The Fur homologue BosR requires Arg39 to activate rpoS transcription in Borrelia burgdorferi and thereby direct spirochaete infection in mice

Katona, Laura I.

doi:10.1099/mic.0.000166

Cited by 13 publications

(15 citation statements)

References 63 publications

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“…Rather, we and others recently reported that BosR functions as a critical virulence factor required by B. burgdorferi to infect mammals (35,37,38), which is linked to BosR's essentiality for activation of the central RpoN-RpoS pathway. More specifically, BosR binds to a DNA element called the BosR box in the rpoS promoter region and then activates the transcription of 54 -dependent rpoS (37,44,45). In addition, our microarray analyses (38) indicated that BosR may also influence the expression of many other genes (other than the RpoS regulon) potentially involved in borrelial physiology and metabolism, thereby substantiating its function as a potential global regulator in B. burgdorferi.…”

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confidence: 75%

Evidence that BosR (BB0647) Is a Positive Autoregulator in Borrelia burgdorferi

2016

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Borrelia burgdorferi survives in nature through a complex tick-mammalian life cycle. During its transit between ticks and mammalian hosts, B. burgdorferi must dramatically alter its outer surface profile in order to interact with and adapt to these two diverse niches. It has been established that the regulator BosR (BB0647) in B. burgdorferi plays important roles in modulating borrelial host adaptation. However, to date, how bosR expression itself is controlled in B. burgdorferi remains largely unknown. Previously, it has been shown that DNA sequences upstream of BosR harbor multiple sites for the binding of recombinant BosR, suggesting that BosR may influence its own expression in B. burgdorferi. However, direct experimental evidence supporting this putative autoregulation of BosR has been lacking. Here, we investigated the expression of bosR throughout the tick-mammal life cycle of B. burgdorferi via quantitative reverse transcription (RT)-PCR analyses. Our data indicated that bosR is expressed not only during mouse infection, but also during the tick acquisition, intermolt, and transmission phases. Further investigation revealed that bosR expression in B. burgdorferi is influenced by environmental stimuli, such as temperature shift and pH change. By employing luciferase reporter assays, we also identified two promoters potentially driving bosR transcription. Our study offers strong support for the long-postulated function of BosR as an autoregulator in B. burgdorferi.

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confidence: 75%

Evidence that BosR (BB0647) Is a Positive Autoregulator in Borrelia burgdorferi

2016

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“…Borrelia burgdorferi strains B31-A3, B31-A3Δ rpoS , B31-A3Δ rpoN , B31-A3Δ bosR -L9, and B31-A3Δ hk2 have been described previously ( Elias et al, 2000 ; Fisher et al, 2005 ; Xu et al, 2010 ; Katona, 2015 ). Membrane-permeable acids were tested as previously described ( Wilks and Slonczewski, 2007 ) with minor modifications.…”

Section: Methodsmentioning

confidence: 99%

Weak Organic Acids Decrease Borrelia burgdorferi Cytoplasmic pH, Eliciting an Acid Stress Response and Impacting RpoN- and RpoS-Dependent Gene Expression

Dulebohn

Richards

et al. 2017

Front. Microbiol.

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The spirochete Borrelia burgdorferi survives in its tick vector, Ixodes scapularis, or within various hosts. To transition between and survive in these distinct niches, B. burgdorferi changes its gene expression in response to environmental cues, both biochemical and physiological. Exposure of B. burgdorferi to weak monocarboxylic organic acids, including those detected in the blood meal of fed ticks, decreased the cytoplasmic pH of B. burgdorferi in vitro. A decrease in the cytoplasmic pH induced the expression of genes encoding enzymes that have been shown to restore pH homeostasis in other bacteria. These include putative coupled proton/cation exchangers, a putative Na+/H+ antiporter, a neutralizing buffer transporter, an amino acid deaminase and a proton exporting vacuolar-type VoV1 ATPase. Data presented in this report suggested that the acid stress response triggered the expression of RpoN- and RpoS-dependent genes including important virulence factors such as outer surface protein C (OspC), BBA66, and some BosR (Borrelia oxidative stress regulator)-dependent genes. Because the expression of virulence factors, like OspC, are so tightly connected by RpoS to general cellular stress responses and cell physiology, it is difficult to separate transmission-promoting conditions in what is clearly a multifactorial and complex regulatory web.

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“…47,55,56 In addition, RpoS represses ospAB transcription. 57 The RpoS-dependent transcriptome, which would be expressed by B. burgdorferi in the vertebrate, includes many other genes and encoding proteins involved in cell envelope biogenesis, transport, and metabolism and the chemotaxis and motility that are required during transmission and in the vertebrate host.…”

Section: Rpon-rpos Alternative Sigma Factor Cascadementioning

confidence: 99%

“…63,65–67 The mechanism by which Rrp2 is activated, presumably by phosphorylation, is enigmatic, because neither any of the annotated Hks, including its cognate Hk2, 63,68 nor acetyl phosphate 69 are culpable. In addition, rpoS transcription is activated by the PerR/Fur homolog Borrelia burgdorferi oxidative stress regulator (BosR) 56,70–74 and repressed by the XylR/NagC homolog BadR. 75,76 BosR not only binds to the rpoS promoter region 74 but also regulates, including via autoactivation 77 and ospAB repression, the expression of many RpoS-independent genes.…”

Section: Rpon-rpos Alternative Sigma Factor Cascadementioning

confidence: 99%

Gene Regulation During the Enzootic Cycle of the Lyme Disease Spirochete

Samuels

2016

Forum Immun Dis Ther

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Borrelia burgdorferi, the spirochete that causes Lyme disease, exists in an enzootic cycle, alternating between a tick vector and a vertebrate host. To adapt to and survive the environmental changes associated with its enzootic cycle, including nutrient availability, B. burgdorferi uses three different systems to regulate the expression of genes: RpoN-RpoS, histidine kinase (Hk)1/response regulator 1 (Rrp1), and RelBbu. The RpoN-RpoS alternative sigma factor cascade activates genes required for transmission from the tick to the vertebrate, maintenance of the vertebrate infection, and persistence in the tick. RelBbu controls the levels of the alarmones guanosine pentaphosphate and guanosine tetraphosphate, which are necessary for surviving the nutrient-deficient conditions in the midgut of the tick following absorption of the blood meal and the subsequent molt. The Hk1/Rrp1 two-component system produces cyclic dimeric guanosine monophosphate that regulates the genes required for the transitions between the tick and vertebrate as well as protective responses to the blood meal.

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The Fur homologue BosR requires Arg39 to activate rpoS transcription in Borrelia burgdorferi and thereby direct spirochaete infection in mice

Cited by 13 publications

References 63 publications

Evidence that BosR (BB0647) Is a Positive Autoregulator in Borrelia burgdorferi

Evidence that BosR (BB0647) Is a Positive Autoregulator in Borrelia burgdorferi

Weak Organic Acids Decrease Borrelia burgdorferi Cytoplasmic pH, Eliciting an Acid Stress Response and Impacting RpoN- and RpoS-Dependent Gene Expression

Gene Regulation During the Enzootic Cycle of the Lyme Disease Spirochete

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