An injected bacterial effector targets chromatin access for transcription factor NF-kappa B to alter transcription of host genes involved in immune responses
- Authors
- Arbibe, Laurence; Kim, Dong Wook; Batsche, Eric; Pedron, Thierry; Mateescu, Bogdan; Muchardt, Christian; Parsot, Claude; Sansonetti, Philippe J.
- Issue Date
- Jan-2007
- Publisher
- NATURE PUBLISHING GROUP
- Keywords
- SHIGELLA-FLEXNERI; MAP KINASE; HISTONE H3; EPITHELIAL-CELLS; ACTIVATION; EXPRESSION; PHOSPHOACETYLATION; PHOSPHORYLATION; RECRUITMENT; SECRETION
- Citation
- NATURE IMMUNOLOGY, v.8, no.1, pp.47 - 56
- Indexed
- SCIE
SCOPUS
- Journal Title
- NATURE IMMUNOLOGY
- Volume
- 8
- Number
- 1
- Start Page
- 47
- End Page
- 56
- URI
- https://scholarworks.bwise.kr/erica/handle/2021.sw.erica/43920
- DOI
- 10.1038/ni1423
- ISSN
- 1529-2908
- Abstract
- Phosphorylation of histone H3 at Ser10 increases chromatin accessibility to transcription factor NF-kappa B on a subset of genes involved in immune responses. Here we report that a bacterial pathogen abrogated phosphorylation of histone H3 to 'shape' the transcriptional responses of infected host cells. We identify the Shigella flexneri protein effector OspF as a dually specific phosphatase that dephosphorylated mitogen-activated protein kinases in the nucleus, thus preventing histone H3 phosphorylation at Ser10 in a gene-specific way. That activity of OspF enabled shigella to block the activation of a subset of NF-kappa B-responsive genes, leading to compromised recruitment of polymorphonuclear leukocytes to infected tissues. S. flexneri has thus evolved the capacity to precisely modulate host cell epigenetic 'information' as a strategy for repressing innate immunity.
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