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Customizing Host Chromatin: a Bacterial Tale

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  • Authors: Michael Connor1, Laurence Arbibe2, Mélanie Hamon3
  • Editors: Pascale Cossart4, Craig R. Roy5, Philippe Sansonetti6
  • VIEW AFFILIATIONS HIDE AFFILIATIONS
    Affiliations: 1: Institut Pasteur, G5 Chromatine et Infection, Paris, France; 2: INSERM U1151, CNRS UMR 8253, Institut Necker Enfants Malades, INEM Institute Department of Immunology, Infectiology and Hematology, Paris, France; 3: Institut Pasteur, G5 Chromatine et Infection, Paris, France; 4: Institut Pasteur, Paris, France; 5: Yale University School of Medicine, New Haven, Connecticut; 6: Institut Pasteur, Paris, France
  • Source: microbiolspec April 2019 vol. 7 no. 2 doi:10.1128/microbiolspec.BAI-0015-2019
  • Received 02 August 2018 Accepted 10 January 2019 Published 05 April 2019
  • Mélanie Hamon, [email protected]
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  • Abstract:

    Successful bacterial colonizers and pathogens have evolved with their hosts and have acquired mechanisms to customize essential processes that benefit their lifestyle. In large part, bacterial survival hinges on shaping the transcriptional signature of the host, a process regulated at the chromatin level. Modifications of chromatin, either on histone proteins or on DNA itself, are common targets during bacterium-host cross talk and are the focus of this article.

  • Citation: Connor M, Arbibe L, Hamon M. 2019. Customizing Host Chromatin: a Bacterial Tale. Microbiol Spectrum 7(2):BAI-0015-2019. doi:10.1128/microbiolspec.BAI-0015-2019.

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/content/journal/microbiolspec/10.1128/microbiolspec.BAI-0015-2019
2019-04-05
2019-10-16

Abstract:

Successful bacterial colonizers and pathogens have evolved with their hosts and have acquired mechanisms to customize essential processes that benefit their lifestyle. In large part, bacterial survival hinges on shaping the transcriptional signature of the host, a process regulated at the chromatin level. Modifications of chromatin, either on histone proteins or on DNA itself, are common targets during bacterium-host cross talk and are the focus of this article.

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Image of FIGURE 1
FIGURE 1

Nuclear effectors targeting histone marks. Secreted effectors from , , and translocate to the nucleus, where they directly act either upon the nucleosome itself (Rv1988 and OspF), bind chromatin readers to displace them (LntA), or bind chromatin readers to dephosphorylate them (OspF). Small black arrows around modifications indicate whether they are being deposited or removed.

Source: microbiolspec April 2019 vol. 7 no. 2 doi:10.1128/microbiolspec.BAI-0015-2019
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Image of FIGURE 2
FIGURE 2

SET domain effectors mediate histone methylation. Effectors of , , and contain the eukaryotic SET domain. Once translocated to the nucleus, these effectors target histones for direct methylation either globally or at specific residues. For and , this leads to repression of the host immune response and is thought to aid pathogen survival.

Source: microbiolspec April 2019 vol. 7 no. 2 doi:10.1128/microbiolspec.BAI-0015-2019
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Image of FIGURE 3
FIGURE 3

Targeting host DNA. Genotoxins such as CDT and colibactin induce host DNA breaks through either DNase activity (CDT) or DNA cross-linking (colibactin). targets host DNA directly for methylation with Rv2966c at non-CpG elements or induces hypomethylation through an unknown effector at CpG islands.

Source: microbiolspec April 2019 vol. 7 no. 2 doi:10.1128/microbiolspec.BAI-0015-2019
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