Histone H3 deacetylation promotes host cell viability for efficient infection by Listeria monocytogenes.

ABSTRACT: For many intracellular bacterial pathogens manipulating host cell survival is essential for maintaining their replicative niche, and is a common strategy used to promote infection. The bacterial pathogen Listeria monocytogenes is well known to hijack host machinery for its own benefit, such as targeting the host histone H3 for modification by SIRT2. However, by what means this modification benefits infection, as well as the molecular players involved, were unknown. Here we show that SIRT2 activity supports Listeria intracellular survival by maintaining genome integrity and host cell viability. This protective effect is dependent on H3K18 deacetylation, which safeguards the host genome by counteracting infection-induced DNA damage. Mechanistically, infection causes SIRT2 to interact with th

SUBMITTER: Eldridge MJG 

PROVIDER: S-EPMC8722725 | biostudies-literature | 2021 Dec

REPOSITORIES: biostudies-literature