期刊
CELL HOST & MICROBE
卷 18, 期 6, 页码 649-658出版社
CELL PRESS
DOI: 10.1016/j.chom.2015.11.007
关键词
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资金
- NIH [5F32NS078954, F31NS076240, F31CA186654, CA181343, R01GM110058, NS042197, GM078366]
- Laboratory of Viral Diseases, Division of Intramural Research, National Institute of Allergy and Infectious Diseases, U.S. National Institutes of Health
Herpes simplex virus (HSV) reactivation from latent neuronal infection requires stimulation of lytic gene expression from promoters associated with repressive heterochromatin. Various neuronal stresses trigger reactivation, but how these stimuli activate silenced promoters remains unknown. We show that a neuronal pathway involving activation of c-Jun N-terminal kinase (JNK), common to many stress responses, is essential for initial HSV gene expression during reactivation. This JNK activation in neurons is mediated by dual leucine zipper kinase (DLK) and JNK-interacting protein 3 (JIP3), which direct JNK toward stress responses instead of other cellular functions. Surprisingly, JNK-mediated viral gene induction occurs independently of histone demethylases that remove repressive lysine modifications. Rather, JNK signaling results in a histone methyl/phospho switch on HSV lytic promoters, a mechanism permitting gene expression in the presence of repressive lysine methylation. JNK is present on viral promoters during reactivation, thereby linking a neuronal-specific stress pathway and HSV reactivation from latency.
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