest as an acute disease (mainly as a self-limiting febrile illness, pneumonia, or 65 hepatitis) or as a chronic disease (mainly endocarditis in patients with previous 66 valvulopathy) [1]. All C. burnetii isolates maintain a large cryptic plasmid or 67 plasmid-like chromosomally integrated sequence [3]. This absolute conservation of 68 plasmid sequences suggests they are critical in C. burnetii survival [4]. Increased 69 knowledge of the plasmid sequences will enhance our understanding of C. burnetii 70 biology and pathogenesis and will be important for guiding the design of live bioRxiv preprint doi: https://doi.org/10.1101/2020.03.22.001875; this version posted March 25, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY-NC-ND 4.0 International license. 71 attenuated vaccine strains for the prevention of Q fever. 72 C. burnetii has at least five different plasmid types: four different plasmids 73 (QpH1, QpRS, QpDV, and QpDG) and one type of QpRS-like chromosomally 74 integrated sequence [5-9]. The plasmids range from 32 to 54 kb in size and share a 25 75 kb core region [3]. Characterization of these plasmid types led to the classification of 76 five associated genomic groups. The hypothesized correlation of plasmid types and 77 genomic groups with the clinical outcomes of Q fever was controversial [3, 10, 11], 78 but the concept of genomic-group specific virulence was supported by mouse and 79 guinea pig infection studies [12, 13]. According to studies on C. burnetii mostly from 80 Europe and North America, this bacterium is considered having a clonal population 81 structure with low genetic diversity [14-16]. Future studies on more C. burnetii 82 isolates especially from other regions will help to understand its global genetic 83 diversity. 84 The sequences of all five representative plasmid types in C. burnetii have been 85 determined [3, 7, 8, 17, 18]. Paul et al. analyzed the diversity of plasmid genes by 86 using DNA microarrays [3]. Nine predicted functional plasmid ORFs are conserved in 87 all plasmid sequences. Two of these ORFs appear to encode proteins similar to phage 88 proteins involved in tail assembly and site-specific recombination, while seven of 89 them encode hypothetical proteins. Three (CBUA0006, -0013 and -0023) of these 90 conserved plasmid hypothetical proteins are secreted effectors of the type IV secretion 91 system [4]. During ectopic expression in HeLa cells, these effectors localize at 92 different subcellular sites, suggesting roles in subversion of host cell functions. In 93 addition, novel plasmid-specific effectors were also identified, supporting the concept 94 of pathotype virulence [19]. Besides the identification of plasmid-encoded secretion 95 effectors, the plasmid is also speculated to be able to be transferred to the host cell bioRxiv preprint doi: https://doi.org/10.1101/2020.03.22.001875; this version posted March 25, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY-NC-ND 4.0 International license. 96 [20]. 97 The advent and foregoing improvement of axenic culture techniques greatly 98 facilitates studies on C. burnetii biology [21-24]. C. burnetii replicates within 99 phagolysosome-like parasitophorous vacuoles (termed Coxiella-containing vacuole, 100 or CCV) in mononuclear phagocytes. Genetic studies revealed that the CCV 101 biogenesis and C. burnetii growth in host cells require a type IV secretion system and 102 a repertoire of type IV effectors [25-28]. The role that these effectors play in C. 103 burnetii pathogenicity is of intense interest. However, regarding the plasmid effectors, 104 reports on their mutants are scarce. By using transposon mutagenesis, Martinez et al. 105 identified mutants of eight QpH1 genes and observed strong phenotypes with mutants 106 of parB and repA, surprisingly, not the mutant of the conserved secretion effector 107 CBUA0023 [29]. Regardless of the identification of plasmid secretion effectors, a role 108 for the plasmid in C. burnetii pathogenesis remains elusive. 109 Since the first development of axenic media, the C. burnetii genetics toolbox has 110 been expanding [30, 31]. Current genetic tools for C. burnetii include, but are not 111 limited to, transposon systems [32], RSF1010 ori-based shuttle vectors [4, 33] and 112 targeted gene inactivation systems [31]. However, there have been no reports of 113 studies using these tools to decipher roles of plasmids in C. burnetii pathogenesis. 114 Here, we describe a set of QpH1-derived shuttle vectors for C. burnetii transformation.
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