Copper tolerance mediated by polyphosphate degradation and low-affinity inorganic phosphate transport system in Escherichia coli

Grillo-Puertas, Mariana; Schurig-Briccio, Lici A.; Rodrı́guez-Montelongo, Luisa; Rintoul, María R.; Rapisarda, Viviana Andrea

doi:10.1186/1471-2180-14-72

Cited by 40 publications

(31 citation statements)

References 39 publications

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“…In addition, polyP has been shown to facilitate export of Cu 2+ from the cell (Figure 2D). The details of this mechanism have recently been elucidated in E. coli , where Cu 2+ tolerance was shown to depend on polyP synthesis by PPK, polyP degradation by PPX, and the metal-phosphate symporters PitA or PitB [24], supporting a model in which Cu 2+ is first chelated by polyP to reduce its toxicity, followed by PPX cleavage of PO 4 3− from polyP and co-export of the resulting PO 4 3− and Cu 2+ via the Pit system. This model is consistent with earlier work on Cu 2+ -resistance in Sulfolobus metallicus [25] and both Cd 2+ and Hg 2+ resistance in E. coli [26,27].…”

Section: Polyphosphate Defends Against the Fenton Reactionmentioning

confidence: 99%

Oxidative stress protection by polyphosphate—new roles for an old player

Gray¹,

Jakob²

2015

Current Opinion in Microbiology

153

133

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Inorganic polyphosphate is a universally conserved biopolymer, whose association with oxidative stress resistance has been documented in many species, but whose mode of action has been poorly understood. Here we review the recent discovery that polyphosphate functions as a protein-protective chaperone, examine the mechanisms by which polyphosphate-metal ion interactions reduce oxidative stress, and summarize polyphosphate’s roles in regulating general stress response pathways. Given the simple chemical structure and ancient pedigree of polyphosphate, these diverse mechanisms are likely to be broadly relevant in many organisms, from bacteria to mammalian cells.

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Section: Polyphosphate Defends Against the Fenton Reactionmentioning

confidence: 99%

Oxidative stress protection by polyphosphate—new roles for an old player

Gray¹,

Jakob²

2015

Current Opinion in Microbiology

153

133

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“…For example, it is involved in metal detoxification and can function as a primitive chaperone to protect against oxidative damage [90][91][92]. Of importance to our discussion here, Keasling hypothesized that E. coli cells could detoxify metals by sequestering them with intracellular polyP.…”

Section: The Response To High Levels Of Extracellular Pimentioning

confidence: 99%

Molecular Mechanisms of Phosphate Homeostasis in <i>Escherichia coli</i>

McCleary¹

2017

≪i>Escherichia Coli

14
2
12
0

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Life's processes absolutely require inorganic phosphate for structural and energetic purposes. Escherichia coli has developed sophisticated mechanisms to acquire phosphate and to maintain intracellular amounts at optimal levels. The processes by which these simple cells maintain stable intracellular concentrations of phosphate are termed phosphate homeostasis, which involves mechanisms to balance the import, assimilation, sequestration, and export of phosphate. This chapter introduces the proteins involved in phosphate homeostasis and reviews information concerning the multiple phosphate transporters and the mechanisms by which they are regulated. It also introduces new concepts of how this bacterium responds to elevated extracellular levels of phosphate and presents a model for the integration of all of these processes to achieve homeostasis. The predominant importers are PitA, PitB, and the PstSCAB complex. Assimilation, or the incorporation of Pi into organic molecules, occurs primarily through the formation of ATP. Gene regulation relies on the PhoB/PhoR two-component system and the formation of a signaling complex at the membrane. The amount of intracellular phosphate can be fine-tuned through the formation or degradation of polyphosphate. Polyphosphate formation requires adequate supplies of ATP. In addition, when intracellular phosphate levels become too high, phosphate can be exported through PitA, PitB, or the YjbB transporters.

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“…Bacteria from diverse phyla synthesize polyP in response to multiple stressors, including amino acid starvation, oxidative stress, heat shock, salt stress, and heavy metal exposure, and mutants lacking the ppk gene, which encodes the polyP-synthesizing kinase PPK, are highly sensitive to these and other stresses (25,(27)(28)(29)(30). The mechanisms by which polyP mediates bacterial stress resistance are not completely characterized, but in E. coli, polyP is known to act as a protein-stabilizing chaperone, as a metal chelator, and as a regulator of RNA polymerase and DNA polymerase IV activity, ribosomal translation fidelity, and transcription, including that of rpoS, which encodes the general stress response sigma factor S (3,25,27,28,(31)(32)(33)(34)(35)(36)(37). Surprisingly, however, very little is currently known about the molecular details of how polyP accumulation is itself regulated in response to different stress conditions.…”

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confidence: 99%

Inorganic Polyphosphate Accumulation in Escherichia coli Is Regulated by DksA but Not by (p)ppGpp
Gray
¹

2019
J Bacteriol
46
11
70
0
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Production of inorganic polyphosphate (polyP) by bacteria is triggered by a variety of different stress conditions. polyP is required for stress survival and virulence in diverse pathogenic microbes. Previous studies have hypothesized a model for regulation of polyP synthesis in which production of the stringent-response second messenger (p)ppGpp directly stimulates polyP accumulation. In this work, I have now shown that this model is incorrect, and (p)ppGpp is not required for polyP synthesis in Escherichia coli. However, stringent mutations of RNA polymerase that frequently arise spontaneously in strains defective in (p)ppGpp synthesis and null mutations of the stringentresponse-associated transcription factor DksA both strongly inhibit polyP accumulation. The loss of polyP synthesis in a mutant lacking DksA was reversed by deletion of the transcription elongation factor GreA, suggesting that competition between these proteins for binding to the secondary channel of RNA polymerase plays an important role in controlling polyP activation. These results provide new insights into the poorly understood regulation of polyP synthesis in bacteria and indicate that the relationship between polyP and the stringent response is more complex than previously suspected. IMPORTANCE Production of polyP in bacteria is required for virulence and stress response, but little is known about how bacteria regulate polyP levels in response to changes in their environments. Understanding this regulation is important for understanding how pathogenic microbes resist killing by disinfectants, antibiotics, and the immune system. In this work, I have clarified the connections between polyP regulation and the stringent response to starvation stress in Escherichia coli and demonstrated an important and previously unknown role for the transcription factor DksA in controlling polyP levels. KEYWORDS (p)ppGpp, DksA, inorganic polyphosphate, stringent response B acteria in nature are rarely found under conditions that are ideal for their growth, and they regulate their gene expression and metabolism to optimize growth and survival under a variety of nonoptimal conditions (1-5). This is known as "stress response" and is key to understanding, for example, how pathogenic bacteria resist attack by antibiotics or the immune system. The intricate regulatory mechanisms that bacteria use to sense and respond to various stresses have been the subject of intense study for many years. While different bacteria have a wide variety of transcription factors and other regulators that sense and respond to particular stressors, general stress response mechanisms, which are triggered by a broad range of conditions that adversely affect bacterial growth, are among the most widely conserved pathways across the bacterial domain.One such highly conserved bacterial general stress response pathway, the stringent response, controls how bacteria respond to a variety of starvation stresses, and it has been studied for nearly 50 years (reviewed in references 6 to 8). When bact...

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Copper tolerance mediated by polyphosphate degradation and low-affinity inorganic phosphate transport system in Escherichia coli

Cited by 40 publications

References 39 publications

Oxidative stress protection by polyphosphate—new roles for an old player

Oxidative stress protection by polyphosphate—new roles for an old player

Molecular Mechanisms of Phosphate Homeostasis in <i>Escherichia coli</i>

Inorganic Polyphosphate Accumulation in Escherichia coli Is Regulated by DksA but Not by (p)ppGpp

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