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• W1890640081 endingPage "821" @default.
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• W1890640081 abstract "Brucella abortus is a facultative intracellular pathogen that grows unipolarly and initiates the replication of its two chromosomes in a specific order. Bacteria at the G1 stage of the cell cycle, that is, before the initiation of their chromosomal replication, are preferentially internalized in host cells. Cell-cycle progression is coordinated with trafficking in the host cell, the endosomal stage being divided into two parts: a first, long, nongrowing part, and a second part in which growth and chromosomal replication are resumed. A cell-cycle control network, conserved with the model bacterium Caulobacter crescentus, is essential for B. abortus virulence. Brucellae are facultative intracellular pathogens. The recent development of methods and genetically engineered strains allowed the description of cell-cycle progression of Brucella abortus, including unipolar growth and the ordered initiation of chromosomal replication. B. abortus cell-cycle progression is coordinated with intracellular trafficking in the endosomal compartments. Bacteria are first blocked at the G1 stage, growth and chromosome replication being resumed shortly before reaching the intracellular proliferation compartment. The control mechanisms of cell cycle are similar to those reported for the bacterium Caulobacter crescentus, and they are crucial for survival in the host cell. The development of single-cell analyses could also be applied to other bacterial pathogens to investigate their cell-cycle progression during infection. Brucellae are facultative intracellular pathogens. The recent development of methods and genetically engineered strains allowed the description of cell-cycle progression of Brucella abortus, including unipolar growth and the ordered initiation of chromosomal replication. B. abortus cell-cycle progression is coordinated with intracellular trafficking in the endosomal compartments. Bacteria are first blocked at the G1 stage, growth and chromosome replication being resumed shortly before reaching the intracellular proliferation compartment. The control mechanisms of cell cycle are similar to those reported for the bacterium Caulobacter crescentus, and they are crucial for survival in the host cell. The development of single-cell analyses could also be applied to other bacterial pathogens to investigate their cell-cycle progression during infection. contains the bacterium during intracellular trafficking. There is usually one bacterium per vacuole, and this vacuole harbours different markers, for example, Lamp1 and calnexin, that respectively allow the discrimination between endosomal BCV (eBCV) and replicative BCV (rBCV). a key stage of the cell cycle is division. After division, the newly generated cells grow. Prior to initiation of DNA replication, cells are classified as G1 bacteria or newborns. After initiation of DNA replication, cells are at the S stage of the cell cycle. The G2 stage corresponds to bacteria that have completed DNA replication but have not completed cell division. Since replication termination (ter) sites can remain associated even after the completion of their duplication [70Deghorain M. et al.A defined terminal region of the E. coli chromosome shows late segregation and high FtsK activity.PLoS ONE. 2011; 6: e22164Crossref PubMed Scopus (25) Google Scholar], it is difficult to distinguish S from G2 phases at the experimental level. the new poles are produced by cell division, while old poles exist before cell division [71Van der Henst C. et al.The Brucella pathogens are polarized bacteria.Microbes Infect. 2013; 15: 998-1004Crossref PubMed Scopus (23) Google Scholar]. In Brucella abortus, two proteins (PdhS and FumC) are known to be associated with the old pole [51Hallez R. et al.The asymmetric distribution of the essential histidine kinase PdhS indicates a differentiation event in Brucella abortus.EMBO J. 2007; 26: 1444-1455Crossref PubMed Scopus (59) Google Scholar, 72Mignolet J. et al.PdhS, an old-pole-localized histidine kinase, recruits the fumarase FumC in Brucella abortus.J. Bacteriol. 2010; 192: 3235-3239Crossref PubMed Scopus (20) Google Scholar], while others, such as IfoP, PopZ, or AidB, are mainly localized at the new pole [22Deghelt M. et al.G1-arrested newborn cells are the predominant infectious form of the pathogen Brucella abortus.Nat. Commun. 2014; 5: 4366Crossref PubMed Scopus (60) Google Scholar, 73Dotreppe D. et al.The alkylation response protein AidB is localized at the new poles and constriction sites in Brucella abortus.BMC Microbiol. 2011; 11: 257Crossref PubMed Scopus (15) Google Scholar]. are signal transduction systems composed of a least two proteins: (i) a histidine kinase (HK) that autophosphorylates on a conserved histidine residue in response to a signal, and (ii) a response regulator (RR) that catalyzes phosphotransfer from the phosphohistidine of the HK to itself, on a conserved aspartate residue. In phosphorelays, hybrid HK proteins such as CckA are frequently involved. They are composed of a classical HK domain followed by a domain typical of RR, with a conserved aspartate residue involved in phosphotransfer. A histidine phosphotransferase (like ChpT) acts as an intermediate to provide a phosphoryl group to an RR, that is often fused to a DNA-binding domain, like CtrA." @default.
• W1890640081 created "2016-06-24" @default.
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• W1890640081 creator A5028480429 @default.
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• W1890640081 creator A5076539728 @default.
• W1890640081 date "2015-12-01" @default.
• W1890640081 modified "2023-10-03" @default.
• W1890640081 title "Brucella abortus Cell Cycle and Infection Are Coordinated" @default.
• W1890640081 cites W1531468991 @default.
• W1890640081 cites W1572283162 @default.
• W1890640081 cites W1601058961 @default.
• W1890640081 cites W1603236694 @default.
• W1890640081 cites W1791474524 @default.
• W1890640081 cites W1875928935 @default.
• W1890640081 cites W1916729042 @default.
• W1890640081 cites W1933176742 @default.
• W1890640081 cites W1975597142 @default.
• W1890640081 cites W1982227919 @default.
• W1890640081 cites W1983937258 @default.
• W1890640081 cites W1987637706 @default.
• W1890640081 cites W1988242871 @default.
• W1890640081 cites W1991862301 @default.
• W1890640081 cites W1995164239 @default.
• W1890640081 cites W1997134402 @default.
• W1890640081 cites W1998258971 @default.
• W1890640081 cites W1998744918 @default.
• W1890640081 cites W2001078622 @default.
• W1890640081 cites W2002467143 @default.
• W1890640081 cites W2006002169 @default.
• W1890640081 cites W2009479311 @default.
• W1890640081 cites W2010009494 @default.
• W1890640081 cites W2014345020 @default.
• W1890640081 cites W2015172896 @default.
• W1890640081 cites W2018635122 @default.
• W1890640081 cites W2020368219 @default.
• W1890640081 cites W2026397514 @default.
• W1890640081 cites W2030581339 @default.
• W1890640081 cites W2032772890 @default.
• W1890640081 cites W2034750183 @default.
• W1890640081 cites W2035356844 @default.
• W1890640081 cites W2037447864 @default.
• W1890640081 cites W2038844415 @default.
• W1890640081 cites W2041594648 @default.
• W1890640081 cites W2046489364 @default.
• W1890640081 cites W2048802523 @default.
• W1890640081 cites W2050478109 @default.
• W1890640081 cites W2050896016 @default.
• W1890640081 cites W2055112546 @default.
• W1890640081 cites W2058681460 @default.
• W1890640081 cites W2059471882 @default.
• W1890640081 cites W2059770256 @default.
• W1890640081 cites W2064102729 @default.
• W1890640081 cites W2064834654 @default.
• W1890640081 cites W2065719622 @default.
• W1890640081 cites W2067912028 @default.
• W1890640081 cites W2076198421 @default.
• W1890640081 cites W2077116102 @default.
• W1890640081 cites W2078805723 @default.
• W1890640081 cites W2080878746 @default.
• W1890640081 cites W2085163337 @default.
• W1890640081 cites W2098259424 @default.
• W1890640081 cites W2099611734 @default.
• W1890640081 cites W2102121381 @default.
• W1890640081 cites W2102543221 @default.
• W1890640081 cites W2106023579 @default.
• W1890640081 cites W2113557404 @default.
• W1890640081 cites W2114849808 @default.
• W1890640081 cites W2115445120 @default.
• W1890640081 cites W2117918973 @default.
• W1890640081 cites W2120470223 @default.
• W1890640081 cites W2122630531 @default.
• W1890640081 cites W2126542112 @default.
• W1890640081 cites W2132043678 @default.
• W1890640081 cites W2133758259 @default.
• W1890640081 cites W2138150103 @default.
• W1890640081 cites W2143475578 @default.
• W1890640081 cites W2147281068 @default.
• W1890640081 cites W2154657387 @default.
• W1890640081 cites W2155608445 @default.
• W1890640081 cites W2156192464 @default.
• W1890640081 cites W2157121604 @default.
• W1890640081 cites W2158034262 @default.
• W1890640081 cites W2160765784 @default.
• W1890640081 cites W2170143290 @default.
• W1890640081 cites W2187120149 @default.
• W1890640081 cites W2460832886 @default.
• W1890640081 doi "https://doi.org/10.1016/j.tim.2015.09.007" @default.
• W1890640081 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/26497941" @default.
• W1890640081 hasPublicationYear "2015" @default.
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