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Comment
. 2014 Nov 18;33(22):2598-600.
doi: 10.15252/embj.201489934. Epub 2014 Sep 22.

Shigella hacks host immune responses by reprogramming the host epigenome

Hiroshi Ashida  1 , Chihiro Sasakawa  2
Affiliations
Comment

Shigella hacks host immune responses by reprogramming the host epigenome

Hiroshi Ashida et al. EMBO J. .

Abstract

Bacterial pathogens alter host transcriptional programs to promote infection. Shigella OspF is an essential virulence protein with a unique phosphothreonine lyase activity. A new study in The EMBO Journal (Harouz et al, 2014) reveals a novel function of OspF: targeting of heterochromatin protein 1γ (HP1γ) and downregulation of a subset of immune genes. These results illustrate how bacterial pathogens exploit epigenetic modifications to counteract host immune responses.

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Figures

Figure 1
Figure 1. Shigella reprograms host transcriptional response by injecting the T3SS effector OspF
(left panel) Shigella WT delivers OspF, which translocates into the nucleus and dephosphorylates MAPK, thereby blocking phosphorylation of histone H3 at Ser10 and HP1γ at Ser83. Dephosphorylated histone H3 and HP1γ repress transcription of specific immunity-related genes such as IL8. (right panel) Shigella ΔospF infection triggers MAPK activation, which induces phosphorylation of histone H3 at Ser10 and HP1γ at Ser83. Phosphorylated histone H3 and HP1γ promote transcriptional activation, resulting in production of IL-8, which in turn recruits neutrophils to limit and clear Shigella infection.
See this image and copyright information in PMC

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References

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