Hamon MA, Cossart PHistone modifications and chromatin remodeling during bacterial infections. Cell Host Microbe 4:100-109

Institut Pasteur, Unité des Interactions Bactéries-Cellules, Paris, F-75015 France.
Cell host & microbe (Impact Factor: 12.33). 09/2008; 4(2):100-9. DOI: 10.1016/j.chom.2008.07.009
Source: PubMed


The long coexistence of bacterial pathogens with their eukaryotic hosts, and their coevolution, have provided pathogens with an amazing capacity to exploit host cell functions for survival, replication inside or outside cells, and escape from early innate immune responses. The fact that bacteria are so well adapted to their host has been of great benefit for cell biologists who are increasingly using them to study fundamental cell processes. In this Review, we will discuss the emergence of chromatin modification as a mechanism by which bacteria affect their host. Similar to viruses, bacteria provoke histone modifications and chromatin remodeling in infected cells, thereby altering the host's transcriptional program and in most cases dampening the host innate immune response. We will review our present knowledge of the effects of lipopolysaccharide (LPS), Mycobacteria, Shigella, Listeria, and Helicobacter on histones and chromatin. The particular case of tolerance to LPS is discussed. In addition, we report on bacterial homologs of eukaryotic chromatin-binding proteins, whose activity on eukaryotic targets are yet to be demonstrated.

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Available from: Mélanie Anne Hamon, Oct 30, 2014
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    • "Several bacteria can influence their host's transcription by secreting protein effectors that mimic host-endogenous transcriptional regulators and alter the epigenetic landscape of the host cells (Bierne 2013; Bierne & Cossart 2012; Bierne et al. 2012; Eskandarian et al. 2013; Hamon & Cossart 2008; Pennini et al. 2010; Rolando et al. 2013). Also certain influenza viruses make use of the hosts epigenetic machinery to replicate or hide within the hosts genome (Minárovits 2009) and the viral encoded histone-mimicking protein NS1 has been described to mediate transcriptional repression of the host cell's antiviral response (Marazzi et al. 2012). "
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