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Author Spotlight: Advancements in Understanding and Combatting Shigella Infections
Published on: February 9, 2024
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Shigella flexneri targets the HP1γ subcode through the phosphothreonine lyase OspF
Habiba Harouz1, Christophe Rachez2, Benoit M Meijer1
1Unité de Pathogénie Microbienne Moléculaire, Unité INSERM 786 Institut Pasteur, Paris, France.
The EMBO Journal
|September 14, 2014
Summary
Shigella bacteria hijack host transcription by altering HP1γ protein phosphorylation, impacting gene expression and potentially reprogramming the mucosal barrier. This bacterial manipulation of host epigenetic regulators offers new insights into host-pathogen interactions.
Area of Science:
- Microbiology
- Epigenetics
- Molecular Biology
Background:
- Heterochromatin protein 1 (HP1) proteins regulate transcription and are modified post-translationally, similar to histones.
- HP1γ phosphorylation, particularly at serine 83 (S83), is a marker for active transcription.
- Shigella enterocolitis involves bacterial manipulation of host cellular processes.
Purpose of the Study:
- To investigate how Shigella flexneri affects HP1γ phosphorylation in a guinea pig model.
- To elucidate the mechanism by which Shigella interferes with HP1γ phosphorylation.
- To understand the transcriptional consequences of Shigella-mediated HP1γ modulation.
Main Methods:
- Utilized a guinea pig model of Shigella enterocolitis.
- Analyzed HP1γ phosphorylation levels in response to wild-type and mxiD mutant Shigella strains.
- Investigated the interaction between Shigella effector OspF and HP1γ.
- Assessed the roles of ERK and MSK1 kinases in HP1γ phosphorylation.
- Performed genome-wide transcriptome analysis.
Main Results:
- A defective Shigella strain (mxiD) induced greater HP1γ phosphorylation in the colon compared to the wild-type strain.
- Shigella's phospholyase OspF inactivates ERK and MSK1, leading to altered HP1γ phosphorylation at S83.
- MSK1 was identified as a novel kinase phosphorylating HP1γ at S83 within an MSK1-HP1γ complex.
- This mechanism promotes HP1γ accumulation on target genes.
- Transcriptome analysis showed upregulation of proliferative genes and fine-tuning of immune gene expression.
Conclusions:
- Bacteria can control host transcription by modulating HP1 protein activity, extending beyond histone modification.
- Shigella utilizes effector proteins like OspF to manipulate host HP1γ phosphorylation, influencing gene expression.
- This bacterial strategy has implications for transcriptional reprogramming at the mucosal barrier and host-pathogen interactions.
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