Analysis of the RpoS regulon in <i>Borrelia burgdorferi</i> in response to mammalian host signals provides insight into RpoS function during the enzootic cycle

Caimano, Melissa J.; Iyer, Radha; Eggers, Christian H.; Gonzalez, Cynthia A.; Morton, Elizabeth A.; Gilbert, Michael A.; Schwartz, Ira; Radolf, Justin D.

doi:10.1111/j.1365-2958.2007.05860.x

Cited by 236 publications

(537 citation statements)

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“…77, 2009 CsrA OF B. BURGDORFERI 5159 following a blood meal (51,52). The significant increase in the levels of BBA64 upon overexpression of CsrA Bb independent of the environmental signals like pH or temperature is indicative of a distinct role for CsrA Bb , as BBA64 has been previously shown to be regulated by the RpoN/RpoS-dependent signaling network (20). It will be interesting to determine if the levels of BBA64 are coregulated by both CsrA and RpoN/ RpoS in response to various environmental signals.…”

Section: Discussionmentioning

confidence: 98%

“…In addition, the genome of B. burgdorferi codes for a limited number of regulators to control myriad metabolic processes, leading to overlapping or discrete networks responding to different environmental signals (32). Currently, much of the information on gene regulation in B. burgdorferi has been obtained from the analysis of a central regulatory pathway mediated by Rrp2-RpoN-RpoS (17,20,31,41,86). The activation of this pathway facilitates a concerted expression of a variety of borrelial determinants, such as OspC, DbpA/B, and BBK32, known to be involved in the pathogenic mechanisms of B. burgdorferi (41,86).…”

Section: Discussionmentioning

confidence: 99%

“…A central regulatory pathway comprising Rrp2-RpoN-RpoS has been characterized as regulating outer surface protein C (OspC), decorin binding protein A (DbpA), fibronectin binding protein BBK32, and several other borrelial determinants involved in various pathogenic processes (11, 17-20, 41, 88). Mutations in one or more of these regulators have also been characterized as having significant global effects on the transcriptional levels of a large number of ORFs in B. burgdorferi (12,17,20,31,61). Recently, it has also been shown that inactivation of ospAB constitutively activates the Rrp2-RpoNRpoS pathway, indicating mechanisms that are unique to B. burgdorferi and to its survival strategies in the tick vector and mammalian hosts (40).…”

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confidence: 99%

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Overexpression of CsrA (BB0184) Alters the Morphology and Antigen Profiles ofBorrelia burgdorferi

et al. 2009

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Section: Discussionmentioning

confidence: 98%

Section: Discussionmentioning

confidence: 99%

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confidence: 99%

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Overexpression of CsrA (BB0184) Alters the Morphology and Antigen Profiles ofBorrelia burgdorferi

et al. 2009

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“…In addition, all of the motility promoters identified so far are 70 -like (19,22,38). However, discrimination between S and 70 promoters in B. burgdorferi based on promoter consensus sequences is problematic (11,66). Recently, using microarray and transcriptional analysis, Caimano et al have shown that whereas flagellum biosynthetic genes are controlled by 70 both in vitro and in vivo, the methyl-accepting chemotaxis genes mcp1, mcp4, and mcp5 and the chemotaxis gene cheW2 are upregulated by S (RpoS) (11) during growth in vivo.…”

Section: Discussionmentioning

confidence: 99%

Borrelia burgdorferi Uniquely Regulates Its Motility Genes and Has an Intricate Flagellar Hook-Basal Body Structure

et al. 2008

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Borrelia burgdorferi is a flat-wave, motile spirochete that causes Lyme disease. Motility is provided by periplasmic flagella (PFs) located between the cell cylinder and an outer membrane sheath. The structure of these PFs, which are composed of a basal body, a hook, and a filament, is similar to the structure of flagella of other bacteria. To determine if hook formation influences flagellin gene transcription in B. burgdorferi, we inactivated the hook structural gene flgE by targeted mutagenesis. In many bacteria, completion of the hook structure serves as a checkpoint for transcriptional control of flagellum synthesis and other chemotaxis and motility genes. Specifically, the hook allows secretion of the anti-sigma factor FlgM and concomitant late gene transcription promoted by 28 . However, the control of B. burgdorferi PF synthesis differs from the control of flagellum synthesis in other bacteria; the gene encoding 28 is not present in the genome of B. burgdorferi, nor are any 28 promoter recognition sequences associated with the motility genes. We found that B. burgdorferi flgE mutants lacked PFs, were rod shaped, and were nonmotile, which substantiates previous evidence that PFs are involved in both cell morphology and motility. Although most motility and chemotaxis gene products accumulated at wild-type levels in the absence of FlgE, mutant cells had markedly decreased levels of the flagellar filament proteins FlaA and FlaB. Further analyses showed that the reduction in the levels of flagellin proteins in the spirochetes lacking FlgE was mediated at the posttranscriptional level. Taken together, our results indicate that in B. burgdorferi, the completion of the hook does not serve as a checkpoint for transcriptional regulation of flagellum synthesis. In addition, we also present evidence that the hook protein in B. burgdorferi forms a high-molecular-weight complex and that formation of this complex occurs in the periplasmic space.Borrelia burgdorferi, the causative agent of Lyme disease, is a spirochete with a characteristic flat-wave morphology (24, 25; for a review, see reference 12). As a result of their unusual morphology, B. burgdorferi and other spirochete species have a highly specialized ability that allows them to traverse viscous gellike media (8). This unique swimming ability enables these bacteria to penetrate into specific host connective tissues and ecological niches (43). The importance of motility as a virulence factor has been implicated in several spirochete species, including Treponema denticola (42), Brachyspira hyodysenteriae (54), Borrelia garinii (60), and B. burgdorferi (10, 56).Motility in B. burgdorferi is provided by bundles of between 7 and 11 periplasmic flagella (PFs) that are subterminally attached near the cell ends. These PFs extend inward along the cell cylinder beneath an outer membrane sheath (6,24,28,46). B. burgdorferi PFs have a structure similar to that of flagella of other bacteria; a PF is composed of a basal body, a hook, and a filament containing a single major ...

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“…A sensor-regulator pair of proteins also contributes to this regulation [154]. When B. burgdorferi mutants were tested in the infection model, rpoS and rpoN expression were found to be required for infecting mice [153,155], demonstrating the importance of this pathway for survival in a mammal.…”

Section: B Burgdorferi Products Required For Mammalian Infectionmentioning

confidence: 99%

Biology of Infection with Borrelia burgdorferi

Tilly

Rosa

Stewart

2008

Infectious Disease Clinics of North America

174

177

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The spirochete Borrelia burgdorferi is a tick-borne obligate parasite whose normal reservoir is a variety of small mammals [1]. Whereas infection of these natural hosts does not lead to disease, infection of humans can result in Lyme disease, as a consequence of the human immunopathological response to B. burgdorferi [2,3]. Consistent with the pathogenesis of Lyme disease, bacterial products that allow B. burgdorferi to replicate and survive, rather than true "virulence factors," appear to be primarily what is required for the bacterium to cause disease in a susceptible host. In support of this idea, the genome sequence of B31, the type strain of B. burgdorferi sensu stricto [4,5], revealed that the bacterium lacks factors common to many bacterial pathogens, such as lipopolysaccharide, toxins, and specialized secretion systems. In this chapter, we will describe the basic biology of B. burgdorferi, and some of the bacterial components required to infect and survive in the mammalian and tick hosts.

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Analysis of the RpoS regulon in Borrelia burgdorferi in response to mammalian host signals provides insight into RpoS function during the enzootic cycle

Abstract: Summary Borrelia burgdorferi (Bb) adapts to its arthropod and mammalian hosts by altering its transcriptional and antigenic profiles in response to

Cited by 236 publications

References 125 publications

Overexpression of CsrA (BB0184) Alters the Morphology and Antigen Profiles ofBorrelia burgdorferi

Overexpression of CsrA (BB0184) Alters the Morphology and Antigen Profiles ofBorrelia burgdorferi

Borrelia burgdorferi Uniquely Regulates Its Motility Genes and Has an Intricate Flagellar Hook-Basal Body Structure

Biology of Infection with Borrelia burgdorferi

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