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© Research
Publication : Science (New York, N.Y.)

A role for SIRT2-dependent histone H3K18 deacetylation in bacterial infection

Team: Biomics
Team: Bacteria-Cell Interactions
Member: Jean-Yves Coppee
Member: Pascale Cossart
Member: Mélanie Hamon
Scientific Fields
Diseases
Organisms
Applications
Technique

Published in Science (New York, N.Y.) - 01 Aug 2013

Eskandarian HA, Impens F, Nahori MA, Soubigou G, Coppée JY, Cossart P, Hamon MA

Link to Pubmed [PMID] – 23908241

Science 2013 Aug;341(6145):1238858

Pathogens dramatically affect host cell transcription programs for their own profit during infection, but in most cases, the underlying mechanisms remain elusive. We found that during infection with the bacterium Listeria monocytogenes, the host deacetylase sirtuin 2 (SIRT2) translocates to the nucleus, in a manner dependent on the bacterial factor InlB. SIRT2 associates with the transcription start site of a subset of genes repressed during infection and deacetylates histone H3 on lysine 18 (H3K18). Infecting cells in which SIRT2 activity was blocked or using SIRT2(-/-) mice resulted in a significant impairment of bacterial infection. Thus, SIRT2-mediated H3K18 deacetylation plays a critical role during infection, which reveals an epigenetic mechanism imposed by a pathogenic bacterium to reprogram its host.