Complete genome sequence of the Q-fever pathogen<i>Coxiella</i><i>burnetii</i>

Seshadri, Rekha; Paulsen, Ian T.; Eisen, Jonathan A.; Read, Timothy D.; Nelson, Karen E.; Nelson, William; Ward, Naomi; Tettelin, Hervé; Davidsen, Tanja M.; Beanan, Maureen J.; DeBoy, Robert T.; Daugherty, Sean C.; Brinkac, Lauren; Madupu, Ramana; Dodson, Robert J.; Khouri, Hoda; Lee, Kathy H.; Carty, Heather A.; Scanlan, David J.; Heinzen, Robert A.; Thompson, Herbert A.; Samuel, James E.; Fraser, Claire M.; Heidelberg, John F.

doi:10.1073/pnas.0931379100

Cited by 509 publications

(561 citation statements)

References 51 publications

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“…4). The C. burnetii genome is 1.9 Mbp, with 2,134 predicted CDSs 16 . Coxiella, Legionella and Francisella are g-proteobacterial pathogens with many lifestyle similarities.…”

Section: Phylogenymentioning

confidence: 99%

The complete genome sequence of Francisella tularensis, the causative agent of tularemia

et al. 2005

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Francisella tularensis is one of the most infectious human pathogens known. In the past, both the former Soviet Union and the US had programs to develop weapons containing the bacterium. We report the complete genome sequence of a highly virulent isolate of F. tularensis (1,892,819 bp). The sequence uncovers previously uncharacterized genes encoding type IV pili, a surface polysaccharide and iron-acquisition systems. Several virulence-associated genes were located in a putative pathogenicity island, which was duplicated in the genome. More than 10% of the putative coding sequences contained insertion-deletion or substitution mutations and seemed to be deteriorating. The genome is rich in IS elements, including IS630 Tc-1 mariner family transposons, which are not expected in a prokaryote. We used a computational method for predicting metabolic pathways and found an unexpectedly high proportion of disrupted pathways, explaining the fastidious nutritional requirements of the bacterium. The loss of biosynthetic pathways indicates that F. tularensis is an obligate host-dependent bacterium in its natural life cycle. Our results have implications for our understanding of how highly virulent human pathogens evolve and will expedite strategies to combat them.

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“…4). The C. burnetii genome is 1.9 Mbp, with 2,134 predicted CDSs 16 . Coxiella, Legionella and Francisella are g-proteobacterial pathogens with many lifestyle similarities.…”

Section: Phylogenymentioning

confidence: 99%

The complete genome sequence of Francisella tularensis, the causative agent of tularemia

et al. 2005

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“…The sequence of the complete genome of C. burnetii Nine Mile phase I RSA493 has been analyzed and suggests a circular topology for the chromosome. Although Coxiella was historically considered as a Rickettsia, gene-sequence analysis classifies the Coxiella genus in the order Legionellale, family Coxiellaceae with Rickettsiella and Aquicella [144]. The genome is predicted to encode 2 134 coding sequences larger than 30 aa, of which 719 (33.7%) are hypothetical.…”

Section: Bacteriologymentioning

confidence: 99%

“…The use of cellular markers (LAMP-1, EEA.1, rab7) [67,68] strongly suggests that the large replicative vacuoles containing Coxiella are derived from fusion with late endosomal-lysosomal organelles. Sequence homologies between the type IV secretion system proteins of Coxiella and Legionella strongly suggest that this secretion system should be involved in the maturation of the phagosome containing Coxiella [144]. Indeed, Coxiella encodes functional components of the type IV secretion system expressed in vivo during host cell infection [188].…”

Section: Entry and Survival Of C Burnetiimentioning

confidence: 99%

Is Q Fever an emerging or re-emerging zoonosis?

2005

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-Q fever is a zoonotic disease considered as emerging or re-emerging in many countries. It is caused by Coxiella burnetii, a bacterium developing spore-like forms that are highly resistant to the environment. The most common animal reservoirs are livestock and the main source of infection is by inhalation of contaminated aerosols. Although the culture process for Coxiella is laborious, advances on the knowledge of the life cycle of the bacterium have been made. New tools have been developed to (i) improve the diagnosis of Q fever in humans and animals, and especially animal shedders, (ii) perform epidemiological studies, and (iii) prevent the disease through the use of vaccines. This review summarizes the state of the knowledge on the bacteriology and clinical manifestations of Q fever as well as its diagnosis, epidemiology, treatment and prevention in order to understand what factors are responsible for its emergence or re-emergence. Coxiella burnetii / epidemiology / bacteriology / diagnostic / control

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“…The ability of Coxiella to develop this unique intracellular niche is entirely dependent on a type IV Dot/Icm secretion system [10,11]. This is a multi-protein apparatus which spans both the bacterial and vacuolar membranes, to enable the translocation of bacterial proteins, termed effectors, into the host cell [12]. The secretion system itself, and a subset of the effectors translocated by this system are essential for intracellular replication [10,11,13].…”

Section: Introductionmentioning

confidence: 99%

Interaction between autophagic vesicles and the Coxiella-containing vacuole requires CLTC (clathrin heavy chain)

Latomanski

Newton

2018

Autophagy

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Coxiella burnetii is an intracellular bacterial pathogen which causes Q fever, a human infection with the ability to cause chronic disease with potentially life-threatening outcomes. In humans, Coxiella infects alveolar macrophages where it replicates to high numbers in a unique, pathogen-directed lysosome-derived vacuole. This compartment, termed the Coxiella-containing vacuole (CCV), has a low internal pH and contains markers both of lysosomes and autophagosomes. The CCV membrane is also enriched with CLTC (clathrin heavy chain) and this contributes to the success of the CCV. Here, we describe a role for CLTC, a scaffolding protein of clathrin-coated vesicles, in facilitating the fusion of autophagosomes with the CCV. During gene silencing of CLTC, CCVs are unable to fuse with each other, a phenotype also seen when silencing genes involved in macroautophagy/autophagy. MAP1LC3B/LC3B, which is normally observed inside the CCV, is excluded from CCVs in the absence of CLTC. Additionally, this study demonstrates that autophagosome fusion contributes to CCV size as cell starvation and subsequent autophagy induction leads to further CCV expansion. This is CLTC dependent, as the absence of CLTC renders autophagosomes no longer able to contribute to the expansion of the CCV. This investigation provides a functional link between CLTC and autophagy in the context of Coxiella infection and highlights the CCV as an important tool to explore the interactions between these vesicular trafficking pathways.

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Complete genome sequence of the Q-fever pathogenCoxiellaburnetii

Cited by 509 publications

References 51 publications

The complete genome sequence of Francisella tularensis, the causative agent of tularemia

The complete genome sequence of Francisella tularensis, the causative agent of tularemia

Is Q Fever an emerging or re-emerging zoonosis?

Interaction between autophagic vesicles and the Coxiella-containing vacuole requires CLTC (clathrin heavy chain)

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