期刊
JOURNAL OF EXPERIMENTAL MEDICINE
卷 207, 期 8, 页码 1727-1743出版社
ROCKEFELLER UNIV PRESS
DOI: 10.1084/jem.20100276
关键词
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资金
- National Institutes of Health [41440, 32497]
- United States Department of Agriculture [58-0790-6-139]
Anaplasma phagocytophilum, the agent of human anaplasmosis, persists in ticks and mammals. We show that A. phagocytophilum induces the phosphorylation of actin in an Ixodes ricinus tick cell line and Ixodes scapularis ticks, to alter the ratio of monomeric/filamentous (G/F) actin. A. phagocytophilum-induced actin phosphorylation was dependent on Ixodes p21-activated kinase (IPAK1)-mediated signaling. A. phagocytophilum stimulated IPAK1 activity via the G protein-coupled receptor G.. subunits, which mediated phosphoinositide 3-kinase (PI3K) activation. Disruption of Ixodes g beta gamma, pi3k, and pak1 reduced actin phosphorylation and bacterial acquisition by ticks. A. phagocytophilum-induced actin phosphorylation resulted in increased nuclear G actin and phosphorylated actin. The latter, in association with RNA polymerase II (RNAPII), enhanced binding of TATA box-binding protein to RNAPII and selectively promoted expression of salp16, a gene crucial for A. phagocytophilum survival. These data define a mechanism that A. phagocytophilum uses to selectively alter arthropod gene expression for its benefit and suggest new strategies to interfere with the life cycle of this intracellular pathogen, and perhaps other Rickettsia-related microbes of medical importance.
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