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Bacterial Iron Homeostasis Regulation by sRNAs

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  • Authors: Sylvia Chareyre1, Pierre Mandin2
  • Editors: Gisela Storz3, Kai Papenfort4
  • VIEW AFFILIATIONS HIDE AFFILIATIONS
    Affiliations: 1: Aix Marseille Université-CNRS, Institut de Microbiologie de la Méditéranée, Laboratoire de Chimie Bactérienne, Marseille 13009, France; 2: Aix Marseille Université-CNRS, Institut de Microbiologie de la Méditéranée, Laboratoire de Chimie Bactérienne, Marseille 13009, France; 3: Division of Molecular and Cellular Biology, Eunice Kennedy Shriver National Institute of Child Health and Human Development, Bethesda, MD; 4: Department of Biology I, Microbiology, LMU Munich, Martinsried, Germany
  • Source: microbiolspec March 2018 vol. 6 no. 2 doi:10.1128/microbiolspec.RWR-0010-2017
  • Received 14 November 2017 Accepted 03 January 2018 Published 23 March 2018
  • Pierre Mandin, pmandin@imm.cnrs.fr
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  • Abstract:

    While iron is essential to sustain growth, its excess can be detrimental to the cell by generating highly toxic reactive oxygen species. Regulation of iron homeostasis thus plays a vital role in almost all living organisms. During the last 15 years, the small RNA (sRNA) RyhB has been shown to be a key actor of iron homeostasis regulation in bacteria. Through multiple molecular mechanisms, RyhB represses expendable iron-utilizing proteins, promotes siderophore production, and coordinates Fe-S cluster cofactor biogenesis, thereby establishing a so-called iron-sparing response. In this review, we will summarize knowledge on how sRNAs control iron homeostasis mainly through studies on RyhB in . The parallel roles and modes of action of other sRNAs in different bacteria will also be described. Finally, we will discuss what questions remain to be answered concerning this important stress response regulation by sRNAs.

  • Citation: Chareyre S, Mandin P. 2018. Bacterial Iron Homeostasis Regulation by sRNAs. Microbiol Spectrum 6(2):RWR-0010-2017. doi:10.1128/microbiolspec.RWR-0010-2017.

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2018-03-23
2018-04-22

Abstract:

While iron is essential to sustain growth, its excess can be detrimental to the cell by generating highly toxic reactive oxygen species. Regulation of iron homeostasis thus plays a vital role in almost all living organisms. During the last 15 years, the small RNA (sRNA) RyhB has been shown to be a key actor of iron homeostasis regulation in bacteria. Through multiple molecular mechanisms, RyhB represses expendable iron-utilizing proteins, promotes siderophore production, and coordinates Fe-S cluster cofactor biogenesis, thereby establishing a so-called iron-sparing response. In this review, we will summarize knowledge on how sRNAs control iron homeostasis mainly through studies on RyhB in . The parallel roles and modes of action of other sRNAs in different bacteria will also be described. Finally, we will discuss what questions remain to be answered concerning this important stress response regulation by sRNAs.

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Figures

Image of FIGURE 1
FIGURE 1

RyhB regulatory mechanisms. (A) RyhB represses expression of multiple mRNAs by inhibiting translation initiation and inducing mRNA degradation. RyhB base-pairing blocks ribosome attachment to the RBS. Consequently, the mRNA is degraded by RNase E recruitment at sites that can be distant from the base-pairing region. (B) RyhB promotes the degradation of the transcript by base-pairing to the translation initiation region of while the 5′ part of the mRNA, encoding , remains stable and is translated. (C) RyhB positively regulates expression by opening a stem-loop structure that otherwise inhibits ribosome attachment to the RBS. (D) RyhB activates translation of by displacing Hfq, which otherwise blocks ribosome attachment. (E) RyhB’s activity can be modulated thanks to the 3′ external transcribed spacer of the tRNA (in purple).

Source: microbiolspec March 2018 vol. 6 no. 2 doi:10.1128/microbiolspec.RWR-0010-2017
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Image of FIGURE 2
FIGURE 2

The iron-sparing response established by RyhB. Under iron-replete conditions, Fur-Fe represses expression. During iron starvation, Fur repression is abolished and RyhB is rapidly expressed. RyhB mediates an Fe-sparing response through three mechanisms: (A) RyhB represses the expression of mRNAs coding for iron-using proteins; (B) RyhB, together with IscR, orchestrates Fe-S biogenesis systems through regulation of the Isc machinery and expression; and (C) RyhB promotes Fe uptake via the upregulation of and and repression of the gene, which leads to serine accumulation used for enterobactin production.

Source: microbiolspec March 2018 vol. 6 no. 2 doi:10.1128/microbiolspec.RWR-0010-2017
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Tables

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TABLE 1

Summary of validated and putative RyhB targets using different set of data

Source: microbiolspec March 2018 vol. 6 no. 2 doi:10.1128/microbiolspec.RWR-0010-2017
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TABLE 2

Overview of Fe-sparing response by sRNA in bacteria

Source: microbiolspec March 2018 vol. 6 no. 2 doi:10.1128/microbiolspec.RWR-0010-2017

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